Israeli fossils are the oldest modern humans ever found outside of Africa

The oldest human fossils ever found outside Africa suggest that Homo sapiens might have spread to the Arabian Peninsula around 180,000 years ago — much earlier than previously thought. The upper jaw and teeth, found in an Israeli cave and reported in Science on 25 January1, pre-date other human fossils from the same region by at least 50,000 years. But scientists say that it is unclear whether the fossils represent a brief incursion or a more-lasting expansion of the species.

Researchers originally thought that H. sapiens emerged in East Africa 200,000 years ago then moved out to populate the rest of the world. Until discoveries in the past decade countered that story, scientists thought that a small group left Africa some 60,000 years ago and that signs of earlier travels, including 80,000–120,000 year-old skulls and other remains from Israel discovered in the 1920s and 1930s, were from failed migrations.

However, recent discoveries have muddied that simple narrative. Some H. sapiens-like fossils from Morocco that are older than 300,000 years, reported last year2, have raised the possibility that humans evolved earlier and perhaps elsewhere in Africa. Teeth from southern China, described in 20153, hint at long-distance migrations some 120,000 years ago. And genome studies have sown more confusion, with some comparisons of global populations pointing to just one human migration from Africa4,5, and others suggesting multiple waves6.

Early start

In the early 2000s, archaeologist Mina Weinstein-Evron, at the University of Haifa in Israel, and palaeoanthropologist Israel Hershkowitz, at Tel Aviv University, began a project to excavate a series of Israeli caves. “We called it ‘Searching for the Origins of the Earliest Modern Humans’. This was what we were looking for,” says Weinstein-Evron.

Their team discovered the jaw fragment in 2002, in Misliya Cave, the highest of Mt Carmel’s caves. It is just a few kilometres away from the Skhul cave, one of the sites where the 80,000–120,000-year-old remains were found in the 1920s and 1930s. Using several different methods, the team estimates the jaw and teeth to be 177,000–194,000 years old.

Misliya Cave

The fossilized jaw and teeth were found in Misliya Cave on Mt Carmel in Israel.Credit: Mina Weinstein-Evron, Haifa Univ.

The remains are unquestionably H. sapiens, says team member María Martinón-Torres, a palaeoanthropologist at the National Research Centre on Human Evolution in Burgos, Spain. The shapes of the teeth match those of both modern and ancient humans, she says. They also lack features typical of Neanderthals, which lived throughout Eurasia at the time.

The dating seems solid and the fossils are H. sapiens, says Huw Groucutt, an archaeologist at the University of Oxford, UK. But he isn’t very surprised to see them in Israel. He and his colleagues have previously said that 175,000-year-old stone tools from other sites in the Middle East resemble those used by H. sapiens in East Africa7.

Close encounters

Hershkowitz says that the jaw and teeth point to a long-term occupation of the Near East by early H. sapiens. “It was a central train station. People were coming and going through this land corridor from one continent to another, and it was occupied all the time.” Once there, humans probably encountered and interbred with Neanderthals, Hershkowitz says, pointing to a 2017 ancient-DNA study that suggested interbreeding had occurred before 200,000 years ago8.

Wet periods could have drawn humans into the Near East, but long, dry spells mean that “the region was probably more often a ‘boulevard of broken dreams’ than a stable haven for early humans”, Chris Stringer and Julia Galway-Witham, palaeoanthropologists at the Natural History Museum in London, write in an essay accompanying the paper9.

The fossil could indicate that Israel and the rest of the Arabian Peninsula were part of a larger region in which H. sapiens evolved, says John Shea, an archaeologist at Stony Brook University in New York. “We tend to think of Israel as part of Asia for geopolitical reasons, but it is really a transition zone between North Africa and western Asia,” he says. “Plenty of Afro–Arabian animals live there, or did so until recently,” including leopards, lions and zebras. “Homo sapiens,” Shea says, “is just another such Afro–Arabian species.”


This article was originally published in Nature. Read the original article.

