Human genetic enhancement or human genetic engineering refers to human enhancement by means of a genetic modification. This could be done in order to cure diseases (gene therapy), prevent the possibility of getting a particular disease[1] (similarly to vaccines), to improve athlete performance in sporting events (gene doping), or to change physical appearance, metabolism, and even improve physical capabilities and mental faculties such as memory and intelligence.These genetic enhancements may or may not be done in such a way that the change is heritable (which has raised concerns within the scientific community).[2]

Genetic modification in order to cure genetic diseases is referred to as gene therapy. Many such gene therapies are available, made it through all phases of clinical research and are approved by the FDA. Between 1989 and December 2018, over 2,900 clinical trials were conducted, with more than half of them in phase I.[3] As of 2017, Spark Therapeutics' Luxturna (RPE65 mutation-induced blindness) and Novartis' Kymriah (Chimeric antigen receptor T cell therapy) are the FDA's first approved gene therapies to enter the market. Since that time, drugs such as Novartis' Zolgensma and Alnylam's Patisiran have also received FDA approval, in addition to other companies' gene therapy drugs. Most of these approaches utilize adeno-associated viruses (AAVs) and lentiviruses for performing gene insertions, in vivo and ex vivo, respectively. ASO / siRNA approaches such as those conducted by Alnylam and Ionis Pharmaceuticals require non-viral delivery systems, and utilize alternative mechanisms for trafficking to liver cells by way of GalNAc transporters.

Some people are immunocompromised and their bodies are hence much less capable of fending off and defeating diseases (i.e. influenza, ...). In some cases this is due to genetic flaws[clarification needed] or even genetic diseases such as SCID. Some gene therapies have already been developed or are being developed to correct these genetic flaws/diseases, hereby making these people less susceptible to catching additional diseases (i.e. influenza, ...).[4]

In November 2018, Lulu and Nana were created.[5] By using clustered regularly interspaced short palindromic repeat (CRISPR)-Cas9, a gene editing technique, they disabled a gene called CCR5 in the embryos, aiming to close the protein doorway that allows HIV to enter a cell and make the subjects immune to the HIV virus.

Athletes might adopt gene therapy technologies to improve their performance.[6] Gene doping is not known to occur, but multiple gene therapies may have such effects. Kayser et al. argue that gene doping could level the playing field if all athletes receive equal access. Critics claim that any therapeutic intervention for non-therapeutic/enhancement purposes compromises the ethical foundations of medicine and sports.[7]

Other hypothetical gene therapies could include changes to physical appearance, metabolism, mental faculties such as memory and intelligence.

Some congenital disorders (such as those affecting the muscoskeletal system) may affect physical appearance, and in some cases may also cause physical discomfort. Modifying the genes causing these congenital diseases (on those diagnosed to have mutations of the gene known to cause these diseases) may prevent this.

Also changes in the mystatin gene[8] may alter appearance.

Behavior may also be modified by genetic intervention.[9] Some people may be aggressive, selfish, ... and may not be able to function well in society.[clarification needed] There is currently research ongoing on genes that are or may be (in part) responsible for selfishness (i.e. ruthlessness gene, aggression (i.e. warrior gene), altruism (i.e. OXTR, CD38, COMT, DRD4, DRD5, IGF2, GABRB2[10])

There is some research going on on the hypothetical treatment of psychiatric disorders by means of gene therapy. It is assumed that, with gene-transfer techniques, it is possible (in experimental settings using animal models) to alter CNS gene expression and thereby the intrinsic generation of molecules involved in neural plasticity and neural regeneration, and thereby modifying ultimately behaviour.[11]

In recent years, it was possible to modify ethanol intake in animal models. Specifically, this was done by targeting the expression of the aldehyde dehydrogenase gene (ALDH2), lead to a significantly altered alcohol-drinking behaviour.[12] Reduction of p11, a serotonin receptor binding protein, in the nucleus accumbens led to depression-like behaviour in rodents, while restoration of the p11 gene expression in this anatomical area reversed this behaviour.[13]

Recently, it was also shown that the gene transfer of CBP (CREB (c-AMP response element binding protein) binding protein) improves cognitive deficits in an animal model of Alzheimers dementia via increasing the expression of BDNF (brain-derived neurotrophic factor).[14] The same authors were also able to show in this study that accumulation of amyloid- (A) interfered with CREB activity which is physiologically involved in memory formation.

In another study, it was shown that A deposition and plaque formation can be reduced by sustained expression of the neprilysin (an endopeptidase) gene which also led to improvements on the behavioural (i.e. cognitive) level.[15]

Similarly, the intracerebral gene transfer of ECE (endothelin-converting enzyme) via a virus vector stereotactically injected in the right anterior cortex and hippocampus, has also shown to reduce A deposits in a transgenic mouse model of Alzeimers dementia.[16]

There is also research going on on genoeconomics, a protoscience that is based on the idea that a person's financial behavior could be traced to their DNA and that genes are related to economic behavior. As of 2015, the results have been inconclusive. Some minor correlations have been identified.[17][18]

George Church has compiled a list of potential genetic modifications based on scientific studies for possibly advantageous traits such as less need for sleep, cognition-related changes that protect against Alzheimer's disease, disease resistances, higher lean muscle mass and enhanced learning abilities along with some of the associated studies and potential negative effects.[19][20]

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Human genetic enhancement - Wikipedia

Health problem caused by one or more abnormalities in the genome

Medical condition

A genetic disorder is a health problem caused by one or more abnormalities in the genome. It can be caused by a mutation in a single gene (monogenic) or multiple genes (polygenic) or by a chromosomal abnormality. Although polygenic disorders are the most common, the term is mostly used when discussing disorders with a single genetic cause, either in a gene or chromosome.[1][2] The mutation responsible can occur spontaneously before embryonic development (a de novo mutation), or it can be inherited from two parents who are carriers of a faulty gene (autosomal recessive inheritance) or from a parent with the disorder (autosomal dominant inheritance). When the genetic disorder is inherited from one or both parents, it is also classified as a hereditary disease. Some disorders are caused by a mutation on the X chromosome and have X-linked inheritance. Very few disorders are inherited on the Y chromosome or mitochondrial DNA (due to their size).[3]

There are well over 6,000 known genetic disorders,[4] and new genetic disorders are constantly being described in medical literature.[5] More than 600 genetic disorders are treatable.[6] Around 1 in 50 people are affected by a known single-gene disorder, while around 1 in 263 are affected by a chromosomal disorder.[7] Around 65% of people have some kind of health problem as a result of congenital genetic mutations.[7] Due to the significantly large number of genetic disorders, approximately 1 in 21 people are affected by a genetic disorder classified as "rare" (usually defined as affecting less than 1 in 2,000 people). Most genetic disorders are rare in themselves.[5][8]

Genetic disorders are present before birth, and some genetic disorders produce birth defects, but birth defects can also be developmental rather than hereditary. The opposite of a hereditary disease is an acquired disease. Most cancers, although they involve genetic mutations to a small proportion of cells in the body, are acquired diseases. Some cancer syndromes, however, such as BRCA mutations, are hereditary genetic disorders.[9]

A single-gene disorder (or monogenic disorder) is the result of a single mutated gene. Single-gene disorders can be passed on to subsequent generations in several ways. Genomic imprinting and uniparental disomy, however, may affect inheritance patterns. The divisions between recessive and dominant types are not "hard and fast", although the divisions between autosomal and X-linked types are (since the latter types are distinguished purely based on the chromosomal location of the gene). For example, the common form of dwarfism, achondroplasia, is typically considered a dominant disorder, but children with two genes for achondroplasia have a severe and usually lethal skeletal disorder, one that achondroplasics could be considered carriers for. Sickle-cell anemia is also considered a recessive condition, but heterozygous carriers have increased resistance to malaria in early childhood, which could be described as a related dominant condition.[17] When a couple where one partner or both are sufferers or carriers of a single-gene disorder wish to have a child, they can do so through in vitro fertilization, which enables preimplantation genetic diagnosis to occur to check whether the embryo has the genetic disorder.[18]

Most congenital metabolic disorders known as inborn errors of metabolism result from single-gene defects. Many such single-gene defects can decrease the fitness of affected people and are therefore present in the population in lower frequencies compared to what would be expected based on simple probabilistic calculations.[19]

Only one mutated copy of the gene will be necessary for a person to be affected by an autosomal dominant disorder. Each affected person usually has one affected parent.[20]:57 The chance a child will inherit the mutated gene is 50%. Autosomal dominant conditions sometimes have reduced penetrance, which means although only one mutated copy is needed, not all individuals who inherit that mutation go on to develop the disease. Examples of this type of disorder are Huntington's disease,[20]:58 neurofibromatosis type 1, neurofibromatosis type 2, Marfan syndrome, hereditary nonpolyposis colorectal cancer, hereditary multiple exostoses (a highly penetrant autosomal dominant disorder), tuberous sclerosis, Von Willebrand disease, and acute intermittent porphyria. Birth defects are also called congenital anomalies.

Two copies of the gene must be mutated for a person to be affected by an autosomal recessive disorder. An affected person usually has unaffected parents who each carry a single copy of the mutated gene and are referred to as genetic carriers. Each parent with a defective gene normally do not have symptoms.[21] Two unaffected people who each carry one copy of the mutated gene have a 25% risk with each pregnancy of having a child affected by the disorder. Examples of this type of disorder are albinism, medium-chain acyl-CoA dehydrogenase deficiency, cystic fibrosis, sickle cell disease, TaySachs disease, NiemannPick disease, spinal muscular atrophy, and Roberts syndrome. Certain other phenotypes, such as wet versus dry earwax, are also determined in an autosomal recessive fashion.[22][23] Some autosomal recessive disorders are common because, in the past, carrying one of the faulty genes led to a slight protection against an infectious disease or toxin such as tuberculosis or malaria.[24] Such disorders include cystic fibrosis,[25] sickle cell disease,[26] phenylketonuria[27] and thalassaemia.[28]

X-linked dominant disorders are caused by mutations in genes on the X chromosome. Only a few disorders have this inheritance pattern, with a prime example being X-linked hypophosphatemic rickets. Males and females are both affected in these disorders, with males typically being more severely affected than females. Some X-linked dominant conditions, such as Rett syndrome, incontinentia pigmenti type 2, and Aicardi syndrome, are usually fatal in males either in utero or shortly after birth, and are therefore predominantly seen in females. Exceptions to this finding are extremely rare cases in which boys with Klinefelter syndrome (44+xxy) also inherit an X-linked dominant condition and exhibit symptoms more similar to those of a female in terms of disease severity. The chance of passing on an X-linked dominant disorder differs between men and women. The sons of a man with an X-linked dominant disorder will all be unaffected (since they receive their father's Y chromosome), but his daughters will all inherit the condition. A woman with an X-linked dominant disorder has a 50% chance of having an affected fetus with each pregnancy, although in cases such as incontinentia pigmenti, only female offspring are generally viable.

