Monthly Archives: June 2021

The knowledge and experience of our advisors will help advance our vision of translating novel gene editing medicines.

"Incisive Genetics' platform technology represents a very promising avenue for gene therapy," said Dr. Hayden. "I look forward to leading the Scientific Advisory Board and working with the greater team at Incisive as they continue to expand upon their delivery platform and pipeline."

The Incisive Genetics SAB is comprised of:

Dr. Michael R. Hayden, CM OBC MB ChB PhD FRCP(C) FRSC

Dr. Michael Hayden is a Killam professor at the University of British Columbia and the founder of the Centre for Molecular Medicine and Therapeutics. He is also a Canada Research Chair in Human Genetics and Molecular Medicine. Dr. Hayden previously served as CSO and President of Global R&D at Teva and has co-founded numerous biotechnology companies, including 89Bio, Prilenia Therapeutics, Xenon Pharmaceuticals, and Aspreva Pharmaceuticals. He is a world-renowned scientist who has sat on many boards of private and public companies across the globe. Dr. Hayden is the recipient of numerous awards and is a pioneer in multiple fields, including genetic medicine. Dr. Hayden is the recipient of the Diamond Jubilee Medal (2012) and is a Member of the Order of Canada (2011), and a Member of the Order of British Columbia (2010).

Dr. Leslie Thompson

Dr. Leslie Thompson is a Donald Bren and Chancellor's Professor in the Departments of Psychiatry and Human Behavior and Neurobiology and Behavior at the University of California Irvine (UCI). Dr. Thompson has studied Huntington's disease (HD) for most of her scientific career and was a member of the international consortium that identified the causative gene for HD in 1993. Dr. Thompson is a member of the Hereditary Disease Foundation SAB, HD CARE SAB, Packard Center SAB, Chair of the Huntington's Disease Society of America SAB and is founding Co-Editor in Chief of the Journal of Huntington's Disease. She is also the PI of the OMICS core of the Answer ALS program, which is a precision medicine approach to understand sporadic ALS in over 1000 ALS subjects.

Dr. David Weiner

Dr. David Weiner is a neurologist and neuropharmacologist with over 20 years of experience in the discovery and development of novel therapeutics for neurological disease. He started his career at ACADIA Pharmaceuticals, where, over a ten-year period, he held a series of discovery research and clinical development roles working on multiple therapeutics, most notably Pimavanserin. He subsequently joined EMD Serono in a late clinical development role, ultimately leading early clinical development activities in neurology globally. Dave has extensive experience in neurological and rare disease drug development, serving as CMO and Interim CEO for Proteostasis Therapeutics Inc., CMO at aTYR Pharma and Lumos Pharmaceuticals, and as CEO at Amathus Therapeutics. He has authored numerous scientific publications, multiple patents, and serves on a number of clinical and scientific advisory boards, including the scientific advisory board of the Michael J. Fox Foundation for Parkinson Research.

About Incisive Genetics Inc.

Incisive Genetics, a privately-held biotechnology company based in Vancouver, Canada, was established in 2018. IG is focused on developing its cutting-edge non-viral delivery platform for genetic therapies. This disruptive and transformational delivery platform enables a one-step encapsulation of the active CRISPR components within lipid nanoparticles. The Company's pre-clinical pipeline includes programs addressing neurologic and ocular genetic diseases. IG is actively seeking partnerships with pharmaceutical companies developing gene therapies to be enabled by its novel delivery platform.

For more information, please visit http://www.incisivegenetics.com

FOR MEDIA INQUIRIES:Austin Hill[emailprotected]604-409-0660

SOURCE Incisive Genetics

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Incisive Genetics Announces Formation Of Scientific Advisory Board And Appointment Of Dr. Michael R. Hayden As Chairperson - PRNewswire

Most mornings, Huda Zoghbi, 67, climbs a glass-encased, curling staircase to reach her lab on the top and 13th floor of the Jan and Dan Duncan Neurological Research Institute in Houston, Texas. The twisting glass tower, which she designed with a team of architects, echoes the double helix of DNA a structure that has been central to her career-long quest to uncover genes underlying neurological conditions.