Big Data Comes to Dieting

At this point in the resolution-heavy month, many of us may be trying to shed pounds, either the ones we added during the holidays or the ones we’ve accumulated stealthily with time. But by the end of the year, most of us won’t have succeeded — and there’s not much established science to tell us why.

An ambitious new study published this month in Cell Systems, however, promises to shed some new light, enumerating for the first time the thousands of changes in genes and various biological systems that may occur after even a small amount of weight gain, and which may — or may not — be reversed if the weight is then dropped. The findings may help researchers better understand why adding weight causes some people to develop diabetes and other conditions, and also underscore the cumulative health risks of so-called yo-yo dieting.

An international consortium of scientists approached 23 overweight men and women who were already part of a large, continuing study — called an “omics” study in the parlance of researchers — that examines participants’ genomes and microbiomes and generates vast amounts of data about the workings of the body.

But an “omics” study had never looked at the effects of weight change. After taking blood and other samples from their volunteers, the scientists asked the men and women to overeat. All of them began the study overweight; about half were insulin-resistant, which is often a precursor to diabetes. For a month, they added on average 880 calories a day to their diets and gained an average of about six pounds.

The scientists then asked the volunteers to cut calories and lose that new weight, which took most of them at least twice as long as the gaining had. After more samples, the researchers asked participants to keep their weight stable and return after another three months for a final round of tests.

In those tests, the scientists found many biological changes related to weight change. They found that 318 genes worked differently after most subjects had gained even a little weight. Some genes were more active, while others were effectively turned off. Many of these genes are thought to be involved in fat metabolism.

The scientists also found multiple new molecular markers in people’s blood after weight gain that can indicate increased inflammation throughout the body and, rather worrisomely, the possible beginnings of cardiomyopathy, or an enlarged heart. Most of these modifications reverted to their previous normal state once the men and women lost the added weight.

Over all, the results indicate that, after even a relatively small amount of weight gain, “imbalances and shifts occur” throughout the body’s biological systems, says Michael Snyder, chairman of the department of genetics at Stanford University and the study’s senior author. Even if you later drop those pounds, the shifts “are not reset completely.”

Snyder says that he and his colleagues have larger “omics” studies of weight and health underway. Results should start arriving later this year.

This article was originally published in The New York Times.  Read the original article.

The key finding is that there is often more time than doctors realized in which brain cells can still be rescued by a procedure to remove the clot.

Many more stroke victims than previously thought can be saved from disability or death if doctors remove blood clots that are choking off circulation to the brain, a new study has shown.

“These striking results will have an immediate impact and save people from lifelong disability or death,” Dr. Walter J. Koroshetz, director of the National Institute of Neurological Disorders and Stroke, said in a statement. “I really cannot overstate the size of this effect.”

The key finding is that there is often more time than doctors realized in which brain cells can still be rescued by a procedure to remove the clot. Traditional guidelines have set a limit of six hours after stroke symptoms begin, and said after that it would be too late to help.

The study showed that the time window could be expanded to 16 hours. However, the findings do not apply to every stroke victim. The researchers used a special type of brain imaging to identify the patients who still had live brain tissue that could be saved if the blood supply was restored. Only about half the patients who were screened qualified for treatment, known as thrombectomy, which uses a mechanical device to pull clots out of a blood vessel.

The study, involving 182 patients at 38 hospitals in the United States, was stopped early because patients who had clots removed fared so much better than those who did not.

Ninety days after treatment, 45 percent of the thrombectomy patients were well enough to be “functionally independent,” as opposed to 17 percent of those who did not have the procedure. The death rates were 14 percent in the thrombectomy group, and 26 percent in those whose clots were not removed.

The results were published on Wednesday in The New England Journal of Medicine. The study was paid for by the National Institutes of Health, and led by researchers from Stanford University. The Stanford team said it expected the study would lead the American Heart Association to change the guidelines for stroke treatment, extending the time window for thrombectomy.

