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Monthly Archives: July 2017
Pence Calls for Return to the Moon, Boots on Mars – Space.com
Posted: July 7, 2017 at 1:49 am
Vice President Mike Pence addresses NASA employees on Thursday, July 6, 2017, at the Vehicle Assembly Building at NASAs Kennedy Space Center in Cape Canaveral, Florida.
CAPE CANAVERAL, Fla. The Trump administration will seek a heavier emphasis on human-spaceflight efforts, including crewed missions to the moon and Mars, Vice President Mike Pence said today (July 6).
During a 25-minute speech at NASA's Kennedy Space Center (KSC) here on Florida's Space Coast, Pence told the 700-plus members of the crowd that the United States is "at the dawn of a new era of space exploration," and called for a return to the moon and "American boots on the face of Mars." He also said the United States will maintain a presence in low-Earth orbit.
Pence standing on a flag-draped podium in KSC's cavernous Vehicle Assembly Building offered no time frame or budget for the expeditions, but said partnerships with commercial companies are key. He repeatedly called for a "re-establishment" of American leadership in space and made no mention of ongoing or future international partnerships or collaborations, such as the International Space Station, a $100 billion project of 15 nations. [The First 100 Days: What Trump Has Done on Space So Far]
Pence chairs the newly revived National Space Council, which will advise the White House on space policy. The council will begin its work with an initial meeting before the end of the summer, the vice president said today.
Pence also stressed that President Donald Trump's initiatives in space will extend well beyond NASA, though the heart of the program will be human spaceflight and exploration.
"President Trump's vision for space is much larger than NASA alone," Pence said, adding that the National Space Council will coordinate policy among several federal agencies and interests, including the military and commercial sectors.
Echoing Trump's "America first" theme, Pence said Trump intended to carry nationalism into space with renewed emphasis on human space exploration and discovery "for the benefit of the American people and all of the world."
"America will lead in space once again," Pence said.
The United States already has the biggest budget for space exploration, according to a 2016 World Economic Forum report.
"From the first moon landing to the International Space Station, the U.S. government agency NASA has been leading space exploration since its creation in 1958," the report states.
Trump's budget request for the fiscal year that begins Oct. 1 drops the Obama Administration's plan to send astronauts to an asteroid as a steppingstone to Mars, but maintains the program's multibillion-dollar, heavy-lift Space Launch System rocket and deep-space Orion capsule. The Trump administration's budget request also continues previous program funding for NASA's commercial partnerships with SpaceX, Boeing and other companies.
Since the end of the shuttle program in 2011, the United States has been dependent on Russia to fly crews to and from the space station, which flies about 250 miles (400 kilometers) above Earth. NASA hopes to turn over crew ferry flights to SpaceX and Boeing before the end of 2018.
Editor's Note:Space.com senior producerSteve Spaletacontributed to this report.
Irene Klotz can be reached on Twitter at @free_space. Follow us @Spacedotcom, Facebookor Google+. Originally published onSpace.com.
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Using Big Data to Hack Autism – Scientific American
Posted: at 1:47 am
Its been 10 years sinceMichael Wiglerhad a breakthrough revelation in autism geneticsone that arguably launched the field as we know it.
In April 2007, Wigler and his then colleague,Jonathan Sebat, reported that de novo mutationsthose that arise spontaneously instead of being inheritedoccur more often in people with autism than in typical people. The mutations they noted were in the form of copy number variants (CNVs), deletions or duplications of long stretches of DNA. CNVs crop up frequently in cancer, an earlier focus of Wiglers work. But his find that they are also involved in autism came as a surprise to those in the field. Genetics was striking out with other efforts based on transmission and inheritance, Wigler says. In that vacuum, the new idea was quickly embraced.
The discovery fast led to further advances. Focusing primarily onde novomutations, three teams of scientists, including one led by Wigler, began hunting for genes that contribute to autism. Their approach was efficient: Rather than looking at the entire genome, they scoured the 2 percent that encodes proteins, called theexome. And they looked specifically at simplex families, which have a single child with autism and unaffected parents and siblings. The premise was that comparing the exomes of the family members might exposede novomutations in the child with autism. The approachyielded a bumper crop: Based on data from more than 600 families, the teams together predicted that there are hundreds of autism genes. They identified six as leading candidates. Some of the genes identified at the time CHD8,DYRK1A,SCN2A quickly became hot areas of research.
In 2014, the number of strong candidates jumped higher. In two massive studies analyzing the sequences of more than 20,000 people, researchers linked 50 genes to autism with high confidence. Wiglers team looked at simplex families and found rarede novomutations in 27 genes. In the second study, researchers screened for both inherited andde novomutations and implicated 33 genes. The two studies identified 10 genes in common.
Two years ago, the tally of autism gene candidates shot up again. Deploying statistical wizardry to combine the data onde novoand inherited mutations, along with CNV data from theAutism Genome Project, researchers pinpointed 65 genes and six CNVsas being key to autism. They also identified 28 genes that they could say with near certainty are autism genes.
For so long, weve been saying if we could just find these genes, wed be able to really make some headway, saysStephan Sanders, assistant professor of psychiatry at the University of California, San Francisco, who co-led the study. Suddenly, youve got this list of 65-plus genes, which we know have a causative role in autism, and as a foundation for going forward, its amazing.
These advances establish beyond doubt that autism is firmly rooted in biology. More and more, we are erasing this idea of autism being a stigmatizing psychiatric disorder, and I think this is true for the whole of psychiatry, Sanders says. These are genetic disorders; this is a consequence of biology, which can be understood, and where traction can be made.
This is just the start, however. As scientists enter the next chapter of autism genetics, they are figuring out how to build on what they have learned, using better sequencing tools and statistics, bigger datasets and more robust models. For example, they are looking for common variantswhich are found in more than 1 percent of the population but may contribute to autism when inherited en masse. And they are also starting to look beyond the exome to the remaining 98 percent of the genome they have largely neglected thus far.
Most of the genetic advances fall into a category of large-effect-sizede novovariants, which is only one piece of the puzzle, saysDaniel Geschwind, professor of human genetics at the University of California, Los Angeles. Its an important piece, but one that still cannot explain why autism clusters in families, for instance, or why close relatives of people with autism often share some of the conditions traits.
So how much of autisms genetic architecture have scientists uncovered? Current estimates suggest that rare mutations, whetherde novoor inherited, contribute to the condition somewhere between 10 and 30 percent of the time. Before the recent spate of discoveries, the proportion of individuals whose autism had a known genetic cause was only 2 to 3 percentmuch of that from rare related genetic syndromes, such asfragile X syndromeand tuberous sclerosis complex, which stem from mutations in a single known gene. These syndromes often involve some core features of autism, along with their own set of characteristic traits, and intellectual disability.
Two generations ago, at least 75 percent of the time autism was comorbid with severe intellectual disability and other neurodevelopmental abnormalities, saysMark Daly, associate professor of medicine at Harvard University. It was also a much rarer diagnosis.
The large increase in diagnoses in recent decades overwhelmingly reflects cases at the mild end of the spectrum, Daly says, creating a new challenge. The genetics of autism has us wrestling with the fact that rare mutations, and especially these spontaneously arising ones, are the strongest risk factors, he says. But at the same time, theres a majority of cases now that dont have any of those high-impact risk factors.
Instead, much of the risk in these instances likely comes from common variants, which have small effects on their own, but can add up to increase overall risk. Researchers have tried to identify those relevant to autism using genome-wide association studies (GWAS), which compare the genomes of people with and without a condition to find differences in single-letter swaps of DNA called single nucleotide polymorphisms.
Because common variants have small effects individually, they are difficult to find, but multiple studies suggest that theyplay a major rolein autism risk. In a 2014 study, for instance, researchers used statistical tools to estimate the heritability of autism from the amount of common variation shared by unrelated people with autism. They applied the method to data from more than 3,000 people in Swedens national health registry. Their calculations indicated thatcommon variants account for 49 percentof the risk for autism in the general population; rare variants, equal partsde novoand inherited, explain 6 percent. Some scientists dispute these figures, but its clear that common variants, rare inherited variants and spontaneous mutations all play a part in autism.