As the institutes director and as a scientist she is known for going beyond the standard job description. Genetics researchers often cast a wide net and sequence thousands of genes at a time. But in her prolific career, Zoghbi has focused on a handful of genes, methodically building up an understanding of their function one careful step at a time.

Thanks to that approach, Zoghbi has made a number of landmark discoveries, including identifying the genetic roots of Rett syndrome, an autism-related condition that primarily affects girls, as well as the genetic mutations that spur spinocerebellar ataxia, a degenerative motor condition. She has authored more than 350 journal articles.

Her accomplishments have earned her almost every major biology and neuroscience research award, including the prestigious Breakthrough Prize in 2017 and the Brain Prize in 2020. Shes clearly the international leader in the field, said the late Stephen Warren, professor of human genetics at Emory University in Atlanta, Georgia.

Zoghbi never set out to lead a large research center, she says her heart is in the lab. That said, she has excelled at it: Since the institutes inception in 2010, it has grown to host more than 200 scientists and fostered more than 70 new disease gene discoveries.

Part of that success may be due to the high expectations she sets for her trainees. They work long hours in what some call the lab that never sleeps, says Vincenzo Alessandro Gennarino, a former postdoctoral fellow in the lab, now assistant professor of genetics and development, pediatrics and neurology at Columbia University. But many say she is also endlessly empathetic and caring toward her lab family, as she describes it. She really kind of sees them as her scientific children in a way, says her son, Anthony Zoghbi, assistant professor of clinical psychiatry at Columbia.

For more than a decade now, this family has worked toward turning the deep biological mechanisms they have uncovered into treatment targets for Rett syndrome and other autism-related conditions. Finding effective therapeutics for such complex conditions is a tall order, Warren said. But shes got good model systems, good ideas, and she attracts very talented people in her lab, so I think she has a crack at it.

Zoghbi grew up in the vibrant city of Beirut, Lebanon, in the 1950s and 60s. Her father filled the familys home with books, which fueled an early passion for Arabic and English literature. She considered studying English literature when she entered the American University of Beirut in 1973, but she switched to biology, swayed by her mother, who saw her talent for the sciences. This path led Zoghbi to medical school at the same institution.

During her first few months of medical training in 1975, the Lebanese Civil War that had erupted earlier that year escalated. Constant bombings made it too dangerous to commute, so Zoghbi and her 62 classmates took shelter on campus. She lived in a closet inside a womens bathroom until the school year ended.

When flying shrapnel injured her 16-year-old brother, Jamal, in the spring, Zoghbis parents decided to send her and her younger siblings to live with their older sister in the United States for the summer. By mid-September, the war had only worsened, and Zoghbi scrambled to find a medical school that would accept a transfer student from another country.

Within weeks, she landed an interview at Meharry Medical College, a historically Black institution in Nashville, Tennessee, and started classes the next day. She spent the rest of the year catching up and feeling achingly homesick, she says, taking solace only in letters from William Zoghbi, a classmate she had started dating before she left Lebanon. Those books were soaked with tears, Zoghbi says. I literally cried my way through that year.

William whom she says she admired for his captivatingly kind smile joined her at Meharry the following year. They later married. (William Zoghbi is now chair of cardiology at Houston Methodist Hospital.)

Zoghbi sought a future in pediatric cardiology at the start of her residency at Houstons Baylor College of Medicine in 1979. And then I rotated in neurology, and everything changed, she says. I fell in love with neurology.

But her excitement wore off soon after she started a neurology fellowship in 1982. It was incredibly frustrating, Zoghbi says, to diagnose children with rare neurological conditions and be unable to provide their families with any information about a cause or hope for a treatment.

This helpless feeling came to a point in October the following year, when she encountered a little girl with a particularly devastating and puzzling condition: Ashley Fry, a 3-year-old girl with sparkling brown eyes, had developed typically for the first 18 months of her life but then suddenly started losing language skills and wringing her hands, rubbing her left hand over and over with her right.