It is not uncommon for strokes to begin during sleep, and some of those patients miss out on treatment because it is not clear what time the stroke began. Medical practice has been to set the beginning of the time window as the last moment they were known to be well, and if they have slept most of the night the six-hour window may be over by the time they wake up. New guidelines may allow such patients to be treated.

About 750,000 people a year suffer strokes in the United States, and 85 percent of those are caused by clots — the same type treated in this study. Symptoms include speech difficulty, arm weakness and facial drooping. Experts urge patients or their families to call 911 immediately so that treatment can be started as soon as possible.

This article was originally published in The New York Times.  Read the original article.

Citing Deaths of Lab Monkeys, F.D.A. Ends an Addiction Study

The deaths of four squirrel monkeys used as subjects in a nicotine addiction study have prompted the Food and Drug Administration to shut down the research permanently and to establish a council to oversee all animal studies under the agency’s purview.

“It is clear the study was not consistent with the agency’s high animal welfare standards,” Dr. Scott Gottlieb, the agency’s commissioner, said in a statement on Friday. “These findings indicate that F.D.A.’s animal program may need to be strengthened in some important areas.”

Dr. Gottlieb has called in an independent investigator to examine the agency’s animal research programs, starting with those at the National Center for Toxicological Research, in Arkansas, where the squirrel monkeys were housed. The 20 or so study animals will be transferred to a sanctuary, the commissioner said.

Federally funded medical research that relies on animals has been contentious for years. The National Institutes for Health has banned the use of chimpanzees in biomedical research and has retired hundreds of lab chimps, some of which have been moved to sanctuaries. The N.I.H. continues to finance research on other nonhuman primates for studies of neurobiology, metabolic illness and other ailments.

F.D.A. researchers are continuing other primate studies, the agency said, although Dr. Gottlieb said he wanted to reduce reliance on them.

The suspended study, begun in 2014, was designed to inform agency officials who have expanded oversight of tobacco products, regulation of e-cigarettes and alternative nicotine delivery devices.

The research was supposed to measure the effects of nicotine on addiction, mostly on young squirrel monkeys although it also included some adults. Researchers taught the squirrel monkeys to press a bar to get a dose of nicotine. After they became addicted, the scientists lowered the doses and observed the effects.

They started with a group of 24 monkeys, but by the end of last summer four had died — three from anesthesia given while catheters were put in, and one from a type of gastric bloat.

Patsie, another squirrel monkey in the study, nearly died while under anesthesia on July 20 of last year. Patsie stopped breathing, but veterinarians were able to revive him.

The mishaps drew the attention of many animal rights activists, including the celebrated primate expert Jane Goodall. In a September letter to Dr. Gottlieb, Dr. Goodall accused the researchers of performing cruel and unnecessary nicotine addiction experiments on the squirrel monkeys.

In September, the F.D.A. suspended the studies and started investigating treatment of the animals. They found numerous deficiencies, although the agency has not released an inspection report with details.

Anthony Bellotti, president of the White Coat Waste Project, which had enlisted Dr. Goodall’s help, praised the agency’s action. ”We applaud the F.D.A. for ending these wasteful baby monkey nicotine tests and for retiring the primates,” he said.

Jack Henningfield, professor of behavioral biology at Johns Hopkins School of Medicine, disagreed with the decision to stop the study.

“These studies are done to address really serious questions about the nature of tobacco addiction,” Dr. Henningfield said. ‘‘This is research in serious service to humanity. If there was an accident leading to the death of someone working in global warming research, you’d correct that situation, not stop doing global warming research. You’d say, ‘We are going to do it better, with more safety and even more care.’”


This article was originally published in The New York Times.  Read the original article.

First monkeys cloned with technique that made Dolly the sheep

Biologists in Shanghai, China, have created the first primates cloned with a technique similar to the one used to clone Dolly the sheep and nearly two dozen other species. The method has failed to produce live primates until now.