X-linked recessive conditions are also caused by mutations in genes on the X chromosome. Males are much more frequently affected than females, because they only have the one X chromosome necessary for the condition to present. The chance of passing on the disorder differs between men and women. The sons of a man with an X-linked recessive disorder will not be affected (since they receive their father's Y chromosome), but his daughters will be carriers of one copy of the mutated gene. A woman who is a carrier of an X-linked recessive disorder (XRXr) has a 50% chance of having sons who are affected and a 50% chance of having daughters who are carriers of one copy of the mutated gene. X-linked recessive conditions include the serious diseases hemophilia A, Duchenne muscular dystrophy, and LeschNyhan syndrome, as well as common and less serious conditions such as male pattern baldness and redgreen color blindness. X-linked recessive conditions can sometimes manifest in females due to skewed X-inactivation or monosomy X (Turner syndrome).

Y-linked disorders are caused by mutations on the Y chromosome. These conditions may only be transmitted from the heterogametic sex (e.g. male humans) to
offspring of the same sex. More simply, this means that Y-linked disorders in humans can only be passed from men to their sons; females can never be affected because they do not possess Y-allosomes.

Y-linked disorders are exceedingly rare but the most well-known examples typically cause infertility. Reproduction in such conditions is only possible through the circumvention of infertility by medical intervention.

This type of inheritance, also known as maternal inheritance, is the rarest and applies to the 13 genes encoded by mitochondrial DNA. Because only egg cells contribute mitochondria to the developing embryo, only mothers (who are affected) can pass on mitochondrial DNA conditions to their children. An example of this type of disorder is Leber's hereditary optic neuropathy.

It is important to stress that the vast majority of mitochondrial diseases (particularly when symptoms develop in early life) are actually caused by a nuclear gene defect, as the mitochondria are mostly developed by non-mitochondrial DNA. These diseases most often follow autosomal recessive inheritance.[29]

Genetic disorders may also be complex, multifactorial, or polygenic, meaning they are likely associated with the effects of multiple genes in combination with lifestyles and environmental factors. Multifactorial disorders include heart disease and diabetes. Although complex disorders often cluster in families, they do not have a clear-cut pattern of inheritance. This makes it difficult to determine a person's risk of inheriting or passing on these disorders. Complex disorders are also difficult to study and treat because the specific factors that cause most of these disorders have not yet been identified. Studies that aim to identify the cause of complex disorders can use several methodological approaches to determine genotypephenotype associations. One method, the genotype-first approach, starts by identifying genetic variants within patients and then determining the associated clinical manifestations. This is opposed to the more traditional phenotype-first approach, and may identify causal factors that have previously been obscured by clinical heterogeneity, penetrance, and expressivity.

On a pedigree, polygenic diseases do tend to "run in families", but the inheritance does not fit simple patterns as with Mendelian diseases. This does not mean that the genes cannot eventually be located and studied. There is also a strong environmental component to many of them (e.g., blood pressure). Other factors include:

A chromosomal disorder is a missing, extra, or irregular portion of chromosomal DNA. It can be from an atypical number of chromosomes or a structural abnormality in one or more chromosomes. An example of these disorders is trisomy 21 (Down syndrome), in which there is an extra copy of chromosome 21.

Due to the wide range of genetic disorders that are known, diagnosis is widely varied and dependent of the disorder. Most genetic disorders are diagnosed pre-birth, at birth, or during early childhood however some, such as Huntington's disease, can escape detection until the patient is well into adulthood.

The basic aspects of a genetic disorder rests on the inheritance of genetic material. With an in depth family history, it is possible to anticipate possible disorders in children which direct medical professionals to specific tests depending on the disorder and allow parents the chance to prepare for potential lifestyle changes, anticipate the possibility of stillbirth, or contemplate termination.[30] Prenatal diagnosis can detect the presence of characteristic abnormalities in fetal development through ultrasound, or detect the presence of characteristic substances via invasive procedures which involve inserting probes or needles into the uterus such as in amniocentesis.[31]

Not all genetic disorders directly result in death; however, there are no known cures for genetic disorders. Many genetic disorders affect stages of development, such as Down syndrome, while others result in purely physical symptoms such as muscular dystrophy. Other disorders, such as Huntington's disease, show no signs until adulthood. During the active time of a genetic disorder, patients mostly rely on maintaining or slowing the degradation of quality of life and maintain patient autonomy. This includes physical therapy, pain management, and may include a selection of alternative medicine programs.

The treatment of genetic disorders is an ongoing battle, with over 1,800 gene therapy clinical trials having been completed, are ongoing, or have been approved worldwide.[32] Despite this, most treatment options revolve around treating the symptoms of the disorders in an attempt to improve patient quality of life.

Gene therapy refers to a form of treatment where a healthy gene is introduced to a patient. This should alleviate the defect caused by a faulty gene or slow the progression of the disease. A major obstacle has been the delivery of genes to the appropriate cell, tissue, and organ affected by the disorder. Researchers have investigated how they can introduce a gene into the potentially trillions of cells that carry the defective copy. Finding an answer to this has been a roadblock between understanding the genetic disorder and correcting the genetic disorder.[33]

Around 1 in 50 people are affected by a known single-gene disorder, while around 1 in 263 are affected by a chromosomal disorder.[7] Around 65% of people have some kind of health problem as a result of congenital genetic mutations.[7] Due to the significantly large number of genetic disorders, approximately 1 in 21 people are affected by a genetic disorder classified as "rare" (usually defined as affecting less than 1 in 2,000 people). Most genetic disorders are rare in themselves.[5][8] There are well over 6,000 known genetic disorders,[4] and new genetic disorders are constantly being described in medical literature.[5]

The earliest known genetic condition in a hominid was in the fossil species Paranthropus robustus, with over a third of individuals displaying amelogenesis imperfecta.[34]

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Genetic disorder - Wikipedia

Genetic Engineering additionally called genetic modification or genetic manipulation is the immediate control of a living being's genes using biotechnology. It is an arrangement of innovations used to change the hereditary forms of cells, including the exchange of qualities inside and across species limits to create enhanced or novel living beings.

Genetic Engineering has been connected in various fields including research, medicine, industrial biotechnology and agriculture. In research, GMOs are utilized to contemplate quality capacity and articulation through loss of function, gain of function, tracking and expression experiments. By thumping out genes responsible for specific conditions it is possible to create animal model organisms of human diseases. And in addition to producing hormones, immunizations and different drug genetic engineering can possibly fix hereditary diseases through quality treatment. Similar strategies that are utilized to create medications can likewise have mechanical applications, for example, producing enzymes for detergents, cheeses and different products.

The ascent of commercialised genetically modified crops has given a financial advantage to agriculturists in a wide range of nations, however, has additionally been the wellspring of a large portion of the debate encompassing the innovation. This has been available since its initial implementation, the primary field trials were destroyed by anti-GM activists. In spite of the fact that there is a logical accord that at presently accessible sustenance got from GM crops represents no more serious hazard to human wellbeing than regular nourishment, GM sustenance security is the main concern with critics.

Genetic engineering is the study of genes and the science of heredity. Genetic engineers or geneticists study living organisms ranging from human being to crops and even bacteria.

These professionals also conduct researches which is a major part of their work profile. The experiments are conducted to determine the origin and governing laws of a particular inherited trait. These traits include medical condition, diseases etc. The study is further used to seek our determinants responsible for the inherited trait.

Genetic engineers or Geneticists keep on finding ways to enhance their work profile depending on the place and organization they are working with. In manufacturing, these professionals will develop new pharmaceutical or agricultural products while in a medical setting, they advise patients on the diagnosed medical conditions that are inherited and also treat patients on the same.

Skill sets for Genetic engineers or Geneticists

Strong understanding of scientific methods and rules

complex problem solving and critical thinking

ability to use computer-aided design (CAD)

graphics or photo imaging

PERL, Python

word processing software programs

excellent mathematical, deductive and inductive reasoning, reading, writing, and oral comprehension skills

ability to use lasers spectrometers, light scattering equipment, binocular light compound microscopes, bench top centrifuges, or similar laboratory equipment

Typical responsibilities of a Genetic Engineering or Geneticist includes:

When a genetic engineer gains a year of experience, one of the regions they can indulge into is hereditary advising, which includes offering data, support and counsel on hereditary conditions to your patients.

An individual aspiring to pursue a professional degree in Genetic Engineering can begin the BTech course after his/her 10+2 Science with Physics, Chemistry, Maths and Biology.

Admission to BTech in Genetic Engineering is made through entrance tests conducted in-house by various universities or through the scores of national engineering entrance examination like JEE for IITs/NITs & CFTIs across the country.

Genetic Engineering professionals require a bachelors or masters degree in Genetic Engineering or Genetic Sciences for entry-level careers. In any case, a doctoral qualification is required for those looking for free research professions. Important fields of study in Genetic Engineering incorporate natural chemistry, biophysics or related fields.

Genetic Engineers require a solid comprehension of logical techniques and guidelines, and in addition complex critical thinking and basic reasoning aptitudes. Phenomenal scientific, deductive and inductive thinking aptitudes, and in addition perusing, composing, and oral cognizance abilities are additionally expected to work in this field.

A semester- wise breakup of the course is tabulated below

SEMESTER I

SEMESTER II

Mathematics 1

Mathematics 2

English

Material Science

Physics

Principles of Environmental Science

Chemistry

Biochemistry

Basic Engineering 1

Basic Engineering 2

-

Cell Biology

-

Value Education

SEMESTER III

SEMESTER IV

Enzyme Technology

Basic Molecular Techniques

Genetics & Cytogenetics

Molecular Biology

Immunology

Stoichiometry and Engineering Thermodynamics

Microbiology

Bio-press Principles

Mechanical Operations & heat Transfer

Biostatistics

German Language Phase 1/French Language Phase 1/Japanese Language Phase 1

German Language Phase 2/Japanese Language Phase 2/French Language Phase 2

-

SEMESTER V

SEMESTER VI

Advanced Molecular Techniques

Recombinant DNA Technology

Functional Genomics and Microarray Technology

Bioinformatics

Momentum Transfer

Chemical Reaction Engineering

Bioprocess Engineering

Gene Therapy

Biophysics

Biosensors and Biochips

Plant Tissue Culture and Transgenic Technology

-

Personality Development

-

SEMESTER VII

SEMESTER VIII

Bio-separation Technology

Project Work

Animal Cell Culture and Transgenic Technology

Bio-Safety, Bio-ethics, IPR & Patients

Nano-biotechnology in Healthcare

-

Stem Cell Biology

-

Aspirants who wish to join the engineering industry as a genetic engineer can apply for the following jobs profiles available:

JOB PROFILE

JOB DESCRIPTION

Genetic Engineer

They apply their knowledge ofengineering, biology, and biomechanical principles into the design, development, and evaluation of biological and health systems and products, such as artificial organs, prostheses, instrumentation, medical information systems, and health care and management.

