Human DNA carries hints of unknown extinct ancestor

Human DNA carries hints of unknown extinct ancestor

 The human family tree may be even more tangled than scientists had thought. A new computer analysis has turned up evidence pointing to some long-lost human cousins. That evidence was found hiding in the DNA — genetic instruction book — of some people alive today.

Ryan Bohlender led the new study. This statistical geneticist works at the University of Texas MD Anderson Cancer Center in Houston. He and his colleagues pored over DNA from people living in Melanesia. This part of the South Pacific includes Papua New Guinea and nearby islands. And here, the new study finds, people inherited genes that appear to come from an unknown extinct hominid. (Hominids are a group of species that includes humans and our ancient relatives.)

Bohlender reported his team’s new conclusions here in Canada, on October 20. It was at the annual meeting of the American Society of Human Genetics.

Earlier research had shown that the ancestors of Melanesians mated with two groups of extinct hominids. One group, Neandertals, left behind fossils in Europe and Asia. The other group had been distant cousins of the Neandertals. Known as Denisovans (Deh-NEES-oh-vuns), this group is known only from DNA found in a finger bone and a couple of teeth. Their fossils came from a cave in Siberia.

The new study found some mysterious DNA in Melanesians that was very old. But it didn’t seem to come from either Neandertals or Denisovans. The mystery DNA likely comes from a third hominid species. Scientists have not yet found fossil evidence for such a species, Bohlender notes.

Other scientists also have dug into the DNA of present-day people and found traces of unknown species. In 2012, another group of researchers suggested some Africans carry heirloom DNA from an unknown extinct hominid. Again, no bones with that particular DNA have yet turned up.

Accounting for missing DNA

After ancestors of humans began migrating out of Africa, they mixed with Neandertals in Europe and Asia. As a result, people whose ancestors came from outside of Africa still carry a small amount of Neandertal DNA. Bohlender and his colleagues calculate that Europeans and Chinese people carry a similar amount of this Neandertal ancestry — some 2.8 percent.

Europeans have no sign of Denisovan ancestry. People in China do, but the amount is very small, just 0.1 percent, according to calculations by Bohlender’s group. But 2.74 percent of the DNA in people in Papua New Guinea comes from Neandertals. And Bohlender estimates the Denisovan DNA in Melanesians at about 1.1 percent. That’s far less than the 3 to 6 percent Denisovan DNA that other researchers have reported in the Melanesians.

But Melanesians carry other bits of old DNA too. These bits may have come from a relative of Neandertals and Denisovans. If true, that would make a third species of extinct hominid that has mixed with human ancestors.

“Human history is a lot more complicated than we thought it was,” Bohlender now says.

Another team recently concluded much the same thing. Eske Willerslev, who led this group, is an evolutionary geneticist. He works at the Natural History Museum of Denmark in Copenhagen. Willerslev’s group examined DNA from 83 aboriginal Australians. They also probed the DNA of 25 people from native populations in Papua New Guinea. DNA similar to Denisovans showed up in the study volunteers. But that DNA didn’t match that of the Denisovans precisely. In fact, it may be from another extinct hominid. That’s what these researchers reported in the October 13 Nature. “Who this group is we don’t know,” Willerslev points out.

Fossils from other extinct human relatives have been found in the South Pacific. Scientists have not yet gotten DNA out of those bones. It’s possible that the not-quite-Denisovan DNA that Willerslev’s team found comes from one those unknown hominids. If researchers can get DNA from the old bones, they’ll try to match it to what’s in people today.

 A possible confounder

It’s hard to know for sure whether such a third group mated with the ancestors of the South Pacific islanders. One reason is that within any group, DNA will vary from person to person. Some groups have quite a bit of this genetic diversity.

Researchers don’t know much about Denisovans, says Mattias Jakobsson. He’s an evolutionary geneticist at Uppsala University in Sweden. But it’s possible that Denisovans formed distant communities. These might have been separated from each other for a long time. If true, those groups could have developed many genetic differences. If there were enough such changes to their DNA, this might have fooled scientists into thinking the groups were different species.