Researchers hope to use this revised technique to develop populations of genetically identical primates to provide improved animal models of human disorders, such as cancer. The technology, described in Cell1 on 24 January, could also be combined with gene-editing tools such as CRISPR–Cas9 to create genetically engineered primate-brain models of human disorders, including Parkinson’s disease.

“This paper really marks the beginning of a new era for biomedical research,” says Xiong Zhi-Qi, a neuroscientist who studies brain disease at the Chinese Academy of Sciences Institute of Neuroscience (ION) in Shanghai. He was not involved in the cloning project.

But the achievement is also likely to raise some concerns among scientists and the public that the technique might be used to create cloned humans. “Technically, there is no barrier to human cloning,” says ION director Mu-Ming Poo, who is a co-author of the study. But ION is interested only in making cloned non-human primates for research groups, says Poo: “We want to produce genetically identical monkeys. That is our only purpose.”

Primates have proved tricky to copy, despite many attempts using the standard cloning technique. In that method, the DNA of a donor cell is injected into an egg that has had its own genetic material removed.

ION researchers Sun Qiang and Liu Zhen combined several techniques developed by other groups to optimize the procedure. One trick was to undo chemical modifications in the DNA that occur when embryonic cells turn into specialized cells. The researchers had more success with DNA from fetal cells, rather than cells from live offspring.

Using fetal cells, they created 109 cloned embryos, and implanted nearly three-quarters of them into 21 surrogate monkeys. This resulted in six pregnancies. Two long-tailed macaques (Macaca fascicularis) survived birth: Zhong Zhong, now eight weeks old, and Hua Hua, six weeks. Poo says that the pair seem healthy so far. The institute is now awaiting the birth of another six clones.

Cloning specialist Shoukhrat Mitalipov of the Oregon Health and Science University in Portland says that the Chinese team should be congratulated. “I know how hard it is,” says Mitalipov, who estimates he used more than 15,000 monkey eggs in cloning attempts in the 2000s. Although he was able to produce stem-cell lines from cloned human and monkey embryos, his team’s primate pregnancies never resulted in a live birth.

Cloned animals offer some significant advantages over non-clones as models for studying human disease. In experiments with non-cloned animals, it is difficult to know whether differences between the test and control groups were caused by the treatment or genetic variation, says Terry Sejnowski, a computational neurobiologist at the Salk Institute for Biological Studies in La Jolla, California. “Working with cloned animals greatly reduces the variability of the genetic background, so fewer animals are needed,” he says.

Parkinson’s studies

Sejnowski also says that primate brains are the best model for studying human mental disorders and degenerative diseases. The ability to clone monkeys might revive primate studies, which have declined in most countries, says Poo. Parkinson’s disease experiments that currently use hundreds of monkeys could be done with just ten clones, he says.

Neuroscientist Chang Hung-Chun, also at ION, says that primate-cloning technology will soon be combined with gene-editing tools to study human genetic disorders in primate brains. Gene editing is already used on developing monkey embryos, but that leaves open the possibility that some cells are not edited, which then affects the results, says Chang.

With cloning, the donor cell can be edited before it is injected into the egg. Within a year, Poo expects the birth of cloned monkeys whose cells have been genetically edited to model circadian-rhythm disorders and Parkinson’s disease.

Spurred by the promise of primate research, the city of Shanghai is planning major funding for an International Primate Research Center, expected to be formally announced in the next few months. The centre will produce clones for scientists around the globe. “This will be the CERN of primate neurobiology,” Poo says. There’s already high demand from pharmaceutical companies that want to use cloned monkeys to test drugs, he says.

Although most reproductive biologists are unlikely to consider using the technique to clone humans because of ethical objections, Mitalipov worries that it might be attempted in a private clinic.

China has guidelines that prohibit reproductive cloning, but no strict laws. It also has a weak record of enforcement of its rules on the use of stem cells for therapy. Some other countries — notably the United States — do not prohibit reproductive cloning at all. “Only regulation can stop it now,” says Poo. “Society has to pay more attention to this.”



This article was originally published in Nature. Read the original article.