That pain was very tangible to me like, to have a girl, shes healthy, and shes beautiful, and youre enjoying her, and then to see her robbed of that, Zoghbi says. I felt that agony.

Zoghbi and her attending physicians diagnosed Ashley with Rett syndrome. Ashley was the first case diagnosed in Texas and among only a handful identified in the U.S. at the time. But a week later, Zoghbi found another case a girl who arrived at a cerebral palsy clinic wringing her hands. Zoghbi pulled more charts from the clinic describing similar symptoms a stark regression, intellectual disability, seizures and hand-wringing and found a few more cases.

Soon Zoghbi and her colleagues started publishing papers on Rett syndrome, and children with suspected cases came in from all over the country. One after the other they looked the same, and I was like, It has to be a gene, and thats when I decided Im going to go into research, Zoghbi says.

In 1984, she approached the renowned geneticist Arthur Beaudet at Baylor about doing a postdoctoral fellowship in his lab. She had collected blood samples from 200 children with Rett syndrome, and she wanted to try to find the gene underlying the condition. Zoghbi had virtually no laboratory experience, but she was just extremely talented and bright and motivated, says Beaudet, now chief executive officer of the Houston-based prenatal genetic testing company Luna Genetics. She was the kind of trainee every scientist hopes to encounter one day.

Beaudet took Zoghbi on but, to her disappointment, said she couldnt focus on Rett syndrome, which he deemed too difficult to trace genetically. Zoghbi agreed instead to study a family in Texas with spinocerebellar ataxia work that later led to a groundbreaking co-discovery of the gene underlying a subtype of the condition.

Even as Zoghbis spinocerebellar ataxia work accelerated, she continued thinking about Rett syndrome. Her urge to help grew even stronger when she had her first child, a daughter named Roula, in 1985. She did little experiments here and there, sometimes under the radar, searching for clues that the causative gene was on the X chromosome, or X-linked. If so, it would explain why all the cases shed seen so far were girls. If a mutation disrupts a gene on the X chromosome, girls, who have two Xs, still have a functioning copy. But boys, who have only one X chromosome, might not survive.

She was able to pursue her ideas further when she started her own lab at Baylor in 1988. With help from geneticist Uta Francke at Stanford University in California, Zoghbi and her team eventually ruled out more than two-thirds of the genes along the X chromosome. That left hundreds of genes to explore, which they started sequencing one by one, taking about a years worth of work each time. Every gene was a labor of love, Zoghbi says.

Negative results piled up, and funding slowed. But Zoghbi kept at it, persistent as ever. Sometimes, during long weekends in the lab, her two children, Roula and Anthony, tagged along, peering into petri dishes or practicing pipetting while she worked.

One afternoon in August 1999, Zoghbis phone rang just as she and her family were returning home from their annual summer trip to Lebanon. She raced to the phone, and on the other end was Ruthie Amir, a postdoctoral fellow in the lab.

I think I found it, Amir said.

Poring over the data together at Zoghbis house later that day, the pair saw that five girls with Rett syndrome all carried a spontaneous mutation in the same gene on the X chromosome. The gene, MECP2, encodes a protein known as methyl-CpG binding protein 2, which regulates the expression of thousands of other genes throughout the body and brain.

The team published their results two months later in Nature Genetics, 16 years after Zoghbi first met Ashley. Zoghbi invited Ashley and her family to the press conference announcing the discovery. She didnt have to explain why she was asking them to come to Houston, recalls Ashleys father, Clifford Fry. I knew it in my heart that she had found the gene.

Zoghbi has meticulously probed the far-reaching effects of MECP2 ever since, tracking the results of removing the gene from different areas or cell types in the brain. Each of these conditional knockouts has helped to account for a subset of Rett-related traits. Deleting MECP2 from the hypothalamus, for example, produces mice that eat uncontrollably and are aggressive and easily stressed, not unlike traits seen in boys with less severe mutations in MECP2.