Lecturer/Professor

They teach at undergraduate and graduate level in areas allocated and reviewed from time to time by the Head of Department.

Research Scientist

They are responsible for designing, undertaking and analyzing information from controlled laboratory-based investigations, experiments and trials.

Scientific/Medical Writer

The research, prepare and coordinate scientific publications. The medical writer is responsible for researching, writing and editing clinical/statistical reports and study protocols, and summarizing data from clinical studies.

Most of the engineering educational institutes shortlist candidates for admission Into BTech in Genetic Engineering course on the basis of engineering entrance exams. These entrance exams are either conducted at the national level like JEE or held in-house by various engineering institutes in the country.

Some of the popular engineering entrance examinations aspirants should consider appearing for admissions to UG and PG level Automobile engineering courses are:

Q. Which college is best for genetic engineering?

A. SRM University Chennai Tamil Nadu, Bharath University Chennai Tamil Nadu, Aryabhatta Knowledge University Patna Bihar, Jawaharlal Nehru Centre for Advanced Scientific Research Bangalore are some of the institutes offering genetic engineering

Q. Is Jee required for genetic engineering?

A. NITs and II
Ts across India does not offer genetic engineering. But there are 23 collages which take admission on the basis of JEE main

Q. What is the qualification for genetic engineering?

A. For admission to BTech Genetic Engineering course, the candidate is needed to have passed the Higher Secondary School Certificate (10+2) examination from a recognized Board of education with Biology, Physics and Chemistry as main subjects with a minimum aggregate score of 60%.

Q. Does IIT offer genetic engineering?

A. No, IIT directly does not offer genetic engineering. Candidates have to take Life Sciences in graduation or Biotechnology from any engineering college in India.

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Genetic Engineering - Courses, Subjects, Eligibility ...

The following points highlight the top four applications of genetic engineering. The applications are: 1. Application in Agriculture 2. Application to Medicine 3. Energy Production 4. Application to Industries.

An important application of recombinant DNA technology is to alter the genotype of crop plants to make them more productive, nutritious, rich in proteins, disease resistant, and less fertilizer consuming. Recombinant DNA technology and tissue culture techniques can produce high yielding cereals, pulses and vegetable crops.

Some plants have been genetically programmed to yield high protein grains that could show resistance to heat, moisture and diseases.

Some plants may even develop their own fertilizers some have been genetically transformed to make their own insecticides. Through genetic engineering some varieties have been produced that could directly fix atmospheric nitrogen and thus there is no dependence on fertilizers.

Scientists have developed transgenic potato, tobacco, cotton, corn, strawberry, rape seeds that are resistant to insect pests and certain weedicides.

Bacterium, Bacillus thurenginesis produces a protein which is toxic to insects. Using the techniques of genetic engineering, the gene coding for this toxic protein called Bt gene has been isolated from bacterium and engineered into tomato and tobacco plants. Such transgenic plants showed nee to tobacco horn worms and tomato fruit worms. These genotypes are awaiting release in USA.

There are certain genetically evolved weed killers which are not specific to weeds alone but kill useful crops also. Glyphosate is a commonly used weed killer which simply inhibits a particular essential enzyme in weeds and other crop plants. A target gene of glyphosate is present in bacterium salmonella typhimurium. A mutant of S. typhimurium is resistant to glyphosate.

The mutant gene was t cloned to E. coli and then recloned to Agrobacterium tumifaciens through its Ti Plasmid. Infection of plants with Ti plasmid containing glyphosate resistant gene has yielded crops such as cotton, tabacco maize, all of which are resistant to glyphosate.

This makes possible to spray the crop fields with glyphosate which will kill the weeds only and the genetically modified crops with resistant genes remain unaffected.

Recently Calogene, a biotech company, has isolated a bacterial gene that detoxifies; side effects of herbicides. Transgenic tobacco plants resistant to T MV mosaic virus and tomato i resistant to Golden mosaic virus have been developed by transferring virus coat protein genes susceptible plants. These are yet to be released.

The gene transfer technology can also play significant role in producing new and improved variety of timber trees.

Several species of microorganisms have been produced that can degrade toxic chemicals and could be used for killing harmful pathogens and insect pests.

For using genetic engineering techniques for transfer of foreign genes into host plant cells, a number of genes have already been cloned and complete libraries of DNA and mt DNA of pea are now known.

Some of the cloned genes include:

(i) Genes for phaseolin of french bean,

(ii) Few phaseolin leg haemoglobin for soybean,

(iii) Genes for small sub-unit RUBP carboxylase of pea, and i genes for storage protein in some cereals.

Efforts are being made to improve several agricultural crops using various techniques of genetic engineering which include:

(i) Transfer of nitrogen fixing genes (nif genes) from leguminous plants into cereals.

(ii) Transfer of resistance against pathogens and pests from wild plants to crop plants.

(iii) Improvement in quality and quantity of seed proteins.

(iv) Transfer of genes for animal proteins to crop plants.

(v) Elimination of unwanted genes for susceptibility to different diseases from cytoplasmic male sterile lines in crop like maize, where cytoplasmic male sterility and susceptibility are located in mitochondrial plasmid.

(vi) Improvement of photosynthetic efficiency by reassembling nuclear and chloroplast genes and by the possible conversion of C3 plants into C4 plants.

(vii) Development of cell lines which may produce nutritious food in bioreactors.

Genetic engineering has been gaining importance over the last few years and it will become more important in the current century as genetic diseases become more prevalent and agricultural area is reduced. Genetic engineering plays significant role in the production of medicines.

Microorganisms and plant based substances are now being manipulated to produce large amount of useful drugs, vaccines, enzymes and hormones at low costs. Genetic engineering is concerned with the study (inheritance pattern of diseases in man and collection of human genes that could provide a complete map for inheritance of healthy individuals.

Gene therapy by which healthy genes can be inserted directly into a person with malfunctioning genes is perhaps the most revolutionary and most promising aspect of genetic engineering. The use of gene therapy has been approved in more than 400 clinical trials for diseases such as cystic fibres emphysema, muscular dystrophy, adenosine deaminase deficiency.

Gene therapy may someday be exploited to cure hereditary human diseases like haemophilia and cystic fibrosis which are caused by missing or defective genes. In one type of gene therapy new functional genes are inserted by genetically engineered viruses into the cells of people who are unable to produce certain hormones or proteins for normal body functions.

Introduction of new genes into an organism through recombinant DNA technology essentially alters protein makeup and finally i body characteristics.

Vaccines:

Recombinant DNA Technology is also used in production of vaccines against diseases. A vaccine contains a form of an infectious organism that does not cause severe disease but does cause immune system of body to form protective antibodies against infective organism. Vaccines are prepared by isolating antigen or protein present on the surface of viral particles.

When a person is vaccinate against viral disease, antigens produce antibodies that acts against the viral proteins and inactivate them. With recombinant DNA technology, scientists have been able to transfer the genes for some viral sheath proteins to vaccinia virus which was used against small pox.

Vaccines produced by gene cloning are contamination free and safe because they contain only coat proteins against which antibodies are made. A few vaccines are being produced by gene cloning, e.g., vaccines against viral hepatitis influenza, herpes simplex virus, virus induced foot and mouth disease in animals.

Hormones:

Until recently the hormone insulin was extracted only in limited quantities from pancreas of cows and pigs. The process was not only costly but the hormone sometimes caused allergic reactions in some patients of diabetes.

The commercial production of insulin was started in 1982 through biogenetic or recombinant DNA technology and the medical use of hormone insulin was approved by food and drug administration (FDA) of USA in 1982.

The human insulin gene has been cloned in large quantities in bacterium E. coli which could be used for synthesis of insulin. Genetically engineered insulin is commercially available as humilin.

Lymphokines:

Lymphokines are proteins which regulate immune system in human body, -Interferon is one of the examples. Interferon is used to fight viral diseases such as hepatitis, herpes, common colds as well as cancer. Such drugs can be manufactured in bacterial cell in large quantities.

Lymphokines can also be helpful for AIDS patients. Genetically engineered interleukin-II, a substance that stimulates multiplication of lymphocytes is also available and is being currently tested on AIDS patients.

Somatostatin:

A fourteen aminoacid polypeptide hormone synthesized by hypothalamus was obtained only in a small quantity from a human cadavers. Somatostatin used as a drug for certain growth related abnormalities appears to be species specific and the polypeptide obtained from other mammals has no effect on human, hence its extraction from hypothalamus of cadavers.

Genetic engineering technique has helped in chemical synthesis of gene which is joined to the pBR 322 plasmid DNA and cloned into a bacterium. The transformed bacterium is converted into somatostatin synthesising factory. ADA (adenosine deaminase) deficiency is a disease like combined immune deficiency which killed the bubble boy David in 1984.

The children with ADA deficiency die before they are two years old. Bone marrow cells of the child after removal from the body were invaded by a harmless virus into which ADA has been inserted.

Erythropoetin, a genetically engineered hormone is used to stimulate the production of red blood cells in people suffering from severe anaemia.

Production of Blood clotting factors:

Normally heart attack is caused when coronary arteries are blocked by cholesterol or blood clot. plasminogen is a substance found in blood clots. Genetically engineered tissue plasminogen activator (tPA) enzyme dissolves blood clots in people who have suffered heart attacks. The plasminogen activator protein is produced by genetech company which is so potent and specific that it may even arrest a heart attack underway.

Cancer:

Cancer is a dreaded disease. Antibodies cloned from a single source and targetted for a specific antigen (monoclonal antibodies) have proved very useful in cancer treatment. Monoclonal antibodies have been target with radioactive elements or cytotoxins like Ricin from castor seed to make them more deadly. Such antibodies seek cancer cells and specifically kill them with their radioactivity or toxin.

Recombinant DNA technology has tremendous scope in energy production. Through this technology Ii is now possible to bioengineer energy crops or biofuels that grow rapidly to yield huge biomass that used as fuel or can be processed into oils, alcohols, diesel, or other energy products.