Still, Jakobsson says he wouldn’t be surprised if other groups of extinct hominids mixed with humans. Modern and ancient humans, he observes, “have met many times and had many children together.”

Scientists discover itch-busting cells

Scientists discover itch-busting cells

A fly tickling the hair on your arm can spark a maddening itch. Now, scientists have spotted nerve cells in mice that curb this light twiddling sensation. If humans have similar itch-busters, the results could lead to treatments for the millions of people who suffer from chronic, unstoppable itch.

For many of these people, there are currently no good treatments. “This is a major problem,” says Gil Yosipovitch. He directs the Temple University Itch Center in Philadelphia, Pa., and was not involved in the new study.

All touch sensations — including itch — start at the skin. In recent years, scientists have started to learn how nerve cells carry itchy signals from there to the spinal cord and on up to the brain. Often the original itch signal is triggered by chemicals, such as those that mosquitoes inject. For another sort of itch, all that’s needed is a light touch on the skin. That’s called a mechanical itch. The fact that this type of itch exists is no surprise, Yosipovitch says. Mechanical itch may help explain why clothes or even dry, scaly skin can be so itchy. It’s also why you might feel a mosquito crawling on your skin before it takes a bite.

The new study, published October 30 in Science, involved mice with one key defect. Scientists had altered their genes so that they lacked a certain type of nerve cell in their spinal cords. Without those cells, the mice “have the urge to scratch all the time,” says study coauthor Qiufu Ma. He’s a neuroscientist at Harvard Medical School in Cambridge, Mass. Even with nothing specifically causing them to itch, the mice scratched so often that they developed bald patches on their skin. A light touch from a thin wire will cause a mechanical itch. This touch led the mice to scratch themselves more than regular mice did. Yet the itchy mice responded to pain and itch-causing chemicals normally.

That suggests some nerve cells detect only mechanical itch, Ma concludes. If a light touch taps into the itch accelerator, then these spinal-cord nerve cells act as the brakes, says Martyn Goulding, who also worked on the study. He’s a neuroscientist at the Salk Institute for Biological Studies in La Jolla, Calif. Removing these nerve cells lets the itch signal more easily get through to the brain, he says.

The discovery of itch-blocking nerve cells opens up new possibilities for understanding itch, Goulding says. Now, scientists can start to piece together the rest of the nerve pathway that detects mechanical itch on the skin and then carries that signal to the brain. These nerve cells produce a chemical signal called neuropeptide Y. Future experiments can test what role that chemical plays in how a mechanical itch makes itself known, he says.

It makes sense that human skin would develop the ability to detect an itchy tickle, Goulding says. An insect crawling on your skin could be harmless. But if it’s carrying germs and bites you, it might cause a nasty infection, he says. A quick scratch, prompted by an itch, might prevent that.

Genes: How few needed for life?

Genes: How few needed for life?

What are the fewest genes needed to sustain life? To test that, scientists started with a microbe having one of the smallest known genomes — or entire sets of genetic instructions. Then scientists figured out the magic minimum for this microbe, which was 473 genes. By whittling down the genes to this number, scientists learned a lot about biology. But there is still much to discover. Researchers still aren’t sure exactly what almost a third of its genes do.

The new microbe is a stripped-down version of Mycoplasma mycoides (MY-ko-PLAZ-ma My-KOY-dees). This bacterium normally has 901 genes. That’s really not very many. Quite a few other bacteria, such as E. coli, may have 4,000 to 5,000 genes. People have more than 22,000 genes, although we don’t need all of them to live and be healthy.

In 2010, researchers at the J. Craig Venter Institute in La Jolla, Calif., copied the entire genome of M. mycoides. Then they popped it into a cell of a different species, Mycoplasma capricolum. Some people called this the first synthetic, or artificial, organism.

More recently, the researchers started by stripping the M. mycoides genome down to its essentials. Then they transplanted them into the M. capricolum shell. The result was a minimal bacterium that they now call syn3.0.

The researchers described their results March 25 in Science.

Learning from minimal life

Researchers hope syn3.0’s simple genome will teach them more about the basics of biology. Minimal life-forms such as this one could also be a starting point for building custom microbes in the future. These microbes might make certain drugs or chemicals that people need or prize.