Wigler says he is skeptical of using GWAS studies for autism precisely because they focus on common variants. Most of the disorders that will cause pain and suffering and require expensive treatments, if theyre genetic, are caused by rare variants that are not going to stay around in the population, he says.
Common variants may turn out to be more relevant at the milder end of the spectrum than in those who are severely affected. The people who havede novomutations, en masse, tend to have lower intelligence quotients and more cognitive problems, Sanders says.
Researchers are grappling with how to fit these pieces together: Finding and diagnosing rare variants linked to severe outcomes is important, but so is unraveling how the core traits of autism relate to other psychiatric conditions and manifest in the general population. Both goals are important, and they shouldnt be seen as at odds with each other, Daly says. In fact, a study published in May reported thatrare and common variants can combineto increase an individuals risk.
The landscape of autism genetics becomes even more complex when considering the sheer number of genes that could be involvedsome researchers estimate up to a thousandand the fact that many high-confidence autism genes are also associated with other conditions, ranging from intellectual disability andepilepsyto schizophrenia and congenital heart disease.
This many-to-one and one-to-many relationship is not surprising, Sanders says. But it does mean there are probably no unique autism genes per se. But I could flip that round and say weve not found anything which is a pure intellectual disability or schizophrenia gene [either]; on a fundamental level, these disorders seem to be related, he says. If I was to say, Can we find something which contributes more to autism than other disorders? then I think the answers yes. The genes that seem particularly tied to autism could offer important clues about the conditions biology.
The genes identified so far have hinted at a handful of underlying mechanisms that contribute to autism. Most of them seem to be involved in three broad categories of tasks: maintaining the function ofsynapses, or the connections between neurons; controlling the expression of genes; and modifying chromatin, structures of DNA wound around protein spools called histones. Chromatin determines which stretches of DNA can be read and so influences gene expression.
The idea of a brain condition originating with atypical neuronal connections made logical sense from the start. There had been a lot of interest in the synapse, Sanders says. But the candidates that control gene expression only emerged in the genetic studies. Two genes that consistently top the high-confidence listsCHD8 and SCN2Awere both somewhat of a surprise. CHD8 encodes a chromatin regulator that controls the expression of thousands of other genes. SCN2A codes for a sodium channel and had primarily been associated with infantile seizures.
Using gene expression maps, such as theBrainSpan Atlas, researchers have traced when and where autism genes are active in the brain. They have found that many of the genes, CHD8 and SCN2A included, are expressed in parts of the cortex during mid- to late fetal developmentwhich happens to be the peak period when neurons are forming. We dont really understand it yet, but theyre more likely than not to disrupt fetal brain development in mid-gestation, Geschwind says. That timing suggests they interfere with processes that are critical to setting up the cortex, including which types of cells form and where in the brain they migrate. If the cortex isnt set up right, he says, you create ongoing problems with how neurons communicate, among other important functions. Within the next few years, he says, researchers will have a refined understanding of the neurons and circuits affected.
Work in animal and cell models reveals similar problems with the genesis, structure and fate of new neurons and the connections between them. In some cell and animal models of syndromic forms of autism, scientists have managed to at least partially correct some of these problems with drugs. The unrealized promise of these findings is that some traits of autism may ultimately prove reversible, even in adults.
The idea that theres something plastic here, not set in stone at birth, is very important, saysMatthew State, chair of psychiatry at the University of California, San Francisco, and lead investigator on many of the big autism genetics studies.
In the meantime, genetic discoveries have delivered some immediate benefits for people with the condition. If you go into a clinic today, theres about a 10 percent chance of you getting a genetic diagnosis, and I would expect to find evidence which was suggestive in about another 5 to 10 percent, Sanders says. We cant then turn round and say, Heres your cure, but what we can do, at least, is put people in touch with other people with that same mutation. Becoming part of such a group gives people a better idea about what the future holds for them and provides them with support and understanding.
Advocacy groups can lobby researchers and funding bodies, contribute to research on their condition and help find participants for clinical trialswhich, by grouping people according to their underlying genetics, would then have a greater chance of success. It becomes very empowering, saysJoseph Buxbaum, director of the Seaver Autism Center for Research and Treatment in New York.
Genetic diagnoses can also help families make decisions about family planning and treatment options. For example, deletion of a region on chromosome 17, called 17q12, is associated with autism and schizophrenia, but treating someone who has this CNV with certain mood stabilizers or antipsychotics could be dangerous: It is also associated with renal failure and adult-onset diabetes, which the drugs would exacerbate. Whats more, certain mutations increase therisk for some types of cancer. Knowing those mutations can be very helpful in those cases, not just in treating autism, but in treating the patient more broadly, Geschwind says.
Debates abound on how best to move the field forward, but one thing most researchers agree on is the need to identify more mutations linked to autism. Theres great benefit now in just doing more exome sequencing, Sanders says. Theres more genes to be found: Those will hopefully help patients; theyll also give us more of an understanding of what autism is.
Much of the variation that predisposes someone to autism, however, may lie in noncoding regions. If half of the variants are outside of the coding region, we need to know how to interpret them, Wigler says. For that reason alone, we have to study that region. Plus, were going to learn an enormous amount of biology in the process.
Noncoding regions make up the dark genome, which is about 98 percent of the whole. Because of the cost and effort involved in sequencing the whole genome, most autism researchers have stayed focused on exomes, until recently. Several teams are now sequencing whole genomes of people with autism, with the aim of identifying risk variants in these noncoding regions. Whole-genome sequencing inevitably will overtake exome sequencing, Sanders says. Its just a question economically of whether its moment is now, or in two years, or five years. Right now, thats a hard question to answer.
In March, researchers in Canada reported results from the largest set of whole genomes of people with autism to date. They sequenced the whole genomes of more than 5,000 individuals, about half of whom have autism. Among the61 variants the researchers identified, 18 had not beenfirmly linked to autismbefore. The team found that many of the CNVs in people with autism rest in noncoding regions.
Some teams are applying other resources, such as gene co-expression maps and protein-protein interaction networks, to understanding the underlying biology of the condition. These networks are only likely to become more powerful as researchers uncover more risk genes for autism. The question is how to integrate all that genetic data with other -omics data, and network-type approaches are probably going to be critical there, Geschwind says.
Most autism research arising from gene discovery is focused on repercussions at the molecular and cellular levels, but theres an important gap from there to whole circuits and behavior. Ultimately, the value of genetics is very likely to play out through an improved understanding of circuit-level function and anatomy, State says.
Stem cells and emerging technologies such as brain organoidsso called mini-brains in a dishcould afford researchers a prime opportunity to study the effects of genetic variation in human neurons. Faced with the limitations of mouse models in studying a condition characterized by behavioral problems, some teams are alsoturning to monkeys, which enable them to study more complex social interactions. Something we should be doing for the future is taking the precise mutations we find in humans and making those in primates, Wigler says.
These days, Wigler is on to another big idea: risk modifiers. Rare variants strongly associated with autism also occur in people without autismespecially women. Researchers know that mutations can contribute to autism by amplifying or attenuating the effects of other genes, so its feasible that two mutations could cancel each other out. But few teams have looked into these combinations as yet. People talk about autism as being an additive disorder, Wigler says, but nobodys really looking at additivity.
This idea brings him to a possible experiment: Take two mutations that individually have damaging effects, and introduce them both into mouse or monkey. Having the combination would be predicted to be worse than having either mutation alone. But what if the net result is correction? Wigler asks. Then we know modifiers exist. Theres not much of that kind of scientific exploration happening now.