The waste from these can be converted into methane. Genetic engineers are trying to transfer gene for cellulase to proper organisms which can be used to convert wastes like sawdust and cornstalks first to sugar and then to alcohol.

Genetically designed bacteria are put into use for generating industrial chemicals. A variety of organic chemicals can be synthesised at large scale with the help of genetically engineered microorganisms. Glucose can be synthesised from sucrose with the help of enzymes obtained from genetically modified organisms.

Now-a-days with the help of genetic engineering strains of bacteria and cyanobacteria have been developed which can synthesize ammonia at large scale that can be used in manufacture of fertilisers at much cheaper costs. Microbes are being developed which will help in conversion of Cellulose to sugar and from sugar to ethanol.

Recombinant DNA technology can also be used to monitor the degradation of garbage, petroleum products, naphthalene and other industrial wastes.

For example bacterium pseudomonas fluorescens genetically altered by transfer of light producing enzyme called luciferase found in bacterium vibrio fischeri, produces light proportionate to the amount of its breaking down activity of naphthalene which provides way to monitor the efficiency of the process.

Maize and soybeans are extensively damaged by black cutworm. Pseudomonas fluorescens is found in association with maize and soybeans. Bacillus thuringiensis contain a gene pathogenic to the pest. The pest has, over the years, not only become dangerous to the crops but has developed resistance to a number of pesticides.

When the gene from B. thuringiensis (Bt) was cloned into pseudomonas fluorescence and inoculated into the soil, it was found that genetically engineered pseudomonas fluorescens could cause the death of cutworms.

Continued here:
Top 4 Applications of Genetic Engineering

Life goes on as gene-edited foods begin to hit the market. Japanese consumers have recently startedbuying tomatoes that fight high blood pressure, and Americans have been consuming soy engineered to produce high amounts of heart-healthy oils for a little over two years. Few people noticed these developments because, as scientists have said for a long time, the safety profile of a crop is not dictated by the breeding method that produced it. For all intents and purposes, it seems that food-safety regulators have done a reasonablejob of safeguarding public health against whatever hypothetical risks gene editing may pose.

But this has not stopped critics of genetic engineering from advocating for more federal oversight of CRISPR and othertechniquesused to make discrete changes to the genomes of plants, animals and other organisms we use for food or medicine. Over at The Conversation, a team of scientists recently made the case for tighter rules in Calling the latest gene technologies natural is a semantic distraction they must still be regulated.

Many scientists have defended gene editing, in part, by arguing that it simply mimics nature. A mutation that boosts the nutrient content of rice, for example, is the same whether it was induced by a plant breeder or some natural phenomenon. Indeed, the DNA of plants and animals we eat contains untold numbers of harmless, naturally occurringmutations. But The Conversation authors will have none of this:

Unfortunately, the risks from technology dont disappear by calling it natural... Proponents of deregulation of gene technology use the naturalness argument to make their case. But we argue this is not a good basis for deciding whether a technology should be regulated.

They have written a very long peer-reviewed article outlining a regulatory framework based on "scale of use."The ideais that the more widely a technology is implemented, the greater risk it may pose to human health and the environment, which necessitates regulatory "control points" to ensure its safe use. It's an interesting proposal, but it's plagued by several serious flaws.

Where's the data?

The most significant issue with a scale-based regulatory approachis that it's a reaction to risks that have never materialized. This isn't to say that a potentially harmful genetically engineered organism will never be commercialized. But if we're going to upend our biotechnology regulatory framework, we need to do so based on real-world evidence. Some experts have actually argued, based on decades of safety data, that the US over-regulates biotech products. As biologist and ACSHadvisorDr. Henry Miller and legal scholar John Cohrssen wrote recently in Nature:

After 35 years of real-world experience with genetically engineered plants and microorganisms, and countless risk-assessment experiments, it is past time to reevaluate the rationale for, and the costs and benefits of, the case-by-case reviews of genetically engineered products now required by the US Environmental Protection Agency (EPA), US Department of Agriculture (USDA) and US Food and Drug Administration (FDA).

The problem with scale

Real-world data aside for the moment, there are some theoretical problems with the scalabilitymodel as well. Theargument assumes thatrisks associated with gene editing proliferate as use of the technology expands, because each gene edit carries a certain level of risk. This is a false assumption, as plant geneticist Kevin Folta pointed out on a recent episode of the podcast we co-host (21 minute mark).

Scientists have a variety of tools with which to monitor and limit the effects of specific gene edits. For example, proteins known as anti-CRISPRs can be utilized to halt the gene-editing machinery so it makes only the changes we want it to. University of Toronto biochemist Karen Maxwell has explained how this could work in practice:

In genome editing applications, anti-CRISPRs may provide a valuable 'off switch for Cas9 activity for therapeutic uses and gene drives. One concern of CRISPR-Cas gene editing technology is the limited ability to control its activity after it has been delivered to the cell . which can lead to off-target mutations. Anti-CRISPRs can potentially be exploited to target Cas9 activity to particular tissues or organs, to particular points of the cell cycle, or to limit the amount of time it is active

Suffice it to say that these and other safeguards significantly alter the risk equation and weaken concerns about a gene-edits-gone-wild scenario. Parenthetically, scientists design these sorts of preventative measures as they develop more genetic engineering applications for widespread use. This is why the wide variety of cars in production today have safety features that would have been unheard of in years past.

Absurdity alert: The A-Bomb analogy

To bolster their argument, The Conversation authors made the following analogy:

Imagine if other technologies with the capacity to harm were governed by resemblance to nature. Should we deregulate nuclear bombs because the natural decay chain of uranium-238 also produces heat, gamma radiation and alpha and beta particles? We inherently recognize the fallacy of this logic. The technology risk equation is more complicated than a supercilious 'its just like nature' argument

If someone has to resort to this kind of rhetoric, the chances are excellent that their argument is weak. Fat Man and Little Boy, the bombs dropped on Japan in 1945, didn't destroy two cities because a nuclear physicist in New Mexico made a technical mistake. These weapons are designed to wreak havoc. Tomatoes bred to produce more of an amino acid, in contrast, are not.

The point of arguing that gene-editing techniques mimic natural processes isn't to assert that natural stuff is good; therefore, gene editing is also good. Instead, the point is to illustrate that inducing mutations in the genomes of plants and animals is not novel or uniquely risky. Even the overpriced products marketed as all-natural have been improved by mutations resulting from many years of plant breeding.

Nonetheless, some scientists have argued that reframing the gene-editing conversation in terms of risk vs benefit would be a smarter approach than making comparisons to nature. I agree with them, so let's start now. The benefits of employing gene editing to improve our food supply and treat disease far outweigh the potential risks, which we can mitigate. Very little about modern life is naturaland it's time we all got over it.

Read more from the original source:
CRISPR Revolution: Do We Need Tighter Gene-Editing Regulations? No - American Council on Science and Health

SARS-CoV-2, the virus that causes Covid-19, has made our future vulnerability to biological pathogens and what we can learn to help prevent the next pandemic a salient concern. We dont have much evidence one way or the other whether Covids emergence into the world was the result of a lab accident or a natural jump from animal to human. And while the US intelligence communitys current best guess is that the virus probably was not genetically engineered, the theory has been the subject of much debate and has not been definitively ruled out.

The many unknowns we confront underscore the need for a much bigger toolkit to deal with pathogenic threats than we currently have which is why a recent paper about a new advance in tracing genetic editing is particularly exciting.

Bioengineering often leaves traces characteristic patterns in the RNA or DNA of an engineered organism that are a product of a plethora of design decisions that go into synthetic biology. That fact about bioengineered genomes raises an interesting question: What if those traces that gene editing leaves behind were more like fingerprints? That is, what if its possible not just to tell if something was engineered but precisely where it was engineered?

Thats the idea behind genetic engineering attribution: the effort to develop tools that let us look at a genetically engineered sequence and determine which lab developed it. A big international contest among researchers earlier this year demonstrates that the technology is within our reach though itll take lots of refining to move from impressive contest results to tools we can reliably use for bio detective work.

The contest, the Genetic Engineering Attribution Challenge, was sponsored by some of the leading bioresearch labs in the world. The idea was to challenge teams to develop techniques in genetic engineering attribution. The most successful entrants in the competition could predict, using machine-learning algorithms, which lab produced a certain genetic sequence with more than 80 percent accuracy, according to a new preprint summing up the results of the contest.

This may seem technical, but it could actually be fairly consequential in the effort to make the world safe from a type of threat we should all be more attuned to post-pandemic: bioengineered weapons and leaks of bioengineered viruses.

One of the challenges of preventing bioweapon research and deployment is that perpetrators can remain hidden its difficult to find the source of a killer virus and hold them accountable.

But if its widely known that bioweapons can immediately and verifiably be traced right back to a bad actor, that could be a valuable deterrent.

Its also extremely important for biosafety more broadly. If an engineered virus is accidentally leaked, tools like these would allow us to identify where they leaked from and know what labs are doing genetic engineering work with inadequate safety procedures.

Hundreds of design choices go into genetic engineering: what genes you use, what enzymes you use to connect them together, what software you use to make those decisions for you, computational immunologist Will Bradshaw, a co-author on the paper, told me.

The enzymes that people use to cut up the DNA cut in different patterns and have different error profiles, Bradshaw says. You can do that in the same way that you can recognize handwriting.

Because different researchers with different training and different equipment have their own distinctive tells, its possible to look at a genetically engineered organism and guess who made it at least if youre using machine-learning algorithms.

The algorithms that are trained to do this work are fed data on more than 60,000 genetic sequences different labs produced. The idea is that, when fed an unfamiliar sequence, the algorithms are able to predict which of the labs theyve encountered (if any) likely produced it.

A year ago, researchers at altLabs, the Johns Hopkins Center for Health Security, and other top bioresearch programs collaborated on the challenge, organizing a competition to find the best approaches to this biological forensics problem. The contest attracted intense interest from academics, industry professionals, and citizen scientists one member of a winning team was a kindergarten teacher. Nearly 300 teams from all over the world submitted at least one machine-learning system for identifying the lab of origin of different sequences.

In that preprint paper (which is still undergoing peer review), the challenges organizers summarize the results: The competitors collectively took a big step forward on this problem. Winning teams achieved dramatically better results than any previous attempt at genetic engineering attribution, with the top-scoring team and all-winners ensemble both beating the previous state-of-the-art by over 10 percentage points, the paper notes.

The big picture is that researchers, aided by machine-learning systems, are getting really good at finding the lab that built a given plasmid, or a specific DNA strand used in gene manipulation.

