TIME animals

You Always Knew Your Cat Was Half Wild But Now There’s Genetic Proof

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Paula Daniëlse—Getty Images/Flickr RM

That kitty curled up on your lap is only one genetic step away from jungle killer

A new study on house cats has found that our feline companions are actually only semi-domesticated.

People began domesticating cats around 9,000 years ago but DNA researchers from Washington University in St. Louis found that house cats still have many of the same traits as their wild cousins. The fact that cats have retained the ability to hunt and survive effortlessly in the wild just underscores how little impact we humans have had on them.

Wes Warren, an associate professor of genomics at the university, told the Los Angeles Times, “We believe we have created the first preliminary evidence that depicts domestic cats as not that far removed from wildcat populations.”

That’s not to say humans haven’t had any influence on cats. We originally took them into our homes to hunt rodents and rewarded that behavior with food. According to researchers, this lead to eventual changes in a group of stem cells that resulted in more docile (but not fully domesticated) felines and produced colors and fur patterns that humans liked.

“Our results suggest that selection for docility, as a result of becoming accustomed to humans for food rewards, was most likely the major force that altered the first domesticated cat genomes,” researchers wrote.

Read more at the Los Angeles Times.

Read next: Celebrate National Cat Day With the Most Ridiculous Cover in TIME History

TIME Archaeology

DNA Study Dates Eurasian Split From East Asians

EU Eurasian Split
The skull of the fossil of Kostenki XIV that was found in 1954 near Kostenki-Borshchevo, in what is now western Russia AP

The study concludes that Kostenki man shared genetic sequences with contemporary Europeans, but not East Asians

(BERLIN) — The human populations now predominant in Eurasia and East Asia probably split between 36,200 and 45,000 years ago, according to a study released Thursday.

Researchers used new techniques to analyze genetic samples from the shin bone of a young man who died at least 36,200 years ago near Kostenki-Borshchevo in what is now western Russia. The study, published in the journal Science, concludes that Kostenki man shared genetic sequences with contemporary Europeans, but not East Asians.

A separate study published last month in the journal Nature determined that a 45,000-year old sample found in Siberia contained sequences ancestral to both modern East Asians and Europeans.

Taken together, these two studies suggest a time frame of about 9,000 years in which the two genetic populations could have diverged, said Eske Willerslev, an evolutionary biologist at the University of Copenhagen, Denmark, one of the authors of the Science paper.

Even on its own the Kostenki sample challenges previous theories that modern Europeans emerged only when hunter-gatherers mixed with a farming population that moved in from the Middle East after Ice Age glaciers receded from Europe about 10,000 years ago, the start of a period known as the Neolithic.

“People had largely tended to think that Europeans today were mostly influenced by the Neolithic expansion from the Middle East,” said Sarah Tishkoff, a professor of genetics at the University of Pennsylvania who wasn’t involved in the latest study. “But if they’re correct they are suggesting that this person 36,000 years ago already had some similarity to the people who contributed to this Neolithic expansion from the Middle East.”

Although Kostenki man — who had dark skin, brown eyes and was relatively short — belonged to a group of humans that ultimately died out, the DNA fragments he left are enough to draw a line in European genetic history going back at least 36,000 years, said evolutionary biologist Marta Mirazon Lahr of the University of Cambridge, another author of the Science study.

TIME Science

Looking to Science for Answers About Race

Theodosius Dobzhansky
Theodosius Dobzhansky, circa 1960s Pictorial Parade / Getty Images

How a forgotten scientist changed the way we talk about race

History News Network

This post is in partnership with the History News Network, the website that puts the news into historical perspective. The article below was originally published at HNN.

Americans are constantly reminded of the contradictions concerning the meaning and impact of race.

We can as a nation claim progress as it pertains to race. After all, a majority of American voters have twice elected President Barack Obama to the most powerful office in the world.