A finding of that nature would herald a whole new wave of advances. It might also help to explain why the mutations identified so far vary in their effector what geneticists call penetranceonly sometimes resulting in autism. And it might help researchers develop therapies. If we ever saw a self-correcting defect in two mutations in autism, Wigler says, I would stand up and cheer.
This story wasoriginally publishedonSpectrum.
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Using Big Data to Hack Autism - Scientific American
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6.8m genetic medicine plan for targeted treatment – BBC News
Posted: at 1:47 am
BBC News | 6.8m genetic medicine plan for targeted treatment BBC News Patients in Wales will benefit from stronger services and more expertise in genetic medicine, under a new strategy. The 6.8m plan has been designed to ensure Wales is able to offer treatment plans revolutionised by better understanding of human DNA. |
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Decoding Brain Evolution – Harvard Medical School (registration)
Posted: at 1:47 am
How did our distinctive brains evolve? What genetic changes, coupled with natural selection, gave us language? What allowed modern humans to form complex societies, pursue science, create art?
While we have some understanding of the genes that differentiate us from other primates, that knowledge cannot fully explain human brain evolution. But with a $10 million grant to some of Bostons most highly evolved minds in genetics, genomics, neuroscience and human evolution, some answers may emerge in the coming years.
The Seattle-based Paul G. Allen Frontiers Group has announced the creation of an Allen Discovery Center for Human Brain Evolution at Boston Childrens Hospital and Harvard Medical School. It will be led by Christopher A. Walsh, the Bullard Professor of Pediatrics and Neurology at HMS and chief of the Division of Genetics and Genomics at Boston Childrens. Michael Greenberg, the Nathan Marsh Pusey Professor of Neurobiology and head of the Department of Neurobiology at HMS, and David Reich, professor of genetics at HMS, will co-lead the center.
Unraveling the mysteries of the human brain will propel our understanding of brain development, brain evolution and human behavior, said George Q. Daley, dean of HMS. It also will help us understand what makes us unique as a species.
The research conducted by these three remarkable scientists spans the gamut from molecule to organism to system and underscores the cross-pollination among basic, translational and clinical discovery as well as across neurobiology, genetics, evolutionary biology and neurology, Daley said.
The centers agenda is a bold one: to catalogue the key genes required for human brain evolution, to analyze their roles in human behavior and cognition and to study their functions to discover evolutionary mechanisms.
To understand when and how our modern brains evolved, we need to take a multi-pronged approach that will reflect how evolution works in nature and identify how experience and environment affect the genes that gave rise to modern human behavior, Walsh said.
The launch of this center is a wonderful opportunity for three laboratories that have been working independently to come together and study the genetic, molecular and evolutionary forces that have given rise to the spectacular capacities of the human brain, said Greenberg.
The funding will allow us to use ancient DNA analysis to track changes in the frequency of genetic mutations over time, which will in turn illuminate our understanding of the nature of human adaptation, added Reich.
An evolving understanding
We already know some basics of human brain evolution. First came the enlargement of the primate brain, culminating perhaps 2 million years ago with the emergence of our genus, Homo, and the use of crude stone tools and fire. Next came a tripling of brain size during the 500,000 years before Homo sapiens arose. Finally, just over 50,000 years ago, there was a great leap forward in human behavior, with archaeological evidence of more efficient manufacturing of stone tools and a rich aesthetic and spiritual life.
What transpired genetically? Prior research has taken a piecemeal approach to occasional genes that have different structures in humans versus non-humans. For example, Walshs lab has identified several genes that regulate cerebral cortical size and patterning, some of them through the study of brain abnormalities. The lab recently found a gene involved in brain foldingthanks to a brain malformation called polymicrogyriathat may have enhanced our language ability.
But such findings only scratch the surface of the cognitive, behavioral and cultural strides humans have made over the past 50,000 years. Thats a blink of the eye in evolutionary terms. What enabled us to invent money, develop agriculture, build factories, write symphonies, tell jokes?
Rosetta Stone(s) to decode brain evolution
The researchers think not one but multiple mechanisms of evolution helped form the modern human brain. Such mechanisms include:
Accordingly, the centers research methods will include, in varying combinations:
No genetic stone unturned
All these approaches will be supported by powerful computational data analysisreaching across genomes, across populations, across hundreds of thousands of years.
The project leaders summed it up: This group will provide the most rigorous possible examination of how, when and where the unique features of the amazing human brain came about.
The $10 million grant will be distributed over four years, with the potential for $30 million over eight years.
Adapted from a post on Vector, the Boston Childrens clinical and research innovation blog.
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At the Bench: Inspired by a Brother, AAN Scholarship Awardee Investigates Brain Metabolism Disorders – LWW Journals
Posted: at 1:47 am
Hurley, Dan
doi: 10.1097/01.NT.0000521715.10826.a9
Features
Isaac Marin-Valencia, MD, recipient of an AAN Clinical Research Training Scholarship, is studying clinical and molecular aspects of pontocerebellar hypoplasia, a brain metabolism disorder so rare it is virtually unseen in the United States. Here, he discusses his research.
BOSTONFrom the Canary Islands to New York by way of Spain and Texas, Isaac Marin-Valencia, MD, has dedicated his career to investigating pediatric neurologic diseases as exotic as his homeland.
The recipient of an AAN Clinical Research Training Scholarship, Dr. Marin-Valencia is studying clinical and molecular aspects of pontocerebellar hypoplasia, a brain metabolism disorder so rare it is virtually unseen in the United States.
All our patients are in the Middle East, because of the high rates of consanguinity, Dr. Marin-Valencia said during a break from the AAN Annual Meeting here in April. I've been to Cairo, to work with collaborators in hospitals there.
Born and raised in the Canary Islands, the Spanish archipelago off the coast of Morocco, Dr. Marin-Valencia grew up with a younger brother, Abimael, who had autism and epilepsy. He decided when he was six to become a doctor to help Abimael.
He was the reason for my career path, Dr. Marin-Valencia said. He's the inspiration for me to continue working on brain disorders that don't have treatments.
After graduating from medical school at the University of Las Palmas de Gran Canaria, he completed his four-year residency in pediatrics at Sant Joan de Deu Hospital of Barcelona. It was there he met Juan Pascual, MD, PhD, a pediatric neurologist who became his mentor.
I was very impressed by his knowledge and expertise is in brain metabolism disorders, Dr. Marin-Valencia said.
It was in Barcelona that he first began seeing young patients with the disorders that Dr. Pascual specialized in treating. I learned a lot about biochemistry and got fascinated, he said.
In 2008, he moved to the University of Texas-Southwestern Medical Center, to pursue postdoctoral research in pediatric neurology. Three years later, a poster of his won a grand prize at the university's postdoctoral research symposium, becoming the basis of a paper, published in the journal Cell Metabolism, that overturned 50 years of scientific dogma.
The so-called Warburg effect, named after Nobel Prize winner Otto Warburg, had been based on his in vitro observation that cancer cells preferentially metabolize glucose to lactate, even in the presence of sufficient oxygen in the mitochondria.
Dr. Marin-Valencia and colleagues disproved the long-held assumption that the same process holds true in vivo, using human glioblastomas implanted into the mouse brain to show that the cells' mitochondria oxidize glucose.
Determined to get back to his primary interest in metabolic disorders of the brain, he moved to Rockefeller University in 2015 to study human genetics and developmental neurobiology.
My background until then was in biochemistry and electrophysiology, Dr. Marin-Valencia said. I was missing two important pieces of the puzzle. Most of these metabolic disorders are genetic, and therefore they affect development of the brain. Learning these two areas have helped me to have a global picture about these disorders. If you're an expert in just one thing, you're going to miss other important facets that could be essential to understand and improve the diseases. Making more connections, meeting other investigators, associating with other laboratories all of that enriches my knowledge and way of thinking.
Under the mentorship of Joseph Gleeson, MD, a pediatric neurologist and neurogeneticist at University of California, San Diego, who has identified some 200 genetic mutations linked to brain disorders, Dr. Marin-Valencia is now looking for genes associated with pontocerebellar hypoplasia.