These monkey twins are the first primate clones made by the method that developed Dolly

Chinese scientists have produced two genetically identical long-tailed macaques using the same technique that gave us Dolly the sheep, the world’s first cloned mammal. The feat is a first for nonhuman primates, and despite limitations, it could lead to batches of genetically uniform monkeys for biomedical research.

Previous attempts to clone monkeys through the Dolly method, known as somatic cell nuclear transfer (SCNT), produced viable embryos but they failed to mature into healthy animals. The technique starts with taking the nucleus of a cell from a tissue like skin, and inserting it into an animal egg that has had its own DNA-carrying nucleus removed. That combination is then treated with enzymes that return it to an early embryonic state from which it can differentiate into every cell type in the body, like a just-fertilized egg. The egg is then implanted in a surrogate mother for development.

Success came from adapting several new techniques, says Mu-ming Poo, director of the Chinese Academy of Sciences’s Institute of Neuroscience in Shanghai, who led the work. These included a new type of microscopy to better view the cells during handling to using several compounds that encourage cell reprogramming, which hadn’t been tried before on primates, they report today in Cell. Still, the success rate was low: Just two healthy baby macaques born from more than 60 surrogate mothers. And the researchers were only able to reprogram cells from fetal monkey tissue, not adult cells. The newborns were named Zhong Zhong and Hua Hua, after a Mandarin term for the Chinese nation and people.

Poo says the new approach is more customizable and can produce a greater number of genetically identical animals than the first technique used to clone primates, a simpler method called embryo splitting. He adds that combining SCNT with gene editing will allow researchers to create “ideal nonhuman primate models” for studying disease mechanisms and screening drugs. And improving their methods could lead to higher success rates and possibly even the ability to use adult tissues.

“It’s a good piece of science,” says Alan Trounson, a stem cell scientist at the Hudson Institute for Medical Research in Clayton, Australia. “[But] I can’t see a high desire to use cloned monkeys for research.” Trounson notes that monkeys are costly, researchers hesitate to use monkeys if alternatives are available, and drug regulatory agencies “don’t demand monkey studies anymore.”

He says one possible use might be to explore how genes and the environment interact in conditions such as Alzheimer’s disease in which the influence of nongenetic factors is poorly understood. Alzheimer’s and Parkinson’s diseases “are the first two we are thinking about” for disease research using cloned monkeys, Poo notes. He adds that the monkeys could be used to study any diseases resulting from one or a few genetic mutations, including certain cancers. But the group’s first research effort will be more basic: regular imaging of the twins’ brains to observe their neurological development. Because the pair have identical genes and are living in the same environment, researchers will be able to see whether their brains develop in similar ways or naturally diverge.

The team acknowledges that the work raises ethical questions, especially because—in principal, at least—the technique could be applied to humans. “[But] I would think society and the general public and governments will not allow extension of this method from nonhuman primates to humans,” Poo says.

Ethicists are also concerned about the monkeys themselves. “At present, it has not been sufficiently demonstrated that there are no alternatives to using macaque monkeys for such research,” Peter Dabrock, an ethicist at Friedrich-Alexander University in Erlangen, Germany, wrote in a statement.

Poo acknowledges that using nonhuman primates for research is more accepted in China than in the West. But he emphasizes his group is following international guidelines for the treatment and care of their monkeys. And he agrees that the minimum number of animals should be used. But, Poo argues: “Once we demonstrate the cloned monkey’s usefulness in curing disease, I hope [Western societies] will gradually change their minds.”



This article was originally published in Science. Read the original article.

Yes, They’ve Cloned Monkeys in China. That Doesn’t Mean You’re Next.

Researchers in China reported on Wednesday that they have created two cloned monkeys, the first time that primates have been cloned with the technique that produced Dolly the sheep more than 20 years ago.

The long-tailed macaques, named Zhong Zhong and Hua Hua, were made from fetal cells grown in a petri dish. The clones are identical twins and carry the DNA of the monkey fetus that originally provided the cells, according to a study published in the journal Cell. They were born at the Chinese Academy of Sciences in Shanghai.