Yet, for as much progress as we have made there is as much work to be done. The recent killings by police of unarmed black men in Ferguson, Missouri and Staten Island, New York remind us how race shapes the often hostile relationship between law enforcement and some communities. Racist comments by several NBA owners remind us that some remain polluted by the foolish belief in the fundamental superiority and inferiority of different groups. Skin color still limits economic and other opportunities. Take home loans: over the past few years the U.S. Justice Department settled cases with several banks for having steered non-whites into expensive subprime loans despite having qualified for standard mortgages.

Race matters, of course, and so too does the meaning we give it. We have often turned to science for that meaning—to justify beliefs and to provide a vocabulary for explaining human differences. But science too struggles with understanding race.

When we talk about the scientific meaning of race today we do so largely because of the work of the distinguished evolutionary biologist Theodosious Dobzhansky, who spent most of his career at Columbia University. Though today forgotten outside of scientific circles, Dobzhansky was almost single-handedly responsible for reshaping the race concept in the 20th century through his classic book, Genetics and the Origin of Species (1937).

Until Dobzhansky’s work appeared, race was defined largely in typological terms, meaning that one member of a race was thought to share the same traits with other members of that race. This kind of thinking helped perpetuate racist actions and stereotypes. For example, from 1932-1972 the infamous Tuskegee Study followed the natural course of syphilis in African American men because it was mistakenly believed that syphilis was a different disease in blacks than it was in whites.

Although Dobzhansky was unaware of the Tuskegee Study at that time, he did understand that such classifications were bad science. Dobzhansky, through new techniques in population genetics and evolutionary biology, came to understand first in the non-human animals he studied like fruit flies and ladybug beetles, and later in humans, that genetic diversity at the racial or population level was far greater than most people knew. Racial groups were much more genetically complex than a typological race concept would allow.

So how did Dobzhansky redefine race? To Dobzhansky, race was simply a methodological tool to facilitate the scientific study of human and other populations. Race was not a fixed entity, it was a way to organize individuals within a species based on the frequency with which a gene or genes appeared in that population. Depending on the genes being investigated, there could be just a few or many races. What made his definition so important and so radical was that he understood that the way we choose to organize differences in gene frequencies within species were about data and methodology, not about an underlying racial hierarchy or about the fixity of certain traits within specific groups. Dobzhansky thus sought to extract racism from the race concept.

By the 1960s, Dobzhansky grew disillusioned with the race concept, and came to believe that the scientific study of race was not only inseparable from its broader social meanings, but that it could also be put in the service of reinforcing those social meanings. The rise of the Civil Rights Movement and his own battles with other scientists over the imprecise and often inappropriate use of the term ‘race’ led him to issue a challenge to the field: devise better and more meaningful methods to investigate genetic diversity.

More than fifty years later biology still struggles with Dobzhansky’s challenge and still operates within a paradox that he himself struggled with. On the one hand, race can be an important tool to help scientists organize genetic diversity. On the other, race is an imprecise marker of genetic diversity and not a great proxy for elucidating the relationship between our ancestry and our genes.

This paradox remains central to the use of race in our genomic age. For example, it is currently too expensive to sequence everyone’s genomes, so the rapidly growing field of personalized medicine relies on race as a proxy to make best guesses about an individual’s disease risk and how one’s genes influence the response (positively or negatively) to drug treatments. Because genetic variants can cluster in populations, the belief is that this can help clinicians and drug companies make medical decisions based on one’s race. The potential danger here is that we inadvertently reinforce a crude understanding of race, forgetting that it is a highly flawed concept that cannot be used as a proxy for an individual’s own genome.

It turns out that muddled thinking about race is as deeply ingrained in scientific as non-scientific thought, and that scientists are as conflicted about race as the rest of society. It is neither cynical nor misguided to acknowledge this. It is only a reflection of a society that continues to struggle with the meaning and impact of racial difference.

Michael Yudell, Interim Chair and Associate Professor at the Drexel University School of Public Health, is author of “Race Unmasked: Biology and Race in the 20th Century,” which was recently published by Columbia University Press.