We use zebrafish and mice, Dr. Marin-Valencia said. We knock out or knock down genes and then see if there is a problem in the development of the brain. From the developmental standpoint, we want to replicate the disease in the animal model, to see what kind of cells are compromised and when the problem is first manifested. Then we go down to the cell and molecular level to localize where the gene is expressed and what the product of the gene is, where the protein is located in the cell and what its role is. Once we know all that, once we sort out the mechanism, we try to development new therapies.
Asked if he has yet identified a particular gene associated with pontocerebellar hypoplasia, he paused and said, I cannot tell you. It's not published yet.
Ultimately, his goal is to identify treatments for diseases that are now untreatable, something Dr. Gleeson's research has already done for a number of pediatric brain diseases.
One of the major problems we have in neurology is that we have few treatments for these devastating diseases that kill children at a very early age, Dr. Marin-Valencia said. There are things we can do to alleviate pain, to alleviate suffering, to provide a better quality of life. But from the biochemical and genetic standpoint, we cannot do much to change the outcome of many of these diseases.
Might his research into pontocerebellar hypoplasia one day lead to a treatment? It's a long way, Dr. Marin-Valencia said, but we are working to get there.
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At the Bench: Inspired by a Brother, AAN Scholarship Awardee Investigates Brain Metabolism Disorders - LWW Journals
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Why You Should Think Twice About Those DNA-By-Mail Results … – NPR
Posted: at 1:47 am
In a new book, University of North Carolina, Charlotte anthropologist Jonathan Marks says that racism in science is alive and well.
This stands in sharp contrast to creationist thinking, Marks says, which is, like racism, decidedly evident in our society but most certainly not welcome in science.
In Is Science Racist? Marks writes:
"If you espouse creationist ideas in science, you are branded as an ideologue, as a close-minded pseudo-scientist who is unable to adopt a modern perspective, and who consequently has no place in the community of scholars. But if you espouse racist ideas in science, that's not quite so bad. People might look at you a little askance, but as a racist you can coexist in science alongside them, which you couldn't do if you were a creationist. Science is racist when it permits scientists who advance racist ideas to exist and to thrive institutionally."
This is a strong set of claims, and Marks uses numerous examples to support them. For example, a 2014 book by science writer Nicholas Wade used genes and race to explain, as Michael Balter put it in Science magazine, "why some people live in tribal societies and some in advanced civilizations, why African-Americans are allegedly more violent than whites, and why the Chinese may be good at business."
The work of psychologist Philippe Rushton, who died in 2012, has been published and even celebrated in scientific circles, Marks explains. Rushton suggested that "the peoples of Africa had undergone eons of natural selection for high reproductive rate and low intelligence, which he measured via surrogate variables notably, sex drive, criminality rates, penis size, and brain size."
In other words, Wade, Rushton, and others working in the same vein take what is cultural, historical and political and conclude it is biologically natural. That's "rationalizing the economic and social disparities in the modern world," Marks notes.
"Race," Marks writes, "is not the discovery of difference; it is the imposition of difference." Inequality comes about because of unequal conditions imposed upon different groups of people through economic and cultural forces.
With this background, we can now tackle a part of Is Science Racist? that deconstructs an activity that has become more and more popular over the past 10 years: sending away our DNA for some type of ancestry testing.
The problem, Marks writes in the book, is the "fabricated meaning" that corporate science superimposes over the raw numbers that emerge from this process. Last week, Marks elaborated on this point in an email to me:
"To understand the ancestry tests, you have to begin by looking at the fine print. This [type of test] says 'for recreational purposes only' or something very similar. It obviously is written by lawyers, not scientists, and it's a way of saying that the results have no scientific or legal standing. This is privatized, corporate science, not ordinary science.
"How do they come up with numbers? They take DNA from people from disparate regions and compare yours to theirs. The numbers reflect a measure of your DNA similarity to those of the divergent gene pools. How do they calculate it? Don't know; the algorithms are protected intellectual property. Are they accurate? About as accurate as looking in the mirror."
OK, so it's a comparative process and we don't know the precise calculation methods. But what's the part about the fabricated meaning? Marks continues:
"Sociologists find that customers make sense of the results, and ignore the nonsense. For example, I've come out 95 percent Ashkenazi Jewish (not a geographical population, but a gene pool with its own minor genetic idiosyncrasies due to history) and 5 percent Korean. A good scientific question would be: +/- how much? 15 percent? 10 percent? Is my 5 percent Korean ancestry the same as 0 percent Korean ancestry?
"Scientific answer: Yes. Corporate answer: Wouldn't you like to know?
"So there is sense, but it blends into nonsense, and may be difficult to distinguish them."
Here's a second example of ancestry nonsense taken from Marks' book. The Denisovan people are named for a Siberian cave where an unusual finger bone, dated to 50,000 years ago, was reported in 2012. By now, we know more about the Denisovans, but still, not a lot.
Despite this, Marks notes, you can pay to find out what percentage Denisovan you are! What genuine meaning can this result possibly have when the meaning of "a Denisovan population" it itself in flux?
All this leads to a question Alva No asked here last year:
"Can it ever be more than fantasy to try to draw meaningful conclusions about an individual's origins on the basis of the sort of DNA information that is available to us now?"
Marks' answer is clearly negative. Again, from his email message:
"The tests often reify as 'natural' human populations that are actually natural/cultural, that is to say, human groups that are genetically different to some extent, but are actually bounded by history, language, politics, or religion, and are thus not 'natural' categories at all. These include particular African tribes, Ashkenazi Jews, or Vikings. The fact that one can detect ancestry in these identities does not mean that they are products of nature."
And as we've seen with work done by Wade and Rushton, the problem is that where we make a habit of seeing biologically natural units of some type instead of complex webs of variables at work, there's a risk of highly unscientific thinking and sometimes worse.
"Scientific racism," Marks told me, "often begins by highlighting (and misrepresenting) patterns of difference in the human species; but regardless of how different they may be from one another, people are entitled to equality."
Yes, they are. Humans vary, and our genes vary. But not very much: The chimpanzee gene pool shows a lot more genetic variation than the human gene pool does.
What can our genome tell us?
Less than we may like to think.
Barbara J. King is an anthropology professor emerita at the College of William and Mary. She often writes about the cognition, emotion and welfare of animals, and about biological anthropology, human evolution and gender issues. Barbara's new book is Personalities on the Plate: The Lives and Minds of Animals We Eat. You can keep up with what she is thinking on Twitter: @bjkingape
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Baboon Study Shows Sexual Bullying May Lie Deep in Our DNA – NBCNews.com
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A female baboon presents to a male, a form of sexual solicitation. Alice Baniel
Why does it matter? If such behavior is found in humanity's closest relatives the chimpanzees and other social primates, it suggests roots deep in evolutionary history, as opposed to behavior that has arisen recently.
"Because sexual intimidation where aggression and matings are not clustered in time is discreet, it may easily go unnoticed," Baniel said.
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"It may therefore be more common than previously appreciated in mammalian societies, and constrain female sexuality even in some species where they seem to enjoy relative freedom."
There's another factor size. The behavior may be more common in species whose males are markedly bigger than females, such as chimpanzees, baboons and humans.
Humanity's other close relative, the bonobo, doesn't have this sexual size difference, and bonobos are notoriously egalitarian when it comes to sex.
"This study adds to growing evidence that males use coercive tactics to constrain female mating decisions in promiscuous primates," Baniel said.
"Such behavior, previously reported only in chimpanzees, may therefore occur in a wider range of primates, strengthening the case for an evolutionary origin of human sexual intimidation," Baniel's team concluded.
Baniel plans to study the two troupes further. She's hoping at least some of the females stand up for better relationships.
"I would like to understand if several mating strategies could coexist among males, i.e., being chosen by females versus intimidating them," she said.