J. Craig Venter is the geneticist who founded the nonprofit institute bearing his name. He worked with a team of researchers there led by Clyde Hutchison III and Daniel Gibson. At first, they wanted to design an organism with a core set of about 300 genes. The researchers thought these would be enough for a microbe to survive on its own. Computers predicted this would work. But when the researchers tried to bring their computer creations to life, “every one of our designs failed,” Venter said in a phone conference with reporters.

Why didn’t the microbes live? The researchers had left out some genes because they didn’t know those genes were important.

In fact, scientists don’t know what many genes do. Here, the scientists thought they already knew the essential ones for survival. They were wrong. Almost one-third of the genes in the minimal genome are secret ingredients that do something important, even though scientists don’t know what that something is. Without these genes, the bacteria died. When the researchers mixed those genes back into their recipe, the bacteria sprung to life.

Most of those 473 genes in the final recipe do one of four essential jobs. Reading DNA instructions and turning them into RNA and proteins, is the job of 195 genes. Another 34 genes copy and repair DNA. There are 84 genes involved in building the cell membrane — the skin around the bacterium — and keeping it working. And 81 genes carry out metabolism, helping the organism use its fuel for growth and reproduction.

That leaves 149 genes in syn3.0 that do jobs researchers don’t completely understand. Scientists can predict what 70 of these genes likely do. But what the remaining 79 mystery ingredients do is entirely unknown.

“I think we’re showing how complex life is in even the simplest of organisms,” Venter says. The results show that researchers still don’t fully understand the basics of life. “These findings are very humbling,” Venter concludes.

Pamela Silver works at Harvard Medical School in Boston, Mass. As a synthetic biologist, she designs and creates new types of organisms from genes. Silver says that lack of knowledge is “frustrating after so many years of molecular biology.” But, she adds, the new stripped-down microbe may help science learn what those mystery genes do.

Other researchers have tried to make minimal genomes by stripping away one gene at a time. Not Venter’s group. His team built its new microbe from the ground up. They made pieces of DNA from scratch, then combined them into a new genome.

Drew Endy is a synthetic biologist at Stanford University. He is one of several scientists who like the made-from-scratch approach. “Only when you try to build something do you find out what’s truly required. Too often in biology we end up with only data, a computer model, or a just-so story. When you actually try to build something, you can’t hide from your ignorance,” Endy said in an e-mail. “What you build either works or it doesn’t.”

And, at first, this bare-bones genome didn’t work. The problem was that the researchers had compiled a list of genes that they thought they could just leave out. Such genes are known as nonessential. But not all of those genes proved nonessential after all. Some genes did the same job as another gene. Researchers could remove one such gene, but never both at the same time. It’s like a twin-engine jet, Gibson says. Knocking out one engine will keep the plane airborne, but disabling both engines will lead to a crash.

How low can you go?

The genome of syn3.0 is far smaller than those of any natural free-living bacterium. But it’s possible that there are life-forms with even smaller starting genomes. For example, other researchers think it’s possible that there could be some cell hosting just a single gene inside a membrane. It sole job would likely be to copy RNA, says George Church. He’s a geneticist at Harvard University.

Researchers might also start with another organism instead of M. mycoides. Or they might grow bacteria under different conditions. This would probably lead to a microbe needing a different minimal set of genes, says Jay Keasling. He’s a synthetic biologist at the University of California, Berkeley. “The minimal genome is in the eye of the beholder,” he says. It also may depend on the environment, stress or other conditions in which a life-form will need to survive.

Gibson and Venter agree that they have created a minimal genome, but not necessarily the most minimal genome. Syn3.0 is streamlined, but still has a few frills. The team kept several “quasi-essential” genes that may not be strictly necessary. Still, these genes let the bacteria grow fast enough to be useful in the lab. It is possible that future minimal life-forms might host even tinier genomes.

Mice with a mutation linked to autism affect their littermates’ behavior

Mice with a mutation linked to autism affect their littermates’ behavior

The company mice keep can change their behavior. In some ways, genetically normal littermates behave like mice that carry an autism-related mutation, despite not having the mutation themselves, scientists report.