Knocking out MECP2 in inhibitory neurons recapitulates almost all the traits of Rett syndrome. The mice even clasp their forepaws repeatedly, which mirrors the girls hand-wringing. And by removing MECP2 from each of two subtypes of inhibitory neurons, or from inhibitory versus excitatory cells, Zoghbi has demonstrated how the gene supports the function of whole brain circuits, not just individual neurons.

Zoghbi and her team also engineered mice with an extra copy of MECP2 to use as controls in Rett experiments. But the animals developed severe seizures, and about a third died prematurely. This unexpected result, published in 2004, showed that a surplus of MECP2 protein can be just as problematic as a deficiency. The following year, another team described some of the first cases of MECP2 duplication syndrome, which causes autism, intellectual disability and seizures mostly in boys.

Zoghbi is particularly attached to her MECP2 duplication work because Tropical Storm Allison nearly washed it away. When the storm slammed into Houston in June 2001, it flooded the animal facility where some of Zoghbis MECP2 duplication mice lived. Zoghbi and one of her graduate students suited up in waders and went searching with a flashlight through the chest-high water for any surviving mice. They found a lone survivor in a top rack of the cages. That mouse is the founder of one of the MECP2 duplication colonies the lab studies to this day.

I learned a lesson from that, Zoghbi says. Always go back and take a second look. You never know.

Zoghbi holds a steady focus on finding what will truly help people with Rett syndrome and the other conditions she studies. Its clear that her approach is not Okay, Ive discovered the gene, Ive done my job, says Michela Fagiolini, associate professor of neurology at Harvard University, who also studies Rett syndrome. And that drive is Zoghbis true legacy: She has built not just an empire in Texas but also created a school of thinking.

In one ongoing line of work, Zoghbis team has used snippets of genetic material, called antisense oligonucleotides, to silence the extra MECP2 gene copy in duplication mice. A drug delivering these genetic strands reverses problems with movement, learning and memory in mice with two human copies of MECP2, suggesting that it might also be effective in people.

The key to these types of treatments, Zoghbi says, will be titrating the dosage of MECP2 expression so that it normalizes protein levels without tipping them too far in the direction of Rett syndrome. As such, Zoghbi is searching for biomarkers that signal when MECP2 levels have reached a safe zone.

Zoghbi has also worked with colleagues at Baylor to show that deep brain stimulation applied to the hippocampus improves learning and memory in a mouse model of Rett. They are exploring whether stimulating motor circuits can similarly ease motor deficits in the mice. And Zoghbi has also tried mimicking the effects of deep brain stimulation in the form of intensive behavioral training to activate some of the same circuits.

Training Rett mice on motor and memory tasks early in life postpones the onset of difficulties in these areas, according to results published in March. If the same holds true in human clinical trials, it would help build the case to offer genetic screening for Rett syndrome in newborns, Zoghbi says. Lets give these girls the maximum opportunity, and lets hopefully delay the disease onset by a year or year and a half or two, until more effective genetic treatments become a reality, she says.

Zoghbi stopped working as a clinician a couple of years ago, but a photo of Ashley, now 41, sits on the windowsill in her office, reminding her of where it all started and what shes working toward. When Ashley and her family are in town, Zoghbi sometimes meets them at their hotel, just to say hi to Ashley and give her a hug and a gift, such as an ornate purple and gold shawl.

Giving people like Ashley a chance to fully engage in their world is at the heart of Zoghbis inexhaustible work ethic, says Laura Lavery, a postdoctoral associate who has worked with Zoghbi for the past seven years. Shes the most driven person Ive ever met, and underlying all of that is really her love and empathy for humankind. She is just not going to stop until she figures out how to help.