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First big efforts to sequence ancient African DNA reveal how early … – Science Magazine
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The Khoe-San in Southern Africa split off early from other Africans, but carry DNA from East African herders.
Roger de la Harpe/Newscom
By Elizabeth PennisiJul. 6, 2017 , 12:45 PM
AUSTINThe study of ancient human DNA has not been an equal opportunity endeavor. Early Europeans and Asians have had portions of their genomes sequenced by the hundreds over the past decade, rewriting Eurasian history in the process. But because genetic material decays rapidly in warm, moist climates, scientists had sequenced the DNA of just one ancient African. Until now.
This week, at the annual meeting of the Society for Molecular Biology & Evolution here, scientists announced that they had partially sequenced 15 ancient African genomes, with representatives from all over sub-Saharan Africa. And another groupwhose work is still unpublishedhas sequenced seven more ancient humans from South Africa. [Finding] ancient genomes from Africa is pretty amazing, says Anna-Sapfo Malaspinas, a population geneticist at the University of Bern, who was not involved in either project.
Africa has long been called the cradle of humanity, from which our earliest human ancestors spread across the rest of the world some 50,000 years ago. Africa is also where peopleancient and modernare most genetically diverse. But how such groups, from the Hadza of East Africa to the Khoe-San of Southern Africa, came to be is a mystery. Thats in part because some 2000 years ago, early adopters of agriculture known as the Bantu spread across the continent, erasing the genetic footprint of other Africans. The one ancient African genome that has been sequencedan Ethiopian who lived some 4500 years agohas shed little light on this mystery.
Pontus Skoglund knew there had to be more to the story. So the Harvard University evolutionary geneticist and his colleagues obtained DNA from 15 ancient Africans from between 500 and 6000 years ago, some before the Bantu expansion. In addition, Skoglunds team got DNA data from 19 modern populations across Africa for comparison, including from large groups like the Bantu and smaller ones like the Khoe-San and the Hadza.
For the most part, the ancient DNA was most similar to that of people living in the same places where the bones were found, Skoglund reported. But some interesting exceptions showed intermingling among various groups. Its really exciting to see in Africa that there was already this ancient admixture, says Simon Aeschbacher, a population geneticist from the University of Bern who was not involved with the work. There must have been population movements in early Africa.
The ancient genomes indicate that Southern Africans split off from Western Africans several thousand years ago, and subsequently evolved key adaptations that honed their taste buds and protected them from the sun. Around 3000 years ago, herderspossibly from todays Tanzaniaspread far and wide, reaching Southern Africa centuries before the first farmers. But modern Malawians, who live just south of Tanzania, are likely descended from West African farmers rather than local hunter-gatherers, Skoglund says. Indeed, the analysis suggests that West Africans were early contributors to the DNA of sub-Saharan Africans. But even these DNA donors were a hodgepodge of what are now two modern groupsthe Mende and the Yoruba. And one ancient African herder showed influence from even farther abroad, with 38% of their DNA coming from outside Africa.
Another study focused on Southern Africa, where some researchers think modern Homo sapiens evolved. Evolutionary geneticist Carina Schlebusch and her colleagues at Uppsala University in Sweden partially sequenced seven ancient genomes: three from 2000-year-old hunter-gatherers and four from 300- to 500-year-old farmers. They also included modern DNA in their analyses.
The more modern farmers did have Bantu DNA in their genomes, but the ancient hunter-gatherers predated the spread of the Bantu, she and her colleagues reported last month on the preprint server bioRxiv. Their other findings parallel Skoglunds discoveries: Nine percent to 22% of the DNA of these farmers modern descendantsincluding the southern Khoe-Sancomes from East Africans and Eurasian herders.
Schlebuschs analysis reaches even deeper into human history than does Skoglunds, as her team used the ancient and modern genomes to estimate that the hunter-gatherers she studied split off from other groups some 260,000 years ago, about the age of the oldest H. sapiens fossil. Having that date lets us start to think about questions like where, and how, anatomically and behaviorally modern humans evolved, says Iain Mathieson, an evolutionary geneticist at Harvard. Whether this date survives peer review after publication is yet to be seen.
Aeaschbacher has a simple solution to resolve such uncertainties: sequencing more ancient African genomes. Theres a deep-seated need to understand this, he says. How ancient Africans divided into groups and when and how they moved around could have a strong impact on what shapes present-day humans.
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DNA evidence is rewriting domestication origin stories – Science News Magazine
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One lab full of rats looks pretty much the same as another. But visiting a lab in Siberia, geneticist Alex Cagan can distinguish rats bred to be tame from those bred to be aggressive as soon as he opens the lab door.
Its a completely different response immediately, he says. All of the tame rats come to the front of the cage very inquisitively. The aggressive rats scurry to the backs of their cages to hide. Exactly how 70 generations of breeding have ingrained friendly or hostile behaviors in the rats DNA is a mystery that domestication researchers are trying to solve. The rats, along with mink and silver foxes, are part of a long-running study at the Institute of Cytology and Genetics in Novosibirsk, Russia. The aim is to replay domestication to determine the genetic underpinnings that set domesticated animals apart from their wild ancestors.
Over thousands of years, humans have found ways to put other species to work, from spinning silk to storing water. These short stories reveal how humans got to know some of their closest companions.
For thousands of years, humans have lived with animals. Some of the creatures are companions hopping onto laps, ready to play fetch. Some have jobs carrying heavy loads, pulling wagons and plows, and herding other animals. Others provide meat, eggs or milk. Plants, too, have been tamed. On nearly every continent, fruits, vegetables, grains, nuts and tubers stand in soldier-straight rows and yield bounty on schedule.
There was a time when the species that now inhabit humans homes, fields and barnyards didnt exist. Then some people, somewhere, brought wild things under human control. Or the wild creatures exploited new ecological niches created by humans, gradually habituating themselves to people and, in essence, domesticating themselves. Both paths scientists are still debating which was more likely for different animals led to the creation of domesticated species or subspecies genetically distinct from their wild ancestors.
Scientists studying evolution and human history want to know how ancient people domesticated animals and plants. What species did humans start with and where did it happen first? How long did it take? Does one group get credit for taming wild horses or subjugating aurochs into milk-giving cows? Or did multiple people in different places have the same idea?
Even for dogs, humans oldest, closest friends, all those things are unknown, says evolutionary geneticist Greger Larson of the University of Oxford. For many domesticated creatures, the questions outweigh the answers. As new studies flood in some based on archaeology, others on modern or ancient DNA the waters get muddy, with one studys results contradicting anothers.
Domestication research right now is really going through an exciting phase, Larson says. Comparing the genetic instruction books, or genomes, of wild and domesticated species is giving evolutionary geneticists fresh clues about the changes that separate domesticated species from wild ones. New techniques (some developed in the last two to three years) for analyzing fragile DNA from ancient bones offer genetic snapshots of domestication as it played out long ago. Marrying that DNA data with archaeological findings, the context in which the bones were discovered, for example, may tell researchers more about when, where and how humans first engaged with plants and animals. Recent results are already rewriting the stories of rice, horse and chicken domestication.
A new hypothesis is also shining a light on core changes in the embryos of many domesticated species. The hypothesis aims to explain how the process of becoming close to people produces comparable changes in the appearance, reproduction and physiology of a whole range of domesticated animals. One central developmental change in a temporary clump of cells called the neural crest may be behind the suite of characteristics known as domestication syndrome.
The pace of research, much of it seemingly contradictory, will only increase in the near future, Larson predicts. Were going to get a lot more confused before we figure out whats really going on.
Deciding when an animal can be called domesticated isnt always easy.
Since 2002, Anna Kukekova has been making annual treks to Novosibirsk. A geneticist at the University of Illinois at Urbana-Champaign, she travels to Siberia each year to collect blood from hundreds of silver foxes to look for genetic changes that produce tame and aggressive behaviors.