The results, published July 31 in eNeuro, suggest that the social environment influences behavior in complex and important ways, says neuroscientist Alice Luo Clayton of the Simons Foundation Autism Research Initiative in New York City. The finding comes from looking past the mutated mice to their nonmutated littermates, which are usually not a subject of scrutiny.  “People almost never look at it from that direction,” says Clayton, who wasn’t involved in the study.

Researchers initially planned to investigate the social behavior of mice that carried a mutation found in some people with autism. Studying nonmutated mice wasn’t part of the plan. “We stumbled into this,” says study coauthor Stéphane Baudouin, a neurobiologist at Cardiff University in Wales.

Baudouin and colleagues studied groups of mice that had been genetically modified to lack neuroligin-3, a gene that is mutated in some people with autism. Without the gene, the mice didn’t have Neuroligin-3 in their brains, a protein that helps nerve cells communicate. Along with other behavioral quirks, these mice didn’t show interest in sniffing other mice, as expected. But Baudouin noticed that the behavior of the nonmutated control mice who lived with the neuroligin-3 mutants also seemed off. He suspected that the behavior of the mutated mice might be to blame.

Experiments confirmed this hunch. Usually, mice form strong social hierarchies, with the most aggressive and vocal males at the top. But in mixed groups of mutated and genetically normal male mice, there was no social hierarchy. “It’s flat,” Baudouin says.

Raised and housed together, the mutated and nonmutated mice all had less testosterone than nonmutated mice raised in genetically similar groups. The testosterone levels in both types of mice were comparable to those found in females — “one of the strongest and most surprising results,” Baudouin says.

The mice’s social curiosity was lacking, too. Usually, mice are interested in the smells of others, and will spend lots of time sniffing a cotton swab that had been swiped across the bedding of unfamiliar mice. But when given a choice of strange mouse scent or banana scent, the nonmutated littermates spent just as much time sniffing banana as did the mutant mice.

When Baudouin and colleagues added back the missing Neuroligin-3 protein to parts of the mutant mice’s brains, aspects of their behavior normalized. The mice became interested in the odor from another mouse’s bedding, for instance. These behaviors also shifted in the mice’s nonmutated littermates. That experiment suggests that the missing protein — and the resulting abnormal behavior of the mutants — was to blame for their littermates’ abnormal actions.

Still, it’s hard to tease apart the mice’s roles, says behavioral neuroscientist Mu Yang of Columbia University. “It is a shared environment, and there is no sure way to tell who is influencing whom, or whether both parties are being impacted.”

Female mice that completely lacked the neuroligin-3 gene also influenced the behaviors of littermates that carried one mutated version of the gene, other behavior tests revealed. More experiments are needed to determine whether the social environment affects male and female mice differently, and if so, whether those differences relate to autism, says Luo Clayton.

The turning of wolves into dogs may have occurred twice

The turning of wolves into dogs may have occurred twice

Dogs were such great friends that humans appear to have domesticated them at least twice, a new study suggests.

Domestication (Doh-MES-ti-KAY-shun) is the gradual process by which humans can produce a tame and useful animal from a wild one. This happens over countless generations. It may take thousands of years, but eventually the tamed animals can become so different from their wild ancestors that they turn into a new species. In this case of wolves, their domestication produced dogs.

Earlier studies had indicated that the wolf-to-dog transformation happened just once. But scientists disagree about where it occurred. Some say dogs became human’s best friend in East Asia. Then, last year, a study of village dogs suggested it had happened in Central Asia. Some studies had even hinted that Europeans were the first to turn wolves into dogs.

In the new study, scientists analyzed the genes of bones from a 4,800-year-old Irish dog and 59 other ancient dogs. These tests suggest that canines and humans became pals in both Europe and East Asia. And it may have been as long as 14,000 years ago. Later, dogs from East Asia accompanied their human companions to Europe. The Asian dogs’ bred with and replaced the European dogs, the team concluded June 3 in Science.