Cite this article: https://doi.org/10.53053/THWT9489

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Huda Zoghbi: Taking genetic inquiry to the next level - Spectrum

LONDON, June 28, 2021 (GLOBE NEWSWIRE) -- Treos Bio Limited (Treos), a clinical stage biotechnology company using data science and proprietary biomarkers to develop precision off-the-shelf and personalized peptide cancer immunotherapies, today announced the publication of a peer-reviewed article titled A Peptide Vaccine Candidate Tailored to Individuals Genetics Mimics the Multi-Targeted T Cell Immunity of COVID-19 Convalescent Subjects in Frontiers in Genetics. The paper reviewed the potential of PolyPEPI-SCoV-2, the Companys peptide vaccine candidate, to potentially address all four structural proteins of the COVID-19 virus in order to generate long-term immunity in virtually all human subjects, independent of ethnicity.

We are gratified to see these promising results published in Frontiers in Genetics, providing another scientific validation for our novel approach to match patients genetic background to T cell responses, which was already successfully applied for the design of our off-the-shelf cancer vaccines. We believe long-term immunity to coronaviruses will likely originate from targeted and broad T cell responses and we think that our technology has the potential to produce long-lasting immunity against this variable virus, said Dr. Christopher C. Gallen, M.D., Ph.D., Chief Executive Officer of Treos. Overall, with the downstream physiological activation shown, these data have compelling implications for the development of highly immunogenic, T cell-focused global vaccines against various pathogens and diseases. We look forward to leveraging our proprietary data science and therapeutic platform to continue investigating this program.

Article highlights include:

The full article is accessible at https://www.frontiersin.org/articles/10.3389/fgene.2021.684152/full and at http://treosbio.com/index.php/publications-2/.

About Treos Bio LimitedTreos Bio uses computational data science and proprietary biomarkers to develop precision off-the-shelf and personalized peptide-based cancer immunotherapies. The Company has developed a unique ability to match the antigens expressed by a specific cancer to the individual patients target recognition mechanism (HLA). This technology aims to address the challenge of the variability of an individual patients clinical responses to cancer immunotherapies. Treos lead candidate is PolyPEPI-1018, an off-the-shelf immunotherapy for the treatment of metastatic colorectal cancer, co-developed with a candidate companion diagnostic. Treos is also developing off-the-shelf personalized immunotherapies (PEPI Panel) for several types of solid tumors and has completed preclinical development of PolyPEPI immunotherapies in ovarian, breast, bladder, gastric and lung cancers and melanoma. The Company is also developing an investigational COVID-19 peptide vaccine, PolyPEPI-SCoV-2. Treos launched in February 2017 and has raised $28 million Series A funding led by shareholders of BXR Group and recently closed a $14 million investment round led by Outsized Ventures (formerly known as Luminous Ventures). More information can be found at http://www.treosbio.com.

Media Contact:

Solebury TroutZara Lockshin +1-646-378-2960zlockshin@soleburytrout.com

Investor Contact:

Solebury TroutAlan Lada +1-646-378-2927alada@soleburytrout.com

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Treos Bio Announces the Publication of Preclinical Data in Frontiers in Genetics Showing its COVID-19 - GlobeNewswire

One of the five authors, who all contributed equally, is Dr Adam Rutherford, a prominent science communicator, author, broadcaster and an Honorary Senior Research Associate at UCL.

He announced the new paper, which he says has been accepted by a journal but not yet published, on his Twitter feed.

"I have been working on this a while: sparking a conversation about the lexicon of genetics, which continues to utilise scientifically redundant, confusing and racist terminology,"he said. "We're definitely not prescribing or policing language, but want to prompt a dialogue with colleagues in similar and adjacent fields about our terminology, datasets and tools, and move towards a lexicon that both serves the science and frees us from a racist past."

Dr Ewan Birney, deputy director of the European Molecular Biology Laboratory at the Wellcome Genome Campus in Cambridgeshire, is also a co-author of the article.

He explains that beyond dropping Caucasian, other terms should also be avoided, including ethnicity labels -such as"Native American", "Hispanic"and "White Irish"-and cultural terms such as "European".

Dr Birney and his colleagues advocate for scientists to replace these commonly used words and phrases with more complex language, based around a two-step genetic analysis.

As a result, he says this more technical language would see the label of "European replaced with "The European-associated PCA cluster, which aims to minimise variation in non-genetic factors and genetic factors".