The top-performing teams had 95 percent accuracy at naming a plasmids creator by one metric called top 10 accuracy meaning if the algorithm identifies 10 candidate labs, the true lab is one of them. They had 82 percent top 1 accuracy that is, 82 percent of the time, the lab they identified as the likely designer of that bioengineered plasmid was, in fact, the lab that designed it.

Top 1 accuracy is showy, but for biological detective work, top 10 accuracy is nearly as good: If you can narrow down the search for culprits to a small number of labs, you can then use other approaches to identify the exact lab.

Theres still a lot of work to do. The competition looked at only simple engineered plasmids; ideally, wed have approaches that work for fully engineered viruses and bacteria. And the competition didnt look at adversarial examples, where researchers deliberately try to conceal the fingerprints of their lab on their work.

Knowing which lab produced a bioweapon can protect us in three ways, biosecurity researchers argued in Nature Communications last year.

First, knowledge of who was responsible can inform response efforts by shedding light on motives and capabilities, and so mitigate the events consequences. That is, figuring out who built something will also give us clues about the goals they might have had and the risk we might be facing.

Second, obviously, it allows the world to sanction and stop any lab or government that is producing bioweapons in violation of international law.

And third, the article argues, hopefully, if these capabilities are widely known, they make the use of bioweapons much less appealing in the first place.

But the techniques have more mundane uses as well.

Bradshaw told me he envisions applications of the technology could be used to find accidental lab leaks, identify plagiarism in academic papers, and protect biological intellectual property and those applications will validate and extend the tools for the really critical uses.

The past year and a half should have us all thinking about how devastating pandemic disease can be and about whether the precautions being taken by research labs and governments are really adequate to prevent the next pandemic.

The answer, to my mind, is that were not doing enough, but more sophisticated biological forensics could certainly help. Genetic engineering attribution is still a new field. With more effort, itll likely be possible to one day make attribution possible on a much larger scale and to do it for viruses and bacteria. That could make for a much safer future.

Correction, October 25, 9:50 am: A previous version of this story stated that SARS-CoV-2 had been definitively proven not to be a bioengineered virus. While an August 2021 US intelligence report concluded, Most agencies assess with low confidence that SARS-CoV-2 probably was not genetically engineer
ed, and many scientists agree with that assessment, it was an overstatement to claim that the theory has been definitively ruled out. The introduction and conclusion of the story have been updated to reflect this lower level of certainty. (h/t to Alina Chan, biologist at the Broad Institute of MIT and Harvard, for her critique and input)

More here:
How biological detective work can reveal who engineered a virus - Vox.com

Earlier this week, surgeons at New York Universitys Langone Transplant Institute successfully performed a pig kidney transplant. This in itself would be unremarkable. What does mark the achievement as unprecedented is the identity of the donor a genetically modified pig.

Some days post-surgery, the recipient, a brain-dead patient whose family consented to the experimental procedure, has not rejected the kidney and tests show that it is functioning normally. This incredible feat is significant both as a demonstration of scientific control over biological systems and as a beacon of hope to others in line for a transplant.

The idea of using other species for organ transplants is not new; we have used pig heart-valves for over 50 years. Yet whole organs have presented several challenges, most notably the risk of rejection. This occurs because the body believes the transplant is an invader that must be destroyed, leading to an immune response that attacks the organ. While the triggers for rejection are not completely understood, one of the biggest barriers to cross-species transplantation is a molecule known as alpha-gal, a carbohydrate that immediately elicits a massive immune response.

To counteract this, scientists used a powerful tool of genetic engineering, CRISPR, to modify the pigs genome so that it does not produce alpha-gal. CRISPR has existed for less than a decade, yet its ability to accurately cut and paste specific pieces of genomes is already leading to breakthroughs in many areas of biology including in the development of COVID-19 vaccines.

At present, over 100,000 people in the United States are awaiting an organ donation, among whom 83%, ~91,000, are in need of a kidney. Though 54% of US citizens are registered organ donors, less than 1% of deaths result in useable organs, so supply will always outstrip demand.

Consequently, wait times for a kidney can range from four months to six years depending on blood type, geographic location, disease severity, immune system activity, and other factors. Most of those on the waiting list must have their blood cleaned via hemodialysis, a process that entails commuting to a dialysis centre and spending four hours a day, three times a week, attached to a machine simply to stay alive. The longer they are on dialysis, the smaller their chance of a successful kidney transplant becomes as the procedure can only partially compensate for the damaged organ.

Every year, 5,000 people die waiting for a transplant and another 5,000 are removed from the list because they are no longer healthy enough to receive it, meaning that only 65% of those placed on transplant lists will receive a kidney in time. This latest development could prove to be a gamechanger.

But there will be difficult questions about the ethics of modifying other species to fit our needs, and the event may spark further dialogue on the conditions pigs and other animals are currently raised in. There are also still many unanswered questions surrounding the efficacy of cross-species transplantation. Can pig kidney transplants to humans save lives? Well, before we get to an answer, more robust, longer-term trials will have to take place.

Yet the significance of this pig kidney transplant demonstration should not be underestimated this is a momentous step towards saving the lives of tens of thousands of people awaiting a transplant, not to mention the half a million with kidney failure who do not even qualify because of scarcity. It also speaks to the potential of biotechnology more broadly to transform the health outcomes of millions of people.

Written by

Cameron Fox, Project Specialist, Shaping the Future of Health and Healthcare, World Economic Forum

The views expressed in this article are those of the author alone and not the World Economic Forum.

Continued here:
A kidney transplant from a pig to a human has worked. What you need to know - World Economic Forum

Left to right: Gary Hon, Ph.D., UTSW Assistant Professor of Obstetrics and Gynecology; Nikhil Munshi, M.D., Ph.D., Associate Professor of Internal Medicine and Molecular Biology; W. Lee Kraus, Ph.D., Professor and Director of the Cecil H. and Ida Green Center for Reproductive Biology Sciences

The Human Genome Project identified and mapped all of the genes of the human genome, achieving the worlds largest international, collaborative biological project. That opened the door to a wide array of innovative research projectsincluding a prestigious one that UT Southwestern has just joined.

A team ofUT Southwestern faculty led by Gary Hon, Ph.D.,has been awarded a five-year, $8.8 million grant to participate in the National Human Genome Research Institutes Impact of Genomic Variation on Function (IGVF) Consortium. The consortiums goal is understanding how developmental variants contribute to developmental diseases.

Dr. Hon is an assistant professor of obstetrics and gynecology in the Cecil H. and Ida Green Center for Reproductive Biology Sciences and a member of the Lyda Hill Department of Bioinformatics.

Hon developed Mosaic-seq, a genome engineering technique that helped lead to the awarding of the $8.8 million grant. In a statement, he saidthe IGVF Consortium is the National Human Genome Research Institutes next step to unveiling the genomes role in disease.

The Human Genome Project told us that most of the genome doesnt contain genes, Hon said. One big surprise from genome-wide association studies is that gene-poor regions contain many disease signatures.

It turns out that the signatures largely overlap with DNA elements, found by the Encyclopedia of DNA Elements (ENCODE) Consortium, that control when genes turn on, Hon added. The goal of this consortium is to fill in the gaps, linking DNA sequences to genes, cell phenotypes, and disease. Ultimately, this knowledge will allow us to interpret the disease potential of any persons genome sequence.

In their work with the consortium, the UTSW teamwill combine molecular biology, genomics, high throughput screens, and computational analyses to focus on potential disease-causing genetic variations in the cardiovascular, nervous, and placental systems.

Besides Hon, the teamalso includes principal investigators Nikhil Munshi, M.D., Ph.D., associate professor of internal medicine and molecular biology, and W. Lee Kraus, Ph.D., professor and director of the Green Center.

Mosaic-seq allows high throughput analysis of the molecular events that occur during programming of embryonic stem cells into other cell types. This technique uses single-cell sequencing to study different regions of the genome at the same time.

Just one experiment can perturb thousands of regions in the genome to better understand their function, according to the UTSW team.

With Mosaic-seq, researchers no critical have to study one region at a time. Hons lab received national attention in 2017 for this significant advance, which was part of his teams grant application.

UTSW now joins Harvard, Stanford, and Yale universities as one of the 30 research sites taking part in the IGVF Consortium nationwide.The consortium will study noncoding regions of the human genome that are known to contribute to genetic diseasesincluding congenital heart disease, autoimmune disease, and blood disorders.

Dr. Kraus, a professor of obstetrics and gynecology and pharmacology who holds the Cecil H. and Ida Green Distinguished Chair in reproductive biology sciences, will use additional CRISPR-based technologies in the consortium research project. Kraus will use them to study how genetic variation in non-coding RNAs originating from the regulatory elements impacts the development of the placenta.

The placentas development is important because it supports the human fetus as it grows, as well as the fetuss heart and central nervous system.

Studying the role of genetic variation in the embryonic development of these key organs could point the way to understanding human diseases in adults, Kraus said in the statement.

Dr. Munshi believes the IGVF Consortium initiativecould potentially fill in huge pieces of the puzzle for many diseases.

If we candetermine all of the noncoding elements in the genome that impact a particular developmental pathway, then those could become candidates fordisease-associated mutations, Munshi said.

By generating catalogs of tens of thousands offunctionalvariants, we dont have to search the billons of basepairs to find where thedisease-causingmutations might lie, he added. We can really focus the search on thesetens of thousands of variants. It really gives us an encyclopediatonarrow the search.

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For years weve been told that human and chimp DNA is some 99 percent identical. The genetic similarity statistic is then used to make an argument for human-ape common ancestry, and human-ape common ancestry is then employed in service of the larger philosophical point that humans are just modified apes, and nothing special. It all amounts to an argument against human exceptionalism. This sort of thinking is embodied by Bill Nye (The Science Guy) in his 2014 bookUndeniable:

As our understanding of DNA has increased, we have come to understand that we share around 98.8 percent of our gene sequence with chimpanzees. This is striking evidence for chimps and chumps to have a common ancestor.

BioLogos-affiliated biologist Dennis Venemahas also arguedthat we are but a hand-breadth away from our evolutionary cousins at the DNA level. But is this really true? In response to the newly released episode ofScience Uprisingon human origins, we have recently received questions about the true degree of human-chimp similarity. With that in mind, lets review some past coverage on the issue.