Understanding process to dog-dom may help people learn more about humans’ distant past. Dogs were probably the first domesticated animal. They may have paved the way for taming other animals and plants.

In the new study, researchers put together the complete set of genes, or genome, of an ancient dog. Genes are made of DNA and carry instructions for building a body and all the bits and pieces inside. So a genome is like an instruction book.

The ancient dog had been found in a tomb near Newgrange, Ireland. To get at the DNA carrying the dog’s genetic instruction book, researchers drilled into a bone from the dog’s inner ear. The bone, called the petrous, is part of a skull bone that makes that knob behind your ear.

That petrous is hard as a rock, says Laurent Frantz. He is an evolutionary geneticist at the University of Oxford in England. He was also one of the scientists that took part in the new study. The hard petrous bone protects the DNA inside. So when scientists examined it after thousands of years, it still was fairly easy to read.

But it didn’t tell the scientists much about what the midsize Irish dog that it came from would have looked like. From its DNA, the scientists can tell that it probably did not resemble modern dog breeds, Frantz says. “He wasn’t black. He wasn’t spotted. He wasn’t white.” Instead, the Newgrange dog was probably a mongrel with fur similar to a wolf’s.

But the ancient mutt has something special in his genes. It had a stretch of mysterious DNA, points out Mietje Germonpré. She is a paleontologist at the Royal Belgian Institute of Natural Sciences in Brussels and was not part of the study. “This Irish dog has a component that can’t be found in recent dogs or recent wolves.” That mystery DNA, she says, could be left over from prehistoric dogs that lived in Europe. And that just might help researchers learn more about what the first dogs were like. Or it could be a trace of an extinct ancient wolf that may have given rise to dogs.

Digging deep into doggy DNA

The idea that dogs came from East Asia or Central Asia is mostly based on the DNA of modern dogs. Claims that dogs have European origins had been staked on the DNA of prehistoric pups. “This paper combines both types of data” to give a more complete picture of dog domestication, says Germonpré.

Frantz’s team gathered DNA data from the Newgrange dog and other ancient dogs. The scientists compared these to data from studies of modern dogs. These included the whole genomes of 80 separate dogs. The researchers also used a less-complete sampling of DNA from 605 additional dogs. They included a collection of 48 breeds and of village dogs of no particular breed.

Eastern and Western dogs are genetically different, the researchers learned. That might indicate that two separate branches of the canine family tree once existed, like distant cousins.

The Newgrange dog’s DNA is more like that of the Western dogs. Since the Irish dog is 4,800 years old, the Eastern and Western dogs must have gone out on separate limbs of family tree before then. That probably happened between about 6,400 to 14,000 years ago. The new finding suggests that dogs may have been domesticated from local wolves in two separate locations during the Stone Age.

The ancient dog’s DNA also may help pinpoint when that domestication took place. Frantz and his colleagues used the Newgrange dog as a known point in time. Then they counted up the genetic changes that have happened to dogs since then. From there they could calculate how quickly dogs’ DNA changes, or mutates. This “mutation rate” is important for figuring out how long ago animals morphed into a new species. It also can tell researchers how fast animals can adapt to new situations.

Dogs’ genes mutate at a slower rate than researchers had calculated before, the study found.

Determining when dogs first emerged

Frantz’s team used this slower mutation rate to calculate when dogs likely became different from wolves.

That split likely occurred between 20,000 and 60,000 years ago. So that could be the time period when humans began domesticating wolves. But Frantz and colleagues say that their estimate doesn’t truly nail down when domestication happened. Different types of wolves could have been hanging around for a long time. Some became grey wolves like the ones living today. Others went extinct. And still others evolved into dogs. The researchers need more data to tell exactly when all of those things occurred.

Although dogs may have started in two different places, our best furry friends have since mixed and mingled. The researchers came to that conclusion from looking at bones and at DNA from dogs’ mitochondria (My-toh-KON-dree-uh). Mitochondria are like power plants inside cells, and have their own DNA. Most of a cell’s DNA is stored in a compartment called a nucleus. Both a mom and dad pass that type of DNA on to their kids. But only moms also pass on their mitochondrial DNA.