These foxes are special. They are part of a long-running biological experiment to repeat domestication by turning a wild canid from the family of animals including wolves, foxes, jackals and dogs into a fox version of a domestic dog (SN: 5/13/17, p. 29). The project was the brainchild of geneticist Dmitry Belyaev. In the 1950s, Belyaev and colleagues started selecting and breeding the least aggressive and fearful silver foxes from those on a fur farm. Since 1960, researcher Lyudmila Trut and her team have selected the farms friendliest foxes to breed. Over more than 60 generations, the foxes have grown more and more tolerant of humans. Kukekova says shes noticed a difference even in the 15 years shes been visiting the farm.
In China, people began domesticating the larvae of silk moths for the fine, strong threads of their cocoons as early as 7,500 years ago, genetic evidence suggests. People bred the larvae to produce more silk and to tolerate human handling and extreme crowding (SN Online: 8/27/09). For more than 2,000 years, the Chinese kept their silk-making methods top secret, and smuggling silkworms out of the country was punishable by death. Silk makers traded their monopolized fabric throughout Eurasia along the Silk Road (SN:5/27/17, p. 4). To this day, the only other insect that is domesticated is the honeybee. Erika Engelhaupt
In Kukekovas early visits, about 70 percent of the tame foxes were considered elite, aquiver with excitement when people came around. The rest of the tame ones didnt mind if you petted them, but they werent super excited to interact with you, she says. Now, almost every tame fox is in the super-friendly elite group. (Foxes bred to be aggressive, on the other hand, are definitely not happy to have people around, much like the fearful rats Cagan encountered at the institute.)
Even though the friendly Novosibirsk foxes are genetically tame some are sold as pets not everyone would call the animals domesticated. In an apartment, they would probably be very difficult pets, Kukekova says. The foxes have a strong odor, are more active at night and they arent easily house-trained. The combination of living with people plus inherited changes in the foxes genomes may eventually make them fully domesticated, but they arent there yet.
Researchers have set out several biological criteria that should determine when silver foxes, or other animals, cross the line that divides merely tame from fully domesticated. Number one: Domesticated animals are genetically distinct from their wild forebears, and they inherit their human-friendly demeanor. Thats different from wild animals that have been tamed but dont pass on that tameness to the next generation.
Two: Domestication makes animals dependent on humans for food and, for the most part, reproduction. Three: Breeding with wild counterparts becomes difficult, if not impossible. For example, domesticated plants dont drop their seeds when ripe; they rely on humans to spread their progeny. Finally, domesticated animals and plants should bear the physical hallmarks of domestication syndrome, such as a smaller skull for animals, and a narrower footprint for plants.
By these criteria, some people argue that cats popular pets worldwide are not fully domesticated. Cats probably started taming themselves about 9,500 years ago by hunting vermin, infesting early farmers grain stores and feasting on food scraps. Farmers brought the mousers with them from the Middle East into Europe around 6,400 years ago, researchers reported June 19 in Nature Ecology & Evolution (SN Online: 06/19/17). But cats may not have been purring lap pets at that time, say molecular biologists Thierry Grange and Eva-Maria Geigl of the Institute Jacques Monod in Paris. That behavioral transformation may have happened later, perhaps in Egyptian cats that were quickly dispersed by boat around the ancient world.
In fact, cats havent changed much physically or genetically from their African wildcat ancestors (Felis silvestris lybica), Grange and Geigl say. Many felines still choose their own mates and hunt for food. Cats famed aloofness may be another clue that their domestication isnt fully complete. Certainly, cats are more like their wild ancestors than dogs are, says Grange. But modern kitties are no longer wild cats, Geigl argues: These couch potatoes are domesticated.
Dogs appear to have been the first species domesticated by humans, followed by many others in Asia and the Middle East. As people spread to the New World, they continued to domesticate animals. Some were domesticated more than once in different locations.
Sources: D.E. MacHugh et al/Annu. Rev. Anim. Biosci. 2017; M. Germonpr et al/J. Archaeol. Sci. 2009
Bonds between humans and their animal companions may be more important than rigid biological criteria, Larson and other researchers argue. Domestication, says zooarchaeologist Alan Outram of the University of Exeter in England, is best looked at with a more cultural definition.
Domestication is a gray area encompassing the point at which a hunter stops being interested in simply killing and eating an animal and starts being interested in controlling the animal, Outram says. The process probably starts slowly, first with animal herding and other forms of husbandry, such as controlling an animals food supply and movement, culling at specific ages and directing breeding. When people start using animals, such as horses, for labor, riding or milking (fermented horse milk is a staple in parts of Central Asia), the animals start moving to being culturally domestic, he says.
Many domestication stories have vague beginnings, but we know exactly when the Syrian golden hamster, now a popular pet, first came under human control. On April 12, 1930, zoologist Israel Aharoni had workers dig up a mother hamster and her 11 babies spied by a farmer in his wheat field near Aleppo, Syria. Aharoni wanted a convenient animal to rear in the laboratory, but the creatures were so easily tamed that breeders began selling them as pets. Now, more than a million hamsters, descended from that first litter, run in wheels and transparent balls in homes across the United States. Erika Engelhaupt
Outram has evidence that the Botai people, hunter-gatherers that lived in Central Asia, were milking and bridling horses about 5,500 years ago (SN: 3/28/09, p. 15). I certainly wouldnt want to make the argument that at the Botai time youve got anything like modern domesticated horses, he says. It was more like equine husbandry and herding.
Scientists have to be careful not to judge how domestication happened in the past by the way animals are treated in modern Western cultures, says evolutionary biologist Ludovic Orlando of the University of Copenhagen. On a trip to collect DNA samples from ancient horse bones in Mongolia, Orlando got a whole new perspective on domestication.
It completely changed my view of horse domestication, because I saw people interacting with this animal in ways I couldnt imagine myself, Orlando says. In Mongolia, horses roam free and their owners catch them, as needed, for riding or milking. Once youve seen that, you cant think that domestication is just about parking animals somewhere. Its about the process of interacting with them and developing a relationship with them.
If its hard to pinpoint what domestication means in foxes tamed in controlled experiments, consider how difficult it is to decide whether the bones of a long-dead animal are from a wild or domesticated critter. Thats the task of paleontologist Mietje Germonpr of the Royal Belgian Institute of Natural Sciences in Brussels, who studies dog domestication. The beloved pets are the subjects of much domestication research.
Scientists used to think that dogs were domesticated toward the end of the Ice Age, about 14,000 years ago (SN Online: 7/22/10). Germonpr and colleagues have studied skulls and jawbones of even more ancient canids in caves and other places where Ice Age people lived more than 25,000 years ago. One skull, found in a Goyet cave in Belgium, may be one of the oldest dogs ever discovered or at least the oldest wolf that looked like a dog. At 36,000 years old, the Goyet pooch pushed dog domestication back to well before glaciers reached their peak coverage of the Northern Hemisphere.
Those early dogs may have been used as pack animals to move mammoth carcasses from hunting grounds to living quarters, says Germonpr. Big dogs may have helped humans hunt dangerous carnivores, such as cave bears, hyenas and cave lions. Its also possible the animals were used for fur or meat.
The ancestor of todays enormous, fleshy sweet watermelons was a surprisingly small, hard and bitter melon with pale green flesh. Just where this fruit was first grown is debatedall thats agreed on is that it was somewhere in Africa. An image of a watermelon appears in an Egyptian tomb dating to at least 4,000 years ago, and five watermelon seeds were found in King Tuts tomb. Its thought that the Egyptians bred the fruit as a tasty, and portable, water supply. Erika Engelhaupt
Germonprs assertion that the Goyet dog is in fact a dog comes from comparing its skull and jaws with those of wolves and modern dogs. Most domesticated mammals, including dogs, tend to have smaller bodies than their wild counterparts, with smaller skulls that have shorter, wider snouts and shorter, lower jaws. Those features make adult dogs look more puppylike than grown wolves do. That type of facial remodeling is part of the domestication syndrome, which also includes curly tails, floppy ears and other characteristics common among domesticated animals but not wild ones. By Germonprs measurements, the Goyet skull more closely resembles modern dogs than it does ancient or modern wolves.