In 2007, not long after the chimp genome was first sequenced, the journalSciencepublished an article, Relative Differences: The Myth of 1%, which called the idea that humans are only 1 percent genetically different from chimps a myth and a truism [that] should be retired. It observed that the genetic differences between humans and chimps amount to 35 million base-pair changes, 5 million indels [sequences of multiple nucleotide bases] in each species, and 689 extra genes in humans. The article further reported that if we consider the number of copies of genes in the human and chimp genomes, human and chimpanzee gene copy numbers differ by a whopping 6.4%.

The old statistic that we are about 99 percent or 98 percent similar to chimps pertains only to alignable protein-coding sequences. In fact the statistic first originated based upon similarity between humans and chimps in just one single gene! But many non-coding sequences are highly dissimilar, and there are sequences of the human and chimp genomes that are so different that they cant be aligned for comparison. For example, there are some parts of our genome, such as thehuman y chromosome, that are radically different from the chimp genome.

Geneticist Richard Buggs has tried to refine the methods for comparing human and chimp genomes. In a 2018 post, he observesthat The percentage of nucleotides in the human genome that had one-to-one exact matches in the chimpanzee genome was 84.38%. In 2020 he co-published anarticle in the journalFrontiers in Geneticsproviding a different method of estimating of human-chimp genetic differences, finding that human-chimp genetic similarity is about 96 percent. This papers estimate of ~4 percent genetic difference includes both coding and non-coding DNA, but it does not include centromeric DNA. If that DNA were included, the percent of genetic similarity between humans and chimps could drop to as low as ~93 percent, but probably not lower. Computational biologist Steve Schaffner has roughly estimated human-chimp genetic similarity to be ~95 percent. However, one criticism Ive heard of all current estimates is that they are based upon versions of the chimp genome that used the human genome as a scaffolding, potentially making certain sections of the chimp genome more humanlike than they ought to be. This could also artificially inflate the degree of human-chimp similarity.

What this means is that until more accurate and complete versions of the chimp genome are produced, any estimate of human-chimp genetic similarity will undoubtedly be refined in the future, and current numbers may very well be overestimates. Nonetheless, any of the above estimates of human-chimp genetic similarity 96 percent, 95 percent, 93 percent, 84 percent carries meaning in different contexts. But what exactly do they mean?

Whatever the exact percentage of human-chimp genetic similarity (however you want to measure it) turns out to be, lets grant that it will be fairly high, probably 84 percent or greater. Does this necessarily require the conclusion of common ancestry? Is the case for common ancestry, based upon the degree of similarity, an objective or rigorous argument thats capable of being falsified? For example, if a 1 percent genetic difference implies common ancestry, but then that statistic turns out to be wrong, then does a 4 percent genetic difference mean common ancestry is false? How about 7 percent or 10 percent genetic difference? 25 percent? At what point does the comparison cease to support common ancestry? Why does the percent genetic similarity even matter? Its not clear that there is an objective standard for falsification here, any identifiable reason why a particular percentage of genetic similarity should be taken to indicate common ancestry.

Indeed, Dennis Venema even seems to acknowledge this point, writing in 2018:

No one is more interested in the % genome identity thing than folks trying to cast doubt on common ancestry. Its just not a precise value that scientists are interested in, because it doesnt answer interesting scientific questions in the way other values do (emphasis added)

Thats quite a bold quote from Professor Venema when earlier he was seen emphasizing how humans are a mere genetic hand-breadth away from chimps, as part of a case for common ancestry. This is in keeping with numerous other evolution apologists over the years who have cited the 1% statistic in favor of human-chimp common ancestry. They are the ones who invented and promoted this fallacious argument, and we are simply responding to it. Yet somehow us Darwin-skeptics get blamed for spreading a fallacious argument.

Perhaps Dr. Venema has changed his mind about the import of the statisticwhich he is fully entitled to do. Whatever the case, we agree with his point here that the % genome identity provides no rigorous argument for common ancestry and does not answer very many interesting questions within this particular debate.

The case for human-chimp common ancestry is further significantly weakened once one realizes that there are other potential explanations for functional similarities: notably, design based upon a common blueprint.

Intelligent agents often re-use parts and components that perform common functions in different designs. Its a good engineering design principle to follow! Everyday examples of this include wheels used on both cars and airplanes, or touchscreen keyboards used on both phones and tablets.

It should be noted that common design, as an argument, is not intended to prove species were specially created or designed separately. Rather, its a rejoinder put forth to defeat the evolutionist assertion that genetic similarity necessarily indicates common ancestry. Genetic similarity doesnt necessarily indicate common ancestry because intelligent agents can and do independently use common parts in different designs to fulfill common functional goals. High genetic similarity could reflect design with a common blueprint rather than common ancestry.Biologist Ann Gauger, mathematician Ola Hssjer, and statistician Colin Reevesexplain this wellin Chapter 15 of the 2017 bookTheistic Evolution:

[T]here are some basic differences between the way evidence is approached by evolutionary biologists and design biologists. The chief assumption made by evolutionary biologists is that the genetic changes responsible for evolutionary change are random, and therefore, if a group of species share a trait in common that is not found in other related species, it is presumed that the common ancestor of the group developed that trait, and they all share it because of common descent. On the other hand, if genetic change is directed rather than random,the trait is most likely shared because the organisms use similar solutions to a physiological need.

Humans and chimps thus have similarities that reflect functional constraints due to design bas
ed upon a common blueprint. Gauger and her team indicate what this means for some of the basic molecular, cellular, metabolic, and physiological similarities between humans and chimps:

First, our basic building blocks, the proteins out of which our cells are made and the enzymes that carry out cellular metabolism, are very similar to those of chimpanzees, almost identical in many cases. One can think of our genes as being like the bricks and mortar, nails and wood, shingles and wires out of which houses are made. Two houses may look different but be composed of the same basic building blocks. By analogy, the building blocks out of which we are made, the genes, are very similar for chimps and humans, even if our bodily forms are different.

Second, the vast majority of our DNA does not code for protein but functions like an operating system, determining what files (genes) should be used when, and where. The routine processes of life are carried out by this operating system, and we share these basic routines with chimps. Thus in many respects our operating systems are the same as those of chimps.

Of course some will cite shared NON-functional (as opposed to functional) genetic similarities between humans and chimps as better evidence for common ancestry. I agree that non-functional shared DNA could be a potential argument for common ancestry, but Im skeptical that many of the DNA elements cited in these arguments are actually non-functional. Aswe saw recently, a new paper inGenome Biology and Evolutiondeclared, The days of junk DNA are over. Even pseudogenes, commonly cited as a form of genetic junk that supports common ancestry, have had their junk status severely questioned in recent years seehere,here,here,here, andherefor discussions.

Since many of the building blocks used by humans and chimps are similar, its no wonder that our protein-coding DNA is also so similar. Common design can explain these similarities. But its important to bear in mind that one can use identical building blocks bricks, mortar, wood, and nails to build very different houses. So its not just about having similar building blocks, but how you use them. This is where genetic similarities between humans and chimps probably arent so meaningful, when you consider how the building blocks being used can be very different.

Gauger and her colleagues thus explain that the percentage of nucleotide similarity does not tell the whole story about human-chimp genetic differences since many of the most crucial differences lie outside the protein-coding DNA:

[C]ounting raw difference is not the best way to calculate how different we are genetically speaking We now know that when, where, and how our DNA is used matters much more than an overall count of nucleotide differences. Human-specific differences in gene regulation, as we will see, are what make us unique.

They recount some of the crucial differences between humans and chimps:

And this leaves aside the vast cognitive and behavioral gulf between humans and chimpanzees. We are the only species that uses fire and technology. We are the only species that composes music, writes poetry, and practices religion. We are also the only species that seeks to investigate the natural world through science. We write papers about chimps; not the other way around. All of this is possible because we humans are the only species that uses complex language.

The human race has unique and unparalleled moral, intellectual, and creative abilities. Regardless of the level of similarity of human protein-coding DNA to chimps, clearly that similarity is only a small part of the story. If anything, it testifies that protein-coding DNA sequences are only one of multiple crucial interacting factors that determine an organisms biology and behavior.

Original post:
Human-Chimp Similarity: What Does It Mean? - Discovery Institute

Completed Business Combination with Big Cypress Acquisition Corp.

Common stock to commence trading on the Nasdaq Global Market October 25, 2021, under the ticker symbol SABS

SIOUX FALLS, S.D., Oct. 25, 2021 (GLOBE NEWSWIRE) --SAB Biotherapeutics, Inc. (Nasdaq: SABS), (SAB), a clinical-stage biopharmaceutical company with a novel immunotherapy platform that produces specifically targeted, high-potency, fully-human polyclonal antibodies without the need for human donors, today announced the completion of its business combination with Big Cypress Acquisition Corp. (Nasdaq: BCYP) (Big Cypress), a publicly-traded special purpose acquisition company (SPAC) focused on innovative biopharmaceutical firms. The common stock and warrants of the resulting combined company, SAB Biotherapeutics Inc. will commence trading on the Nasdaq Global Market (the NASDAQ) under the ticker symbol SABS and SABSW, respectively, on October 25, 2021.

The stockholders of Big Cypress approved the transaction at a Special Meeting held on October 20, 2021. The transaction was previously approved by SABs shareholders. SABs management team will be led by Eddie Sullivan, Ph.D., Co-Founder, President, and Chief Executive Officer, who previously served as President, and Chief Executive Officer. Samuel J. Reich, formerly Chief Executive Officer and Chief Financial Officer of Big Cypress, and Jeffrey G. Spragens, Big Cypress Chairman of the Board of Directors, will join the SAB Board of Directors, with Mr. Reich assuming the role of Executive Chairman.

We are excited to enter the public markets at such a pivotal time when next-generation immunotherapies like ours are essential in driving improvement in the global health landscape. We extend our gratitude to the Big Cypress team for being our partner in driving our vision of developing scalable and highly potent polyclonal antibody therapies, said Dr. Eddie Sullivan. We would also like to thank the SAB team, as well as our new and existing shareholders, who are making our important work possible. The SAB team is committed to progressing our science and expanding the reach of our unique DiversitAb platform, now as a public company.

Dr. Sullivan added, We look forward to reporting clinical data from a number of our programs in the coming months. SAB expects to announce topline clinical data for our seasonal influenza program before the end of the year, and we expect to report clinical data from our NIH-sponsored COVID-19 clinical trials as soon as it becomes available.

SABs innovative and versatile DiversitAb platform and talented team bring a unique approach to the development of immunotherapies, which is why we chose them as our merger partner, said Samuel Reich. Our experienced biopharmaceutical team was initially impressed by the ability of SABs platform to produce high-potency fully-human polyclonal antibodies with the potential to address a variety of serious diseases with high unmet medical need. In the few months since we announced our intention to merge, SAB has achieved multiple significant milestones, reinforcing our confidence in their ability to execute and deliver on the promise of their technology. Im delighted to be joining the SAB team to advance the companys clinical programs and business strategy, with the goal of building a differentiated biopharmaceutical company committed to creating shareholder value and having a significant positive impact on human health.