Mitochrondrial DNA comes in different “flavors” called haplogroups. Researchers can use those different types to figure out where a dog’s mother, grandmother, great-grandmother and so on came from. The researchers compared mitochondrial DNA from 59 ancient European dogs and 167 modern European dogs. Haplogroups in the ancient European dogs were different from those in the modern dogs, the researchers found.

Still, the authors of the latest study admit they can’t yet rule out that dogs were domesticated only once. Dogs could have then moved to different places early on. There, isolation, random chance and other factors might have caused them to drift apart genetically so that now their DNA looks like they started as different groups.

Ancient enzymes adapted to a cooler Earth to keep life’s chemical reactions going

Ancient enzymes adapted to a cooler Earth to keep life’s chemical reactions going

Like lifelong Floridians dropped into a Wisconsin winter, enzymes accustomed to warmth don’t always fare well in colder climes. But ancient heat-loving enzymes forced to adapt to a cooling Earth managed to swap out parts to keep chemical reactions going, scientists report online December 22 in Science.

By reconstructing enzymes as they might have looked billions of years ago, the research “helps to explain the natural evolutionary history of life on this planet,” says Yousif Shamoo, a biochemist at Rice University in Houston who wasn’t part of the study. And the findings question the idea that enzymes must sacrifice their stability to become more active.

Enzymes are natural catalysts that jump-start essential chemical reactions inside living things. Most work only within a specific temperature range. Too cold, and they can’t get going. Too hot, and they lose their shape — and by extension, their function.

Life on Earth is believed to have started out in warm environments like hot springs or hydrothermal vents, so the first enzymes probably worked best in those toasty temperatures, says study coauthor Dorothee Kern, a biochemist at Brandeis University in Waltham, Mass. But gradually, Earth cooled. For life to continue, early enzymes had to shift their optimal temperature range.

Kern and her colleagues looked at the evolutionary history of an enzyme called adenylate kinase. Some version of this protein is found in every cell, and it’s essential for life to survive.

The researchers used a technique called ancestral sequence reconstruction to figure out what the enzyme’s genes might have looked like at different points in the last 3 billion years. The scientists edited E. coli’s genes to make the bacteria produce those probable ancient enzymes, and then looked at how the reincarnated molecules held up under different temperatures.

“These very old enzymes were way more lousy at low temperatures than anyone expected,” says Kern. But over time, natural selection gradually pushed the enzymes to work better at cooler temperatures, she found. The enzymes accumulated mutations that swapped some of their amino acid building blocks, ultimately lowering the enzymes’ energy demands. That let the enzymes keep moving essential reactions along at a fast-enough pace for life to survive.

There wasn’t a corresponding disadvantage to also working well in heat, so the enzymes didn’t immediately lose their heat tolerance. Some of them became what Kern calls “superenzymes” — they worked impressively fast and could catalyze reactions at low temperatures, but they remained stable at high temperatures.

That finding goes against a widely held assumption that an increase in an enzyme’s activity — which would allow it to keep trucking at the same speed at lower temperatures — typically comes with a corresponding decrease in stability.

That assumption was a logical one: Like chilly fingers struggling to tie shoelaces, enzymes get stiffer and don’t work as well when the temperature drops. To up their activity, they‘d need to increase their flexibility. That could make them less stable at higher temperatures — more likely to lose their shape and stop working. But now, it seems that some enzymes can have the best of both worlds.

The idea of a generalist enzyme that works well across a wide temperature range isn’t new — scientists have engineered such proteins in the lab, Shamoo says. But this work shows it might have happened in a real-world setting. “Just because I can do something in the laboratory, that I can build an enzyme that’s a true generalist, doesn’t mean that’s how it happened on this planet,” he says.

Cleaner water helps male fish again look and act like guys

Cleaner water helps male fish again look and act like guys

Some types of water pollution can make male fish look and act like females. But a new study shows that better water treatment can prevent that. And that could allow  fish populations to thrive.