This suggestion is, by Dr Birneys own admission, "bamboozling"and "a bit complex"for non-geneticists.

PCA - orprincipal component analysis - is a tool for analysing genes that picks up similar physical or biochemical characteristics of species,

However, in the article the scientists say they prioritised "technical accuracy over concision".

"Some of these suggestions may meet with disagreement; we present them partly to stimulate discussion of these and other terms, and in the hope that this will lead to better and more accurate language conventions and less misunderstanding, particularly outside of human genetics,"the researchers add.

Dr Aylwyn Scally is another of the authors. Heworks in the genetics department at the University of Cambridge and is based at Darwin College.

Darwin College was set up and named after Sir Charles Galton Darwin -a noted proponent of eugenics and grandson of Charles Darwin -upon his death in 1962.

In a tweet, Dr Scally revealed the opinion piece he co-authored received "constructive input"from Dr Agustin Fuentes, a professor of anthropology at Princeton University, who last month penned a scathing editorial criticisingCharles Darwin.

He accused him of letting his scientific process become "warped" by his prejudices, which included racism, sexism and misogyny.

Dr Michael Inouye, of the University of Cambridge, and Dr Jennifer Raff, of the University of Kansas, also co-authored the article.

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The word Caucasian is racist and must be banned, say academics - Telegraph.co.uk

Humans are testing the limits of most species survival, with their planet-wide changes. As urbanisation, deforestation, loss of wildlife, and human-wildlife conflicts continue to spiral up, there is a need to use every available tool available, to help protect what is left of the natural world. Molecular ecology is one such tool for conservation and can help in wildlife disease management and forensics in illegal trade.

Molecular ecology is a hybrid field that combines molecular biology techniques with ecological data to make sense of natural processes such as the growth or decline of populations, formation of new species, extinctions and invasiveness.

In modern molecular ecology, genetic data is analysed in the context of field and observational studies to address ecological problems.

Molecular ecology is used to estimate population genetic diversities to aid wildlife breeding and conservation efforts, define species for conservation policy, track diseases, and combat poaching.

Genetic data from organisms is collected in the form of molecular markers, which are biological molecules that may be used to distinguish between species, populations, or individuals.

When molecular biologists first began identifying genetic differences between individuals, they extracted proteins from animal or plant tissues, and used them as molecular markers. However, DNA-based markers soon became more popular than protein markers as they could be obtained from very small samples of tissue. They were also easier to handle and showed more variations than protein-based markers. Molecular ecology now relies on extracting DNA from animals using tissue samples (typically hair, scales, skin, bones, horns, or blood) or even fecal matter.

Different individuals within a species can have different forms or variants of a particular gene or molecular marker. A familiar example of this is blood type one of the genes that determine blood type in humans comes in three different forms/variants known as A, B, and O. Such genes are known as polymorphic (poly = many, morphic = form) genes. Genes that are the same in all individuals of a population are called monomorphic (mono = one, morphic = form).

By studying and documenting the variations in the genes and molecular markers, one can measure the genetic diversity of a population of animals with the help of statistics.

Genetic diversity is the fuel for natural selection. It is a source of inheritable variations in characteristics that can allow populations to survive changing environments. Higher the genetic diversity of a population, higher the chance that some individuals in that population can adapt to new environmental conditions. Thus, the population will not go extinct due to any changes.

Large populations typically have high genetic diversities, whereas small populations have low genetic diversities. If the population size of a species drops sharply due to natural disasters or human negligence and anthropogenic activities, its genetic diversity is reduced, creating a genetic bottleneck. When this happens, not only is the population robbed of its potential to survive, it also becomes vulnerable to inbreeding. Inbreeding occurs in small populations, where genetically related individuals are more likely to mate with each other.

Over time, such populations suffer from inbreeding depression, a condition where genetic variants with harmful mutations begin to accumulate.