She also has evidence of early dogs in Russia and the Czech Republic dating to 25,000 years ago or more. Other groups have reported data suggesting that a 33,000-year-old canid from the Altai Mountains of Russia was also an early dog.
Other researchers disagree, saying the animals were really wolves. Three-dimensional reconstructions of the skulls of the Goyet dog and another Ice Age dog show that the animals snouts didnt angle from the skull the way modern dogs do, and the ancient versions didnt have some other features of modern dogs (SN Online: 2/5/15).
Larson says hes not bothered that the Goyet hound didnt physically measure up in the 3-D study. The canid may have behaved very much like a dog and had close ties to humans. Those early dogs didnt have thousands of years of intense breeding selection to sculpt them into the image of modern dogs. Even modern dogs have been transformed dramatically in just 200 to 300 years of breeding (SN Online: 4/26/17; SN:1/31/09, p. 26). What was a dog 15,000 to 30,000 years ago is not what a dog is now, Larson says.
The timing of Fidos taming isnt the only dispute. Researchers also wrangle over where and how many times it happened. Dueling genetic studies based on the DNA of modern dogs and wolves suggest the fellowship between humans and dogs could have been forged in the Middle East, Central Asia, East Asia or, as Goyets archaeological evidence suggests, in Europe. Research reported by Larson and colleagues last year in Science suggests that dog domestication happened at least twice, once in Europe and once in East Asia (SN: 7/9/16, p. 15).
DNA evidence indicates that the Goyet dog and the 33,000-year-old Russian dog are not the ancestors of todays dogs or wolves (SN: 12/14/13, p. 6). Scientists examined mitochondrial DNA, which is passed from mothers to offspring, to trace maternal lineages of ancient and modern dogs and wolves. The mitochondrial DNA of the Goyet and Russian dogs belongs to a maternal lineage that didnt leave any modern descendants, researchers reported in Science in 2013. But it doesnt mean the animals werent on the way toward being domesticated, Germonpr says.
Perhaps those dogs were part of an early, failed attempt at domestication, she says. The domesticated animals became extinct, and domestication started up again somewhere else.
Locating the cradle of most species domestication is difficult. Many were domesticated before writing was even invented. So scientists have to extract the story from artifacts and bones or from DNA.
The origin of Asian rice has been hotly debated for many years. Scientists used to think modern rice, Oryza sativa, was domesticated twice: sticky, short-grained japonica rice was domesticated in China, and in India, rice was domesticated into long-grained varieties indica and aus. Archaeological finds suggest that rice cultivation started about 9,000 years ago in China and 8,000 years ago in India. But true domestication probably happened only once in China, says Dorian Fuller, an archaeobotanist at University College London.
People were certainly cultivating rice in India, but thats just one step in the domestication process. The final threshold that separates a fully domesticated crop from a cultivated one is that domesticated plants require human intervention to spread their seeds, Fuller says. Wild grains, for instance, shatter their seed heads when ripe. But domesticated grains, including rice, wheat, barley, sorghum and millet, have mutations that prevent shattering. The only way the grain crops can propagate is if humans collect and plant the seeds.
Though the Inca built great cities and had a sophisticated understanding of astronomy, they didnt use wheels to transport goods. Instead, llamas carried the heavy loads along the empires vast road system. And llama dung fertilized Inca fields, possibly helping to grow maize at high altitudes. South Americas llamas and alpacas are domesticated versions of two wild camel species: guanaco (ancestor of llamas) and the smaller vicua (alpacas ancestor). The earliest evidence of the animals domestication is from bones found at archaeological sites in the Peruvian Andes, dating to at least 6,000 years ago. Erika Engelhaupt
It may have taken nearly 2,000 years for people in Chinas Yangtze River basin to wrest complete control over rice, researchers reported last year in Scientific Reports. Scientists examined rice fossils to determine how easily the plant shattered its seed. Although people were growing an early rice 9,000 to 8,400 years ago, about 60 percent of plants were still dispersing seeds via shattering. It wasnt until about 7,000 to 6,500 years ago that nonshattering rice began to edge out shattering varieties.
By examining DNA from modern rice strains, Fuller and evolutionary geneticist Michael Purugganan of New York University think theyve pieced together the rest of the rice domestication story. DNA evidence clearly shows that Chinas wild O. rufipogon was domesticated into O. sativa japonica. Traders carried domesticated japonica from China to India, where it was bred with the cultivated rice species O. nivara to produce domesticated aus about 4,000 years ago, Fuller, Purugganan and colleagues reported in January in Molecular Biology and Evolution. Indicas story is less clear because its cultivated predecessor in India is still unknown. But the genetic evidence indicates that it got its domestication genes from Chinas japonica.
Working out the step-by-step history of domesticated animals is just as complicated. Until recently, researchers compared DNA from modern domestic animals with that of wild relatives, preferably the wild species that gave rise to the domesticated species. Sometimes thats impossible to do. There are no wild cattle, for instance. Aurochs massive cattle that eventually gave rise to domesticated cows went extinct when the last one died in 1627 in Polands Jaktorw Forest.
Horses wild ancestors are also extinct, but remains from the warrior steeds of Genghis Khan and medieval knights, the Romans chariot horses and the mounts of the ancient Scythians, Greeks and Persians might fill in gaps in horse history and prehistory. Through the Pegasus project, begun in 2015, Orlando and colleagues have collected ancient DNA from horse fossils from a wide variety of time periods and cultures. Were looking at every possible ancient equine culture on the planet, Orlando says.
Before the project, scientists mostly had to rely on DNA from modern horses to piece together the story of how the beasts of burden were domesticated. Findings of those studies may be misleading, Orlando and colleagues have concluded. For instance, studies of modern horses mitochondrial DNA plus Y chromosomes (passed from fathers to sons) told a nice, neat story: At the beginning of horse domestication, people must have captured just a few stallions and bred those stallions to many different mares.
But when Orlando and colleagues examined DNA of ancient horses, they found that the story started completely differently. Domesticated horses living 2,300 to 2,700 years ago about the midpoint of horse domestication had a wide variety of Y chromosomes, the researchers reported April 28 in Science (SN: 5/27/17, p. 10). That means many stallions contributed DNA to horses gene pool for at least the first few thousand years of domestication. It wasnt until sometime after 2,300 years ago that people started winnowing down the number of stallions that were allowed to breed. Orlando doesnt know yet when most Y chromosomes were lost.
The story of chicken domestication is being retold as well, also thanks to DNA evidence. Modern chickens carry a version of the thyroid-stimulating hormone receptor gene, TSHR, that has been linked to several domesticated chicken characteristics: year-round egg laying, faster egg production at sexual maturity, reduced aggression toward other chickens and less fear of people. Because that version of the gene is ubiquitous in present-day chickens and is responsible for those attractive traits, researchers thought that people probably selected the most prolific egg layers right from the very beginning, about 4,000 years ago. Picking better laying hens would also mean unwittingly choosing the domesticated version of TSHR.
But, the egg-laying version of the gene didnt become popular among chickens in Europe until about A.D. 920, around the time that Christians started giving up meat on fasting days in favor of fish and fowl, Larson and colleagues reported May 2 in Molecular Biology and Evolution. (Rabbit domestication followed a religious proclamation, as well. In 600, Pope Gregory I declared that fetal rabbits, called laurices, are aquatic, which made them fish, suitable to eat during Lent. Rabbit breeding took off in monasteries in southern France, and bunnies quickly became domesticated.)