Dolly the sheep was produced from udder cells that had been frozen for six years. Until that feat, many researchers had thought that type of cloning was impossible, because it required taking adult cells and bringing them back to their original state, when sperm first fertilized egg.

The cell would then have to start to grow in a surrogate’s womb and to differentiate into an entire animal, genetically identical to the one that provided the initial cell.

But once cloning proved possible, researchers began improving their method and testing it on other species. Since Dolly was born, researchers have cloned 23 mammal species, including cattle, cats, deer, dogs, horses, mules, oxen, rabbits and rats.

The new monkey clones stand out, though. “It’s the first primate ever to be cloned,” said Dr. Leonard Zon, director of the stem cell program at Boston Children’s Hospital. “We are closer to humans than we’ve ever been before.”

“That raises questions of where we would want to go,” he added.

Still, the techniques used to make those clones are not new, and other researchers previously had initiated the process in primates.

An initial step was reported in 2007 by Shoukhrat Mitalipov at Oregon Health and Science University. He and his colleagues removed skin cells from a 9-year-old macaque and inserted them into eggs from which the original DNA had been removed.

The eggs adopted genes from the inserted cells, and the resulting clones were grown to an early embryo stage. Dr. Mitalipov and his colleagues did similar work with human embryos in 2013.

The researchers, led by Qiang Sun, director of the primate research facility at the Chinese Academy of Sciences Institute of Neuroscience, began with cells taken from an aborted female monkey fetus.

From those, he and his colleagues created 149 early embryos, clones whose DNA was entirely derived from the fetal cells. Seventy-nine embryos survived in the lab, apparently healthy enough to transfer into the uteruses of surrogate monkey mothers.

Zhong Zhong, left, and Hua Hua were cloned using the method that created Dolly the sheep, the first cloned mammal.CreditAgence France-Presse — Getty Images

Four of those surrogates remained pregnant, but two soon miscarried. In the end, there were two live births.

The investigators say they followed international guidelines for animal research set by the National Institutes of Health. They anticipate that the method could be used to produce monkeys for research. (The United States, however, is backing away from the use of primates in medical research.)

The genes of cloned monkeys could be manipulated before the process begins, yielding animals that have edited genes in every cell of their bodies, the researchers suggested. This might allow scientists to probe the genes’ functions and to test experimental drugs on monkeys custom-made to have various genetic conditions.

The scientists tried cloning adult cells, but those attempts failed. The older a starting cell, the more difficult it is to clone and the more likely the resulting embryo or fetus will be miscarried in a surrogate female.

If scientists wanted to create a monkey identical to an adult, or even an adolescent, this method so far would not succeed. And the technique used by the Chinese scientists is still a long way from producing human babies, even if that were ethically permissible.

“It is unlikely it can be applied to humans,” Dr. Mitalipov said.




This article was originally published in The New York Times.  Read the original article.

The development heralds the possibility of genetically engineered primates for drug testing, gene editing and brain research

In a world-wide first, Chinese scientists cloned two monkeys by transplanting donor cells into eggs, they said on Wednesday, a feat that could lead to genetically engineered primates for drug testing, gene editing and brain research.

The cloned macaque monkeys are the latest application of a test-tube technique called somatic cell nuclear transfer pioneered 20 years ago with the creation of the cloned sheep named Dolly. It has been used to clone 23 species from rodeo bulls to polo ponies and pet cats. But the ability to clone primates eluded scientists until the project made public Wednesday in the journal Cell.

“For the cloning of a primate species, including humans, the technical barrier is now broken,” said senior author Qiang Sun, director of the Nonhuman Primate Research Facility at the Chinese Academy of Sciences Institute of Neuroscience in Shanghai, in an interview. “In principle it could be used in humans, but there is no intention for us to apply this method to humans.”

The Chinese bioengineers made the two female monkeys by surgically replacing the nucleus of an egg with fetal donor tissue and then using special chemicals designed to trigger genes required for embryo development. The monkeys appear to be healthy and developing normally, the scientists said.