TIME ebola

This Might Be Why Some Survive Ebola

A new mice study may help explain Ebola's varying impacts

Scientists in a biosafety level 4 lab have discovered that genetics are likely involved in how susceptible someone is to Ebola, finds a new mice study published in the journal Science.

Why some people survive Ebola and others do not, even when they’re treated in the same conditions, is a question that’s long intrigued researchers. The current outbreak has also revealed that humans show symptoms of the disease differently; a significant number do not present hemorrhagic fever symptoms like heavy diarrhea, vomiting and bleeding before death.

So far, researchers have primarily used monkeys to study the Ebola virus, but in the new study, the researchers discovered that a genetically diverse population of mice had wide variations in their responses and symptoms to the Ebola virus—similar to how humans have reacted. It’s notable because mice very rarely have similar immune responses to humans, which is why discoveries made in mouse models are evaluated skeptically.

When the researchers infected the mice with Ebola, they found that some of the mice survived with mild disease symptoms, some died, and some died with severe hemorrhagic fever symptoms similar to those observed in humans. Researchers Michael G. Katze and Angela L. Rasmussen of the University of Washington also identified a few potential genetic pathways that might differ in mice who survive the disease versus those who die from it. The hope is that these pathways could help researchers develop drugs for the disease.

“We now have a model that represents the human Ebola disease that we could test vaccines in, we could test novel therapeutics in, and we also could start getting information about the genes that are responsible for the resistance to Ebola and the susceptibility to Ebola,” said Katze in a video about the study. Before the researchers can make the leap to developing drugs for humans, they will have to confirm that the pathways also exist in humans and work in the same way. But the new research is a starting point.

The team started studying the progression of the Ebola virus in mice a few years ago, before the current outbreak of Ebola started in West Africa. Only a handful of of scientists work in the few high-security containment labs in the United States. The training, Katze told TIME, is intense and requires psychological testing. “We’ve been studying Ebola for almost a decade. We’ve always been interested in Ebola because it’s a very interesting virus. It’s like the rockstar of viruses,” Katze told TIME in early October.

Read on for more about the scientists’ emerging Ebola research.

TIME Autism

Major Autism Studies Identify Dozens of Contributing Genes

Researchers collaborate on two large studies identifying the genetic basis of autism

Two new studies exploring the genetic basis of autism tie mutations in hundreds of genes to the disease.

Several teams of researchers collaborated on the studies, both published in the journal Nature, and found that about 60 of the genes are considered “high confidence,” meaning there’s a 90% chance that mutations within those genes contribute to risk for autism. Both studies show through genomic sequencing that many of these mutations are de novo, meaning that parents do not have the gene mutation, but they present spontaneously just before a child is conceived in either the sperm or egg.

It’s long been believed that autism is genetic, but a lack of large studies and advanced genomic sequencing has precluded any sort of consensus about what genes might be at play. But in the last couple years, scientists have been able to look at the genetic mutations in hundreds of people with autism and identify genes that likely factor into a child’s development of the disorder. In the two new studies, scientists were able to expand their work and look at thousands of people.

In one of the studies, several institutions used data from the Simons Simplex Collection (SSC), which is a collection of DNA samples from 3,000 families. In each of the families, one individual had autism. The researchers compared the gene sequences of the individual with autism to their unaffected family members. After analysis, they estimated that de novo mutations contribute to autism in at least 27% of families, where only one member has the disorder.

The other study, by researchers at 37 different institutions as part of the Autism Sequencing Consortium, looked at 14,000 DNA samples of parents with affected children. It found 33 genes the researchers say definitely increase risk for autism, should there be a mutation.

Even though there may be hundreds or even thousands of genes that contribute to a child’s risk of developing autism, the researchers on both studies found that the mutations appear to converge on a much smaller number of biological functions, like nerve-cell communication or proteins known to cause inherited disability. “In my view, the real importance of these studies is not diagnosis, and it’s not figuring out exactly what percentage of people have de novo mutations, it’s about laying the foundation to transform the understanding of the biological mechanisms of autism,” says Dr. Matthew State, chair of the psychiatry department at University of California, San Francisco and a co-leader of the SSC study, as well as a senior participant on the other study.