Turkeys are one of the most recently domesticated animals. In 2016, researchers found 1,500-year-old turkey eggs plus bones of both chicks and adult birds in the Oaxaca region of Mexico. The presence of turkeys at all life stages suggests they were being raised as food. They may have been important symbolically too; remains have been found buried alongside humans. The birds have changed a great deal since those early days: Some commercially bred turkeys have breast muscles so large that the birds cant get close enough to mate. Humans must artificially inseminate them, a sign of true domestication. Erika Engelhaupt
If Larsons calculations are correct, egg laying wasnt the main criterion for selecting which chickens to keep until the Middle Ages. By that time, the birds had been domesticated for thousands of years. So what were ancient people looking for when striking up friendships with the feathered animals or any other creatures? Many people think it was about the relationship; tameness and docility were the most attractive qualities in potential animal pals. Its hard to be buddies with a creature that constantly runs from you, or worse, attacks.
A breeding experiment with wild red jungle fowl, the precursor to the domesticated chicken, may help explain whether selecting for tameness is the triggering event of domestication and all its characteristics. Behavioral geneticist Per Jensen of Linkping University in Sweden is in the middle of a domestication redo. He and colleagues have bred eight generations of the rust-feathered birds. Like the rats, mink and foxes in Novosibirsk, Jensens jungle fowl are bred to be more (or less) fearful of humans than their ancestors were.
From the beginning, the researchers took great pains to select birds only for their behavior: Jungle fowl were tested for tameness at 12 weeks old, before they reached sexual maturity. One researcher would approach the fowl and attempt to touch it, while an outside observer scored the birds reaction. Neither researcher knew whether they were testing a jungle fowl from the tame or fearful line.
Mind you, this went well for two or three generations but then the difference started to be so big it was difficult to keep a secret, Jensen says. After that, the tame birds were so calm they didnt react when a human entered the room. You basically had to kick them out of your way, he jokes. By the sixth generation, tame birds were bigger and had a higher metabolism than their fearful counterparts, Jensen and colleagues reported in Biology Letters in 2015. Changes in body size, reproduction and metabolism happened quickly, even though the researchers were only choosing birds for tameness.
The tame birds, Jensen says, show a lot of traits that you really associate with domesticated animals, but Im not sure anyone would accept that, he says. Becoming what other people think of as domesticated chickens may take more time: jungle fowl hens that lay eggs year-round and are big enough to eat. I dont think were talking about hundreds of generations, maybe dozens. Its a much faster process than we used to think.
Again and again, animals of various species domesticated at different times in different parts of the world develop the same domestication syndrome characteristics: more extensive breeding periods; smaller brains, hearts and teeth; small or floppy ears; spotted coats; curly hair and tails; variable numbers of vertebrae in the spine; and juvenile faces with shorter snouts. Researchers have found evidence that pigmentation genes differ between domestic and wild animals. Others have pinpointed changes in brain chemistry or genes involved in face development that may separate tame and wild animals. But scientists didnt have a unifying explanation for why the physical traits of domestication syndrome were linked to tameness until three years ago.
Humans may have selected animals for tameness (left column), with those choices leading to unintended features seen in many domesticated species (right column). One hypothesis is that tameness, which involves a calmer nervous system and a dampened stress hormone response, results from alterations in neural crest cells. Those cells migrate throughout the embryo to form many tissues. Changes in the cells migration might account for many physical traits linked to tameness in domesticated animals.
Source: A.S. Wilkins, R.W. Wrangham and W.T. Fitch/Genetics 2014
Thats when geneticist Adam Wilkins of Humboldt University of Berlin, primatologist Richard Wrangham of Harvard University and evolutionary biologist and cognitive scientist W. Tecumseh Fitch of the University of Vienna introduced a new hypothesis. Selecting animals for tameness, they said, could alter genes that control a group of developmentally important cells called neural crest cells. Those embryonic cells migrate in the embryo and contribute to tissues involved in the fight-or-flight response, facial development and coloring.
Choosing animals for tameness might be selecting for ones that have changes in how their neural crest cells function, the researchers proposed in Genetics in 2014 (SN: 8/23/14, p. 7). Calmer domesticated animals might have neural crest cells that move or work differently than the cells in more fearful wild animals. Because neural crest cells contribute to so many tissues in the body, altering their function could change an animals behavior, appearance and biology, the researchers reasoned. For the first time, domestication researchers had a hypothesis about the link between tameness and physical traits that could really be put to the scientific test.
It would be hard to recognize todays toothsome corncobs from the plants wild progenitor, a grass called teosinte. When Native Americans began domesticating teosinte, its ears were two or three inches long, holding a sparse five to 12 kernels each. In fact, teosinte looks so different from maize that scientists questioned the link, first proposed in the 1930s, until genetics could prove it more than half a century later. In 2009, archaeologists found the earliest known evidence of domesticated maize at an 8,700-year-old site in southwestern Mexico, alongside stone tools used to grind the plants. Erika Engelhaupt
Since the neural crest hypothesis surfaced, geneticists have found tantalizing clues that Wilkins, Wrangham and Fitch are onto something. Analysis of cat DNA found that house cats and wild cats have different versions of genes implicated in neural crest cell migration (SN: 12/13/14, p. 7). When Orlando and colleagues examined horse DNA for genes that may have rapidly changed during domestication, they too found genes involved in neural crest cell function.
While at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, Cagan compared DNA from the tame rats and mink at Novosibirsk, and from other domesticated species, with DNA from aggressive counterparts and wild ancestors. In unpublished research, Cagan (now at the Wellcome Trust Sanger Institute in Hinxton, England) found that genes involved in helping neural crest cells migrate differed between the tame and wild animals (SN: 6/13/15, p. 11). That might explain the white patches of fur, shorter snouts and curly tails of the tame animals.
Jensen calls the neural crest cell hypothesis a very speculative idea that may not be applicable across species. He is looking more closely at the neural crest in the jungle fowl. He and colleagues are collecting eggs to track the cells movements in tame and fearful birds. Even if the researchers find differences, he says, we still need to find the genetic mechanisms that are causing the neural crest cells to act as they do.
Larson expects many revelations in the next year or two about when, where and how domestication happened. Even the big themes are going to be radically revised, he says. Domestication is likely to be a far more complicated process than researchers expected, but Larson hopes people will find it all the more interesting for its lack of simplicity. We want to get people to embrace the ambiguity and to love the complexity.
This article appears in the July 8, 2017, issue of Science News with the headline: "The road to tameness: Fresh ideas emerge about the origins of humans' relationships with their favorite species."
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DNA evidence is rewriting domestication origin stories - Science News Magazine
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Making macrocyclic compounds for DNA-encoded libraries – The Biological SCENE
Posted: at 1:47 am
A simple tweak to a tool for making macrocyclic compounds could help increase the diversity of DNA-encoded libraries used by drug developers to rapidly screen and identify promising drug candidates (Bioconjugate Chem. 2017, DOI: 10.1021/acs.bioconjchem.7b00292).
Building such libraries involves attaching short, unique DNA sequences to small molecules and then reacting those DNA-tagged building blocks together to create myriad products, which are tagged with additional unique DNA sequences. The chain of DNA markers serves as a sort of bar code to identify the compounds in a library that successfully bind to a particular drug target and to trace their synthesis history. However, these libraries generally have not been able to include ring compounds in the drug screening because transition-metal catalysts essential for ring-closing reactions are incompatible with DNA. These catalysts are central to many important organic transformations such as olefin metathesis, but they can bind to charged DNA backbones and cause the strands to fall apart.
A team led by Xiaojie Lu and Lijun Fan at GlaxoSmithKline has found that by protecting the DNA tags with magnesium ions, they can produce a variety of DNA-encoded heterocycles and macrocycles using ruthenium-catalyzed ring-closing metathesis. The team hypothesizes that because the magnesium ions occupy all the DNAs binding sites, the ruthenium catalyst is forced to react with the substrates instead of the DNA. Preliminary tests to perform cross-metathesis reactions between two DNA-tagged primary alkenes to produce a secondary alkene were also successful.
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Making macrocyclic compounds for DNA-encoded libraries - The Biological SCENE
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