Two others, made at the same time using adult donor cells instead of fetal tissue, died within hours of birth, said the scientists, who couldn’t explain why. The failure is significant because adult cells are easier to obtain for cloning than cells from aborted monkey fetuses.

These microphotographs show the step-by-step process by which researchers in China created the first cloned monkeys.
These microphotographs show the step-by-step process by which researchers in China created the first cloned monkeys. PHOTO: QIANG SUN AND MU-MING POO / CHINESE ACADEMY OF SCIENCES

The cloning project reflects China’s growing attention to primate research at a time when funding for primate studies has declined in Europe and the U.S. due to budget constraints, tighter regulations and growing reservations about the morality of animal research.

China sees primate research as the best way to find treatments or cures for a variety of brain diseases and disorders, and many Western scientists agree. But many Americans and Europeans think that using animals for medical research or drug testing is cruel.

China singled out the creation of primate disease models as a national goal in 2011. The number of businesses there breeding macaque monkeys—a mainstay of biomedical research—tripled between 2004 and 2013 to 34 from 10, according to data published in Nature.

“China has definitely taken the ball and run with it,” said primate reproductive biologist Catherine VandeVoort at the California National Primate Research Center, who wasn’t involved in the project.

Once they are available in larger numbers, cloned monkeys would be ideal as test subjects in many conventional medical studies because they are genetically identical. “You can treat one of them with a drug and leave the other one as a control. Then the only difference between them is the treatment,” Dr. VandeVoort said.

While technical hurdles remain, cloning also could become a way to speed up the breeding of primates given new traits through modern gene-editing techniques. Already, several research teams in China have altered monkeys by adding human genes, to make them better laboratory models than mice for probing brain-related disorders such as autism.

“Scientifically, there is an urgent need for nonhuman primate models of disease,” said reproductive biologist Keith Latham at Michigan State University, who uses gene-editing technology to alter rhesus monkey embryos. “The ability now to clone monkeys using this technique is a powerful tool in the toolbox.”


This article was originally published in The Wall Street Journal. Read the original article.

It has over five times as much DNA as the human genome

THE domestication of wheat and other staple crops in the Levant some 10,000 years ago allowed for persistent settlement above a level of mere subsistence—one possible definition of the beginning of civilisation. Early farmers grew naturally occurring hybrids of wheat, and over time tamed them into a robust, easy-to-harvest and high-yielding species, the history of which is revealed in the genome of modern bread wheat. It is an enormously dense, complicated genome. And unlike the genetic codes of staples like rice, soya and maize, scientists struggled until 2017 to crack it. Why was it so hard to decipher and was it worth the effort?

The genomes of ancient wheats, such as wild emmer, contain more of the DNA base pairs required to create proteins than that of humans. Domesticated hybrids, like bread wheat, are even larger. Bread wheat has nearly six times the number of DNA base pairs as humans (about 17bn compared with humans’ 3bn). That is in part because humans are diploid, with two sets of chromosomes, whereas the chromosomes of bread wheat come in sets of six (which correspond to the three ancient wheats of which bread wheat is a hybrid). Furthermore, the DNA of ancient wheat contained a huge amount of duplication. This means that bread wheat not only contains an enormous amount of genetic information, but that much of it is repeated. That makes decoding its genome complex. With fewer unique pieces, it is harder to fit the jigsaw together.

Other staple food crops had their genomes sequenced long before bread wheat. But then they are much simpler: popular strains of maize, soya and rice have 2.3bn, 1.1bn and 420m DNA base pairs respectively. The breakthrough with bread wheat came last year, when several different academic and industry projects matured. Both the International Wheat Genome Sequencing Consortium (IWGSC), which includes wheat farmers, breeders and scientists, and an independent group led by Johns Hopkins University managed to sequence it. Others decoded wild emmer, an ancestor of both bread and durum wheat, and Aegilops tauschii, another of bread wheat’s ancestors.