State doesn’t believe that the findings will mean that families will one day get their genomes sequenced to spot hundreds of possible mutations. Instead, they could lay the groundwork for discovering how autism develops, and what potential treatments, or even drugs, could help fight it.

TIME Innovation

Five Best Ideas of the Day: October 14

The Aspen Institute is an educational and policy studies organization based in Washington, D.C.

1. Fix the system, don’t fight individual diseases: Why Ebola may change how aid dollars are spent on healthcare in Africa.

By Lesley Wroughton at Reuters

2. Plan for a global body to regulate the great promise of genetics — balancing unfettered innovation with sensible rules to prevent abuse.

By Jamie F. Metzl in Foreign Affairs

3. Because it increases disease and exacerbates resource scarcity, the Pentagon sees climate change as a threat multiplier.

By Laura Barron-Lopez in the Hill

4. The U.S. should call out Egypt’s rising authoritarian leadership and the plight of repressed people there.

By the Editorial Board of the Washington Post

5. Successful community collaborations build civic confidence for increasingly audacious projects that can improve lives.

By Monique Miles in the Collective Impact Forum blog

The Aspen Institute is an educational and policy studies organization based in Washington, D.C.

TIME Ideas hosts the world's leading voices, providing commentary and expertise on the most compelling events in news, society, and culture. We welcome outside contributions. To submit a piece, email ideas@time.com.

TIME Genetics

Gene-Therapy Trial Shows Promise Fighting ‘Bubble Boy’ Syndrome

The immune system-related disease affects about 1 in 100,000 babies each year

A new gene-therapy treatment is showing promise in treating a rare and severe congenital condition that involves extreme immune-system deficiencies.

“Bubble boy” syndrome, an X-linked condition, takes its name from a famous case in which an affected boy, vulnerable to infection, lived inside a plastic bubble that protected him from the world’s germs. Outside of such sterile environments, babies with the syndrome seldom live longer than a year, the Wall Street Journal reports.

The condition has for decades bested medical researchers, despite occasional bouts of optimism — hope for one previous gene-therapy treatment was felled when some recipients developed leukemia.

Gene-therapy treatment works, essentially, by replacing unperforming genes with functional ones. Dysfunctional cells are removed from the child’s immune system and exposed to a genetically engineered virus that can reprogram the cells to function properly, explains Reuters. Those cells are then reinserted back into the patient.

In the earlier treatment, the virus to which the cells were exposed apparently activated a part of their genetic code that leads to leukemia, Reuters says.

But initial results reported in the New England Journal of Medicine show that none of the nine babies from the U.S. and Europe who received the latest treatment are exhibiting any signs of cancer.

Of the nine infant participants in the research — who were between 4 and 10½ months old when they began receiving the therapy — eight were still alive 16 to 43 months later, without living in a protective “bubble.” (The ninth child died four months after treatment began from an earlier infection he had been fighting.)

Out of the eight boys still living, the treatment upped blood T-cell levels, rebuilding the immune system, of seven. In the case of the eighth child, the treatment did not rebuild his immune system, but a successful stem-cell transplant has kept him in improved health, Reuters reports.

TIME Addiction

Addicted to Coffee? It’s Probably in Your Genes

coffee crema
Getty Images

A new genetic explanation for your caffeine cravings

If you feel like you literally could not survive a day without coffee, you might have your genes to thank (or blame).

A new genome-wide study published in Molecular Psychiatry has identified genetic variants that may have a lot to do with your coffee obsession. Researchers from Harvard School of Public Health and Brigham and Women’s Hospital looked at more than 120,000 coffee drinkers and found six markers linked to responsiveness to caffeine—some of which had been previously identified as being related to smoking initiation and other types of potentially addictive behaviors, but had never before been linked to coffee consumption, says Marilyn Cornelis, research associate in the Department of Nutrition at Harvard School of Public Health and lead author of the study.

MORE: You Asked: Is Coffee Bad For You?