Cheetahs are a classic example of how inbreeding depression can bring a species to the brink of extinction, despite extensive efforts at conservation through captive breeding programmes. To understand why captive breeding efforts in cheetahs were failing, a series of genetic analyses were done. These analyses showed that due to the combined effects of the past natural disasters and indiscriminate human hunting, cheetahs were highly inbred. The inbreeding not only caused reproductive issues with low fertility and high infant death rates, but also left cheetahs vulnerable to diseases. The cheetahs genetic diversity was so severely decimated, that a crucial immune-related gene complex, which is usually very polymorphic in most species, was monomorphic (had no genetic variation) in cheetahs. This caused feline infectious peritonitis a common viral disease that kills <1% of domestic cats to wipe out nearly 80% of a captive breeding population of cheetahs in the USA.

To offset inbreeding in captive and protected populations of other endangered species (Mexican red wolves, Puerto Rican crested toads, and African lions to name a few), conservationists have attempted genetic rescues. Genetic rescues are carried out by introducing new individuals (which can add more genetic variation) into inbred populations to increase genetic diversity.

However, such measures can backfire in some species like the Ibex and the Arabian oryx, which ironically, suffer from outbreeding depression. Gene flow between populations in such species is usually low, as their populations are insular with very limited immigration and emigration; therefore, each population seems genetically inbred. This, however, is advantageous for the population as it has developed local adaptation and maintains a specific combination of gene variants that allow for better survival in local conditions.

In misplaced attempts at genetic rescue by reversing this local inbreeding to recover genetic diversity in such systems, breeding programmes mate individuals from different populations. The outcomes of these efforts are usually poor. The offspring of such pairings often end up with genetic combinations that leave them unable to survive in either of the two local conditions. For example, in an attempt to genetically rescue the Alpine ibex, Nubian ibex were introduced into the Tatra mountains. Unfortunately, the introduced ibex which were adapted to warmer climates, rutted in autumn and birthed hybrid young in February, the coldest time of the year. Obviously, these offspring did not survive, and the rescue attempt failed.

Based on the lessons learned from both inbreeding and outbreeding depression, it is clear that molecular ecology is essential for successful wildlife conservation.

In India, molecular ecology studies on the critically endangered gharial and blackbuck reveal that the genetic diversities in managed populations of these animals are not high, painting a grim picture for their chances of survival.

Recent work using genome-wide data on tigers suggests that compared to the tigers from Amur, Sumatran, and Malayan populations, Indian tigers have very high genetic diversity. However, this data also indicates that certain tiger populations in India are so isolated and small, that local inbreeding is occurring.

Although we have many tigers in Indiaroughly two-thirds of all the worlds tigerstheir populations in some parts of India are fragmented, which has caused local inbreeding. The Amur tigers, on the other hand, are much fewer in numbers, but they are not inbred because they are not isolated from each other, says Uma Ramakrishnan a molecular ecologist from the National Centre for Biological Sciences (NCBS), Bangalore.

Ramakrishnan and her team have worked on tigers for over 15 years, and their molecular data is now being used to formulate plans for genetically rescuing some of Indias inbred tiger populations. Our work can help collecting data regarding which tigers are least inbred and which ones can be moved between populations, she adds.

Defining a species seems more like an esoteric academic undertaking rather than a serious and practical conservation issue. However, the conservation status of a species and the legal protection it is accorded is based on its taxonomic classification. Therefore, any ambiguity in how or what constitutes a particular species can have a major impact on that organisms survival.

Traditional methods of defining a species based on physical characteristics and behavioral observations are no longer considered reliable. Molecular taxonomy, which depends on genetic information, is now being increasingly used to resolve taxonomic disagreements and correct misclassifications.

Errors in taxonomy have resulted in the mismanagement of conservation efforts of many species. Two examples that stand out, are the cases of the colonial pocket gophers and the dusky seaside sparrow.

A single population of pocket gophers (<100 in number) within a tiny range in the State of Georgia, USA, was managed as an endangered species for more than 10 years as it was described as a distinct species (Geomys colonus) based on physical characteristics. Molecular ecology later proved that this population was genetically no different from Geomys pinetus, a pocket gopher species that is common in southeastern USA.