Summary of TransactionOn June 22, 2021, SAB entered into a definitive business combination agreement with Big Cypress Acquisition Corp., a blank check company focused on innovative biopharmaceutical firms, which was created for the purpose of entering into a business combination with a selected biopharmaceutical company and bringing the combined entity to the NASDAQ.

The gross proceeds from the transaction after redemptions and before deducting transaction fees are approximately $30 million. SAB intends to use the proceeds from the transaction to progress its pipeline programs and to augment its recent $60.5 million award from the government, in addition to approximately $27 million remaining from previous awards.

Recent Developments Demonstrate Momentum Across Key Initiatives

AdvisorsLazard served as exclusive financial advisor to SAB. Stradling Yocca Carlson & Rauth is serving as legal counsel to SAB. Chardan served as exclusive M&A advisor and financial advisor to Big Cypress and Dentons US LLP is serving as legal counsel. Ladenburg Thalmann & Co. Inc. is acting as a capital markets advisor to Big Cypress.

About SAB Biotherapeutics, Inc.SAB Biotherapeutics, Inc. (SAB) is a clinical-stage, biopharmaceutical company advancing a new class of immunotherapies leveraging fully human polyclonal antibodies. SAB has applied advanced genetic engineering and antibody science to develop transchromosomic (Tc) Bovine that produce fully-human antibodies targeted at specific diseases, including infectious diseases such as COVID-19 and influenza, immune system disorders including type 1 diabetes and organ transplantation, and cancer. SABs versatile DiversitAb platform is applicable to a wide range of serious unmet needs in human diseases. It produces natural, specifically targeted, high-potency, human polyclonal immunotherapies. SAB is currently advancing multiple clinical programs and has collaborations with the US government and global pharmaceutical companies. For more information on SAB, visit: https://www.sabbiotherapeutics.com and follow @SABBantibody on Twitter.

Contact:Melissa Ullerich+1 605-679-4609mullerich@sabbiotherapeutics.com

Courtney Turiano (investors)Stern IR212-698-8687Courtney.Turiano@sternir.com

Forward-Looking Statements Certain statements made herein that are not historical facts are forward-looking statements for purposes of the safe harbor provisions under The Private Securities Litigation Reform Act of 1995. Forward-looking statements generally are accompanied by words such as believe, may, will, estimate, continue, anticipate, intend, expect, should, would, plan, predict, potential, seem, seek, future, outlook and similar expressions that predict or indicate future events or trends or that are not statements of historical matters. These forward-looking statements include, but are not limited to, statements regarding future events. These statements are based on the current expectations of SAB and are not predictions of actual performance. These forward-looking statements are provided for illustrative purposes only and are not intended to serve as, and must not be relied on, by any investor as a guarantee, an assurance, a prediction or a definitive statement of fact or probability. Actual events and circumstances are difficult or impossible to predict, will differ from assumption and are beyond the control of SAB.

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SAB Biotherapeutics Debuts as Publicly Traded Next-Generation Immunotherapy Company - BioSpace

Click on any icon to hear that co-authors perspective on what the proposed guidelines mean for the region in which they work. Map compiled by Stephanie Dutchen

HMNews: What is the main goal of having a set of international guidelines?

Kendra Sirak: While some countries have developed rigorous standards that guide the scientific analysis of human remains, many others have few or no guidelines that ensure that this work is carried out responsibly and is both scientifically robust and sensitive to community perspectives. Everyone wants practical guidance that will be positive about the research enterprise while embracing high ethical standards.

Its our hope that these guidelines will raise the integrity of ancient DNA research around the world by minimizing damage to collections of human remains; ensuring sensitivity to the perspectives of stakeholder groups, especially when these groups are marginalized; and reducing opportunities for the misuse of results. We expect these guidelines will undergo further development as the field continues to evolve.

HMNews: Why now?

Jakob Sedig: Ancient DNA as a field has been growing rapidly, evolving from a promising technology to a mature field. The discussion about how to handle human remains and how to meaningfully involve diverse stakeholders has not yet caught up. More and more people are calling for clear, strong guidance that all researchers engaged in ancient DNA work can embrace.

Ancient DNA analysis has contributed vital new insights about the human past and has helped us understand the genetic roots of human diversity. It has disrupted nationalist and xenophobic narratives. It has challenged what many of us thought we knew about who we are and where we came from. But like any field that matters, its complex.

Because of the number of ancient individuals being analyzed, the socialand political nature of the work, and the challenges that ancient DNA findings have raised about theories proposed before we had such data, people are paying attention to ancient DNA. That makes it even more vital to articulate and adopt strong guidelines that work well everywhere.

HMNews: How did the team come up with these five guidelines?

Sedig: We took cues from archaeology and modern human genetics, which have established protocols for carrying out analyses on human remains and establishing stakeholder consent. We built on aspects of existing guidelines, such as those crafted by a group of North American scholars, including Indigenous scholars, published last year in the American Journal of Human Genetics.

Our diverse co-author groupparticularly those in Central and South America, Africa, Europe, South Asia, the Pacific, and East Asiafelt that these and other suggestions, while valuable, were not applicable in all world regions. Our virtual workshop led to monthslong discussions that took many different value systems and histories into account and sought balance between local contexts and general principles. We then wrote the manuscript.

Given that there was near-unanimous support and excitement about the final document among the workshop participants, we hope the broader community will embrace and build on these proposals. It would be wonderful if the proposals form a basis for official guidelines in the future.

HMNews: Why not just follow national or local government regulations wherever a project is being conducted?

Sirak: There are some places where laws are robust enough for that to be appropriate, but in other locales, we feel that researchers need to hold themselves to a higher standard than required by the laws currently in place.

HMNews: What are some of the needs and unique circumstances in different regions that shaped the guidelines?

Sirak: We have found that guidelines that work well for one region can come across as condescending or even colonialist in another. Many co-authors on this manuscript raised the point that indigeneity has different meanings in different places and is even used in some regions as a framework for oppression and discrimination against minority groups argued to be non-Indigenous. Thus, basing research ethics on a single definition can inadvertently reinforce rather than mitigate power imbalances in conducting and interpreting genetic analyses.

The videos our co-authors have shared speak to the many nuances of ethical ancient DNA research in the places where they live and work.

HMNews: Some critics say that ancient DNA research, which to a large extent has focused on and been conducted by white people from wealthy nations, has been a colonialist endeavor that siphons agency from marginalized groups. How do the proposed guidelines address these discussions about power and ownership?

Sedig: These are important conversations. We cant reiterate enough that our goal is to learn about the past in a sensitive, thoughtful, and ethical way. We do not want to contribute to exploitation; we want to do the opposite. We need to listen to and respect the people who are stakeholders in ancient DNA studiesincluding groups from the place of origin of the human remains being studiedand make sure their perspectives are represented in discussions about study design, research questions, and whether a project should proceed at all. Theres been a huge amount of progress in recent years in seeking local perspectives from the start to the conclusion of a study and incorporating that feedback into the project and publication. We have increasingly diverse groups of people who conduct the research as well.

We want to minimize harm and reduce inequity, and I believe the ancient DNA community has an extraordinary track record of providing arguments that do so. We know that in regions with histories of settler colonialism, we have to center Indigenous perspectives. We have to confront the colonial legacies of human remains collected in unethical ways and often sent abroad, and we should seek ways to mend the harms done, such as by considering how our research findings or the methods we are using might be helpful tools for facilitating repatriation of remains. We must ensure that local scientists and communities are as engaged as can be in ancient DNA research, particularly in places with histories of scientists conducting exploitative research. Researchers working in countries outside their own must prioritize establishing equitable collaborations that benefit local scholars and avoid carrying out parachute research at all costs.

When possible, those of us in positions of privilege should contribute to reducing structural inequities. Some ideas we propose in the guidelines are to help educate and train local community members and other stakeholders, assist with raising the curatorial standards of collections or developing museum exhibits, provide funds for training or attending professional meetings, and advocate for funding agencies to build more capacity for equitable ancient DNA research. We also need to ensure that we communicate results in ways that are accessible to nonscientists and the broader scholarly community. Lastly, we have to oppose those who use genetic data to support narratives of group superiority or to justify exclusionary policies.

At the same time, as scientists we need to make sure we can proceed in a way consistent with the scientific method. We cant ethically conduct a study without the guarantee that we can follow the data where they lead. This means that once stakeholder communities agree that publishing results would not cause them harm, the relevant portion of a manuscript wont be restricted. It also means the data must be made accessible at least so others can replicate or reevaluate results.

We have a loyalty to the facts we uncover as we learn about our shared humanity. In cases where the data we generate dont align with other forms of knowledge, such as traditional expertise or cultural beliefs, it is not our job to discredit or diminish that knowledge. Rather, those discrepancies highlight how comple
x an undertaking it is to understand the past and should be flagged in papers that result from the work.

Regarding ownership, we believe that whenever researchers are granted permission to study the remains of ancient individuals, they become stewards of that material with a responsibility to care for and respect it. They do not assume ownership of the remainsor of the data that arise from sequencing it.

HMNews: Some groups assert that stakeholder communities should decide whether and how certain kinds of ancient DNA data can be used in future analyses. How does this fit with the teams push for open data?

Sirak: We advocate for stakeholders having input into how data should be distributed and we advocate for open data. We believe that both goals can coexist.

Many of our co-authors felt strongly that ancient DNA data should always be made fully and publicly available. Other co-authors argued that when it comes to data from remains that might be meaningfully connected to present-day Indigenous communities, it could be appropriate to have usage restrictions. This was one of many debates we had, and in listening to one another, some of us changed our positions.

We all agreed that open data for ancient DNA is something to strive for. The data must be made available after publicationeither through full open access, which is ideal, or distributed by a professional organization without a stake in the research resultsso scholars can reproduce or challenge analyses. This also lowers the chances study results will be misused. We are proud that the raw data for nearly all ancient genomes published so far was made publicly available at or before the time of publication.

Finally, we agreed that Indigenous-led data repositories such as those now being developed could help mediate permissions when scholars wish to use data for purposes beyond those articulated in an original study plan.

HMNews: Given that equity is a priority, how accessible will this paper be to those who, for example, dont have paid access to the journal in which its being published or who arent fluent in English?