Caffeine is a drug—a fact many of us forget until we madly crave a double shot. “There is controversy as to whether it can be addictive, and some of the genes that come up in the study suggest that’s quite possible,” Cornelis says. “The stimulating effects caffeine has would suggest that caffeine is a major driving in habitual coffee consumption at the genetic level.”

MORE: How Coffee Might Lower the Risk of Heart Failure

The results might help add nuance to coffee research, she says, which generally treats everyone as the same. It could also help pinpoint people who’d most benefit from coffee consumption, and who should stick to decaf. “We assume that any health effects from one cup of coffee will be the same for everyone, but this data suggests that’s not true,” Cornelis says.

Scientists have known for a long time that genetics play a role in coffee consumption and caffeine response, Cornelis says. “But it’s only until just recently that we’ve actually been able to pinpoint these exact genetics. That’s an important step forward in the research.”

TIME medicine

New Genes Found that Determine Your Height

The latest analysis doubles the number of genes connected to height

How tall you are is strongly related to the genes you inherit, and previous studies suggested that as much as 80% of the variance in height among people is due to their DNA.

And in the largest genetic study of height-related genes to date, scientists involved in the appropriately titled GIANT consortium (Genetic Investigation of Anthropometric Traits) identified 423 genetic regions connected to height — which could explain as much as 60% of that genetic component.

Dr. Joel Hirschhorn, leader of the GIANT consortium at Boston Children’s Hospital, Harvard Medical School and the Broad Institute of MIT says that for a trait like height, which isn’t determined by a single gene but likely the combined effects of multiple genes involved in multiple different processes from bone growth to cell growth, the new findings are like finding biggest nuggets of gold in a riverbed. The latest analysis, published in the journal Nature Genetics, describes the gene variants most commonly shared among people (not the rare mutations) that likely contribute to height.

They emerged from a sweep of the genomes of more than 250,000 people of various heights, and from correlating their stature with their genetics. Many of the known and familiar factors related to height, including those dealing with skeletal growth and collagen that are mutated in people with medically short stature, for example, appeared in the study, confirming their role in determining how tall people get.

But there were also some surprises — genetic regions that previous had never been thought to be related to height, including a gene known to be involved in cell growth but not in skeletal functions. “It’s a mix ranging from completely known things, to those that make sense to things that are completely surprising and things we don’t even know what to think about them,” says Hirschhorn.

What the group has identified are gene regions of interest, and a new round of studies will have to delve deeper into those areas to isolate specific genes — and the proteins they make, such as growth factors, enzymes, or other agents — that are actually responsible for determining height. But it’s a critical first step, and could lead to potential new ways of treating medical conditions of short stature or gigantism that can have health negative health effects on the heart and joints.

TIME Genetics

New Study Makes Great Strides in Understanding Human Height

Nearly 700 gene variants linked to height have been identified

What makes tall people tall and short people short is becoming less of a mystery to scientists. An international team of researchers has identified nearly 700 gene variants in more than 400 gene regions that are connected to height — an estimated 20 percent of all the gene variants that play a role in determining one’s size.

The findings of the study were published in the journal Nature Genetics, Reuters reports. It is believed to be the biggest study of its kind to date.

Scientists believe that about 80 percent of a person’s height is hereditarily determined, with environmental factors such as nutrition determining the rest. The average height of humans around the world has risen throughout the last few generations as world nutrition generally improves.

Researchers studied the genomes of 253,288 people from Europe, North America and Australia, all with European ancestry and found 424 gene regions with 697 gene variants that are linked to height. Many of the genes identified were not previously known to have an effect on skeletal growth.

“For over 100 years, [height has] been a great model for studying the genetics of diseases like obesity, diabetes, asthma that are also caused by the combined influence of many genes acting together,” Dr. Joel Hirschhorn, a pediatric endocrinologist and geneticist at Boston Children’s Hospital and the Broad Institute. “So by understanding how the genetics of height works, we can understand how the genetics of human disease works.”

[Reuters]

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