Similarly, when a darker form of the seaside sparrow (Ammodramus maritimus) was discovered in Florida, USA, it was identified as a separate species (A. nigrensis) and listed as endangered due to its low numbers and restricted range. After a seven-year long unsuccessful captive breeding program, the last dusky sparrow died in captivity. Two years later, however, molecular data revealed that this species had been genetically indistinct from the seaside sparrow.

In both these cases, conservation efforts were wasted on populations that had been misclassified as distinct species.

Another area in which molecular taxonomy is becoming important is in identifying areas rich in endemic species.

India has a huge amount of biodiversity, but many of its landscapes, like savannahs, and organisms, like arthropods, have hardly been studied. Now, with more field expeditions across these landscapes, and better taxonomic tools based on DNA that complement traditional morphology-based classification, we are making some surprising discoveries in the field of systematics, says Jahnavi Joshi, a molecular ecologist and taxonomist from the Centre for Cellular and Molecular Biology (CCMB), Hyderabad.

Recent studies on the molecular taxonomies of geckos and centipedes have shown that previously ignored regions like peninsular India, the Eastern Ghats, and the drier northern parts of the Western Ghats are unexpectedly rich in endemic species. Such areas need to be protected to conserve the range-restricted flora and fauna that are exclusively found there.

Molecular ecology has now become an important part of wildlife disease management. Rapid detection of even low intensities of viral, bacterial, and parasitic infections is now possible using tests based on PCR (polymerase chain reaction a technique that amplifies or makes more copies of specific DNA regions). Currently, PCR-based diagnostic tests allow for the swift detection of a number of diseases in wildlife such as the Kyasanur forest disease (a tick-borne viral disease in South India), Ebola, Nipah, tuberculosis, rabies, and malaria, all of which are directly responsible for endangering wildlife and spilling over into domestic livestock and human populations.

By studying molecular interactions between pathogens and their vectors (insects like ticks and mosquitoes, or wildlife like raccoons), scientists can even track routes of transmission and reservoir hosts for diseases such as monkey fever, avian malaria, and rabies. In addition, molecular ecology studies on host-pathogen interactions can help conservationists understand how some species or individuals are more tolerant, resistant, or susceptible to certain diseases. For example, molecular genetics work on frogs is showing that individuals with stronger immune systems are actually more likely to die of chytridomycosis, a fungal skin infection that has caused mass die-offs and extinctions in amphibians globally.

When law enforcement authorities seize illegal wildlife products, the first problem they encounter is identification what animal does a pelt, skin, hair, horn, flesh, or bone belong to? Molecular forensics using DNA barcoding has been used to identify species even from processed samples such as dried meat and powdered bones or horns. Similar to how supermarket scanners can identify products from a series of black and white stripes using the universal product code, DNA barcoding matches short sequences from samples with those in a reference database to identify which species the sample belongs to. For animals, sequences from the mitochondrial gene COX1 or CO1 (cytochrome oxidase 1) are usually used. Currently, reference databases such as the Barcode of Life Data System (BOLD) and the International Barcode of Life contain nearly 9.5 million DNA barcodes for thousands of species of animals, plants, and other organisms.

The usefulness of molecular tools does not end there. Other molecular markers such as microsatellites, minisatellites, and SNPs (single nucleotide polymorphisms), as well as techniques such as DNA profiling/fingerprinting (which has been used in criminal investigations), can be applied to identify which country or population the poached animal came from. Researchers have used microsatellite data to identify the species, sex, and even geographic origins of seized tiger parts, elephant tusks, and a variety of other animal parts.

Banner image: Although Amur tigers have much smaller population sizes and genetic diversity than Indian tigers, they are not isolated from one another, and so, do not suffer from inbreeding. In India, however, some tiger populations are so small and isolated, that local inbreeding has occurred. Photo by S. Brickman/Flickr.

Excerpt from:
What is molecular ecology and how does it help in conservation? - Mongabay-India