Sirak: Weve made our paper open access and applied the most flexible Creative Commons license to it, known as CC BY 4.0. That means its available for free to anyone in the public to read, distribute, adapt, and build upon. Our team members also have translated the text into more than 20 languages that they speak.

HMNews: Do you expect pushback from scientists who feel that the guidelines are too onerous and will make it harder to carry out research?

Sedig: We did receive feedback during the review process that the guidelines were too strongthat they would create a heavy burden for researchers from smaller labs or who are in the early stages of their careers. We respect this perspective and understand that were requesting a lot in terms of engaging with stakeholders and what could be called overhead beyond the research itself. However, we firmly believe that all ancient DNA studies, from an early-career stage onwards, should meet these ethical standards.

In a way, the proposals are merely concretizing the standards that are already emerging in the field. We believe that authors and journal editors feel their way toward this ethical framework during the review process. We believe that the proposals are practical and that early-career researchersincluding many who co-authored our articlewill benefit from having the principles clearly articulated and the guesswork reduced as they aim to carry out their research in an ethically principled way.

HMNews: What enforcement would there be if someone involved in ancient DNA research didnt follow these guidelines?

Sirak: Our co-authors do not represent any official organization, so we cannot make or enforce rules for anyone except ourselves. What our paper does represent is a grassroots, community-led pledge from representatives of a nontrivial faction of worldwide researchers engaged in this type of work. We have committed to adhering to a set of strong principles, and we invite others to hold us accountable to them.

It would be a great outcome if scientific journals, professional societies, or granting agencies found these proposals useful enough to turn into official guidelines, which would mean there could be professional repercussions for not adhering to them. The fact that scholars from such a diverse array of nations and disciplines have signed on to the guidelines at this stage makes us optimistic that they will be embraced in practice by laboratories and research groups as well as other groups engaged in ancient DNA research all over the world. But either way, its important to continue the global conversation.

This work was supported by the Australian Research Council Discovery Project (DP160100811), National Research Foundation South Africa, Brazilian National Council for Scientific and Technological Development (302163/2017-4), So Paulo Research Foundation/FAPESP (2018/23282-5), Francis Crick Institute (FC001595), Cancer Research UK, UK Medical Research Council, Wellcome Trust, Dutch Research Council (VI.C.191.070), Hungarian Academy of Sciences, Science and Engineering Research Board of India, Council of Scientific and Industrial Research in India (Ministry of Science and Technology, Government of India), European Research Council (ERC-2017-StG 804844-DAIRYCULTURES), Werner Siemens-Stiftung, John Templeton Foundation (6122), Howard Hughes Medical Institute, Max Planck Society, and the Max Planck Harvard Research Center for the Archaeoscience of the Ancient Mediterranean, and the National Geographic Society.

Interviews were edited for length and clarity.

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Proceeding with Caution | Harvard Medical School - Harvard Medical School

September 24, 2019

The Pew Research Center has reported that more and more people identify themselves as spiritual but not religious. How can this be explained in our highly technoscientific age? Since technoscience is taken to be secular, how can we make sense of the relationship between our radical technoscientific advances and our search for spirituality?

A group of Arizona State University researchers will explore these and other questions through a project titled Beyond Secularization: A New Approach to Religion, Science and Technology, which has received a $1.7M grant from the Templeton Religion Trust.

The Center for the Study of Religion and Conflict will serve as the lead unit for this major interdisciplinary initiative that seeks to explore the underlying assumptions about science and technology research, exploring whether religious ideas shape scientific research directions and revealing new models for understanding ideas of progress.

Conflicts at the borders of religion, science and technology have been a major research area of the centers since its inception in 2003. Partnering withHava Tirosh-Samuelson, now a Regents Professor and director of Jewish studies, the center launched a faculty seminar in 2004 that met for almost 15 years. Several externally funded projects that grew out of the seminar supported a major lecture series, international research conferences and numerous publications.

All of this work positioned the center for this latest project, which has the potential to have a major impact in how we understand not only the interplay between religion, science and technology in public life, but also how we understand ideas and meanings of progress.

Beyond Secularization builds on a small pilot project that produced over 20 articles, including a cover story in the January issue of Sojourners magazine. It will establish a collaboratory that will include graduate students, postdocs and faculty who will develop and advance new research methods and understandings over the next three to four years.

To learn more about the subject, ASU Now sat down with Tirosh-Samuelson,Ben Hurlbut,School of Life Sciences associate professor,andGaymon Bennett, School of Historical, Philosophical and Religious Studies associate director of research and associate professor,who will serve as co-principal investigators.

Question: What does the title of this project refer to?

Hurlbut: The project looks at the relationships between religion, science and technology in several important domains of public life: in environmental movements, in shifting ideas of the spiritual self that draw upon science, in arenas of high-technology innovation that are reshaping how we live and in the ways societies debate and govern the ethical implications of biotechnological transformation of life, including human life. We want to understand how science, technology and religion are related in those domains, including how lines are drawn between them. There is a pretty widespread assumption that as scientific knowledge and technological capacity increase, religion retreats into the background. And yet, if you look at how people think and talk, things are a lot messier. Go to Silicon Valley and you will encounter a lot of people who are imagining a technological future in terms of its potential to bring a kind of redemption and transcendence, a kind of eschatology. In other domains, like in public debate about biotechnologies, like human genome editing, there is a lot of drawing of lines between scientifically-grounded ethical views versus religious ones. But in all these areas, the boundaries are less clear than we tend to assume. They are a lot more mixed, a lot more hybrid, a lot fuzzier. And understanding that is important for how we think about the relationships between science, technology and religion in contemporary public life.

Q: How is this project unique?

Tirosh-Samuelson: The core work of this project will be done by a collaborative lab (co-lab, for short), which will include the three principal investigators, invited faculty, postdoctoral fellows and graduate students. This group will be studying together and will host visiting scholars from other universities around the world who will help enrich the discussion about big picture questions. The work of the co-lab will be distinctly interdisciplinary, crossing boundaries between history, science and technology studies, religious studies, sociology and anthropology. Our basic conviction is that to understand the interplay between religion, science and technology, we need to pose new questions and engage new methods. The artificial dichotomy between science and religion is no longer valid and even talking about a dialogue between religion and science is insufficient. We need to develop deeper ways to understand how these domains operate in our public life, and to do so, we must engage new disciplines that previously have not been applied to this field of inquiry. Since the project engages religion, science and technology in public life, it will have a public component, including public lectures that will involve the entire ASU community as well as an outreach program to people outside the ASU community, such as high-tech innovators in various innovations enclaves (e.g. Silicon Valley). The public aspect of the project exemplifies ASUs commitment to social embeddedness and to breaking the boundaries between the academy and the community.

"Theres been this sort of assumption that as technology progresses, as knowledge progresses, we get less religious, we become more secular."

Ben Hurlbut,School of Life Sciences associate professor

Q: Why do we see such pronounced boundaries between the religious and the secular in academia?

Hurlbut: Theres been this sort of assumption that as technology progresses, as knowledge progresses, we get less religious, we become more secular. That assumption has also been built into the way some fields study modern life, whether or not that actually corresponds with people's lived experience. So one of the things that we want to do is ask, "What are the things that we're overlooking?" Because we have operated in the social sciences, to a very significant degree, under the assumption that secularization is an inevitable result of modernization and progress, religion is either left behind or pushed to the side. It drops out of public life and becomes privatized. So, the disciplines have sort of carved themselves up in ways that are mapped onto assumptions about the world and knowledge that may not actually be correct.

Q: How have the boundaries between the religious and the secular changed over time?

Bennett: Theres this widespread belief today that if you want to transform the world, you don't really need religion. Your just need science and technology. And yet if you go someplace like Silicon Valley and you walk down Sand Hill Road and walk into a coffee shop and you sit and listen to innovators talk about what they're doing, theyre all talking about transforming the most fundamental aspects of what it means to be human. And if you tune in closely, all sorts of kinds of topics that we used to associate with religion or spirituality are being talked about in relation to technology. Questions like what does it mean to be a being with a finite body? Can we overcome our own frailty and even cure aging? What does it mean to be connected to other people and to our environments? What does it mean for us to be able to build infrastructures in the world that promised to united us together but have become the engine for so much division?

"When we study religious environmentalism, we have to think anew about terms such as 'secular,' 'religious,' 'worldliness' and 'otherworldliness.'"

Hava Tirosh-Samuelson, Regents Professor and director of Jewish studies

Q: What are some other areas where we see this happening?

Tirosh-Samuelson: The area that I wor
k on is religious environmentalism. This movement emerged in the U.S. in the 1960s when people began to be aware of the ecological crisis. Interestingly, some of the scientists who were first to note the crisis were religious practitioners who considered the environmental crisis an assault on Gods created world. The interreligious movement of religious environmentalism and the academic discourse on religion and ecology illustrate the porous boundaries between science and religion or between the religious and secular aspects of life. For religious environmentalists, the natural world, or the environment, is not simply inert matter that can be known only through science, but rather the expression of divine creativity. When we study religious environmentalism, we have to think anew about terms such as secular, religious, worldliness and otherworldliness. Our analysis of religious environmentalism is not only historically grounded, it is also attentive to religious diversity and religious differences. The way we think about the relationship between religion and science reflects the legacy of Christianity. But other world religions, for example Judaism, Islam, Hinduism or Buddhism approach these issues quite differently. In addition to religious diversity, we are going to interrogate the category of spirituality as a hybrid category that fuses the secular and the religious. We can see it in regard to environmentalism but also in other domains such as medicine and the wellness industry. But what does it mean to be spiritual but not religious and how does spirituality express itself? We will seek to address these questions.

"What does it mean to alter a world our children will inherit?"

Gaymon Bennett,School of Historical, Philosophical and Religious Studies associate director of research

Q: How are these questions relevant to peoples everyday lives?

Bennett: It's not incidental that the three research areas for this project are three areas that are some of the major areas of collective crisis in the world today. On one level, these areas seem so timely, so current the question of bioengineering will transform our bodies, or how digital innovation will change our sense of ourselves. But on another level, these are really old, really fundamental questions: What does it mean to alter a world our children will inherit? How do our religious and spiritual views of reality shape what gets to count as important, or desirable or dangerous? Our lives are saturated with science and technology. Its fundamentally changing how we relate to ourselves our bodies, our planet, our food, our lovers, our sense of a higher reality. And then of course theres the environmental crisis and the question of what we modern people have done to our relationship with nature, whether it has intrinsic meaning and what that might be. All of these areas cut across time, place, culture and tradition, and are some of the most pressing issues that humanity is facing today.

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ASU event to address human dignity and technoscience - ASU Now