The value of the decoding is two-fold. First, it allows researchers to manipulate wheat without recourse to so much trial and error. Second, it allows them to insert attractive traits from ancient wheats into modern ones, rather than introduce genes from other organisms altogether (a process known as transgenics). These may have better resistance to pests or better tolerance of drought, but yet have poorer yields and quality, says Catherine Feuillet, head of trait research at Bayer, a German pharmaceuticals firm and an important part of IWGSC’s gene project. Without the genome operating as a sort of index of the wheat’s positive traits, it would take ten years using conventional techniques to cross a new wheat with an ancient one and recover all the desired traits. With the genome to hand, and in the public domain (the IWGSC is eschewing patents), iteration and improvement can be done rather faster. More researchers can get involved. Help may even come from unexpected corners. Ms Feuillet talks of finding “a high-school student who may finally be able to find a key resistance gene for a fungal disease.”



This article was originally published in The Economist. Read the original article.

This Worm Evolved Self-Fertilization and Lost a Quarter of Its DNA

Inspecting the tiny roundworms Caenorhabditis briggsae and Caenorhabditis nigoni through a microscope, you’d have trouble telling them apart. Both are about a millimeter long and transparent. On the evolutionary tree, they’re closer together than horses and donkeys.

The key distinction between the two nematodes is their sex lives. Sex in C. nigoni takes place between a male and female. But only a small minority of C. briggsae are males. The rest are hermaphroditic females that reproduce by self-fertilizing, or selfing. They have evolved the ability to produce sperm that merge with their own eggs.

This sexual switch may have caused profound changes at the genetic level for C. briggsae. In a study published last week in Science, biologists reported that C. briggsae lost thousands of genes — a staggering quarter of its genome — since it diverged from C. nigoni a million years ago.

“Many of these genes had been around, and were presumably needed, for tens of millions of years or longer,” said Eric Haag, a biology professor at the University of Maryland, College Park, and an author of the paper. “In the blink of an eye, they disappeared.” He and his co-authors believe that a large portion of the genes shed are related to male reproduction.

In their study, the biologists compared C. briggsae and C. nigoni, and discovered that C. briggsae has about 7,000 fewer genes. A disproportionately high number of shed genes, they found, were more heavily expressed in male than female C. nigoni.

“That tells us that the stuff being lost in Caenorhabditis briggsae is disproportionately involved in male biology,” said Erich Schwarz, an assistant research professor at Cornell University who led the sequencing efforts for the study.

Digging into a specific example of what C. briggsae lost when it dumped all those genes, the researchers studied male secreted short (or m.s.s.) genes, which have been found in all studied Caenorhabditis species except those with selfing hermaphrodites. “We thought this gene family was maybe emblematic of a larger phenomenon,” Dr. Haag said.

Da Yin, a graduate student in Dr. Haag’s lab and lead author of the study, showed in lab experiments that C. briggsae fathered more offspring when those genes were added to their genomes, suggesting that these genes contributed to a reproductive edge in males.

This bolsters the scientists’ hypothesis that C. briggsae’s dramatic reduction in DNA had to do with its change in sexual strategy. Over time, the species possibly gave up many genes facilitating male-dependent procreation because a mostly hermaphroditic lifestyle offered an advantage, Mr. Yin said.

C. briggsae are opportunistic creatures that often colonize isolated oases — say a rotting apple — as lone individuals. If the wrigglers always had to rely on mates to multiply, it would be harder for them to kick-start these new colonies. As a result, it might be more efficient for the species to skew heavily toward hermaphrodites — having more males may “put a brake on population growth,” Dr. Haag said.

Being able to examine the genetic underpinnings of C. briggsae, particularly in relation to such a close relative, C. nigoni, has been a gift, he added.

“We have this natural experiment where a species has given up the way it used to reproduce,” he said. “It shows us how much of the genome is involved in the subtleties of mating and reproduction — and it’s startling just how much of it is.”


This article was originally published in The New York Times.  Read the original article.