Water treatment plants are supposed to clean the water from our toilets, showers and sinks before releasing it into rivers, lakes and oceans. They are also supposed to treat water from manufacturing plants. But these water-cleanup plants were never designed to remove all pollutants. Most were built before anyone realized that hormones and hormone-like chemicals could show up in the water. And such chemicals can prove a big problem for fish.

How? They can fake out cells of a male’s body by sending signals telling those cells that this he fish is actually a she. These feminized guy fish may then have little interest in fertilizing a female’s eggs — or he may do so poorly. The result: Fewer baby fish. Or at least that’s the risk.

Male feminization of fish has been showing up in rivers throughout North America.

Mark Servos and his team have been monitoring it in Canada’s Grand River. Servos is an aquatic toxicologist at the University of Waterloo in Ontario. There, he studies the effects of water pollution on rainbow darter fish.

At least once a year from 2007 to 2012, his team caught and examined rainbow darters at a site downstream of a water treatment plant. And depending on the year, between 80 and 100 percent of the males had eggs in them. Egg-making is something that only female fish should do. Moreover, those eggs were in the males’ testes — reproductive organs that normally make sperm (cells used to fertilize a female’s eggs).

Many affected males didn’t even look right on the outside. “Male rainbow darter fish are really colorful,” Servos says. Or at least they should be. “This color is important for attracting mates.” Yet some local males were becoming drab. That could make it hard for them to find a mate.

Clearly, something was very wrong in these male fish. Until 2013, that is. Suddenly, the number of feminized male fish started to fall. This happened at the same time that the local treatment plant changed how it cleaned the water.

The team’s data now link these two observations in a paper published early online in Environmental Science and Technology.

The problem with feminized males

The bodies of animals — including humans — use hormones to tell their cells when to switch various activities on or off. Those hormones fit like keys into “locks” on the outside of a cell. Scientists call these locks receptors. When hormones connect with their locks, they affect how an animal will develop and act. But certain pollutants act like fake keys. These hormone mimics are known as endocrine (EN-doe-krin) disruptors. They can turn on or off some normal function of an animals’ cells — but at the wrong time. That can make an animal develop or act in a way that isn’t natural.

From 2007 to 2012, Servos’ team found high levels of endocrine disruptors in the water downstream of the water treatment plant. Many of these chemicals mimicked the action of estrogen, a female sex hormone. Some endocrine disruptors came from birth control pills. Their synthetic hormones left a woman’s body in urine. Flushed down the toilet, they ended up at a water-treatment plant. Another common endocrine disruptor is nonylphenol (NON-ul-FEE-nul). It’s a breakdown product of certain surfactants. (Surfactants are chemicals that let liquids mix that would not ordinarily do so.) The problem: Nonylphenol, too, can mimic estrogen.

Some male rainbow darters exposed to these pollutants produced eggs in their testes. This took a lot of energy. That reduced the energy available for them to make sperm. Affected fish may have made damaged sperm — or no sperm at all. Eggs laid in the water by females won’t mature and hatch unless males release sperm to fertilize those eggs. So egg-making by males could cause fish populations  to shrink. Oh, and the eggs made by those males: They’re worthless. The bodies of males lack the tubes needed to release those eggs. So the eggs just collect and take up space in the males’ bodies.

Bacteria, bubbles and healthier fish

The good news: Changes to the wastewater-treatment plant in 2013 led to changes in those males.

The plant had always used bacteria to break down harmful chemicals in the water. But workers upgraded the system to give the bacteria more time to break down chemicals. The plant now also bubbled oxygen into the wastewater. This extra oxygen helped the hard-working bacteria grow faster.

Servos and his team tested the water and fish for three years after these water-cleaning changes. As expected, levels of various pollutants dropped. These included the estrogen-mimicking chemicals.

“We don’t know exactly how estrogens are reduced,” Servos says of the water treatment plant. “The key seems to be giving bacteria more time to break down harmful compounds and to feed them oxygen to speed the process.”

And as levels of these chemicals in the water fell, so did the number of feminized males. Within three years, nearly all male fish appeared normal again, inside and out. The researchers suspect the males’ bodies had re-absorbed the useless eggs. The male darters also regained their rainbow colors.

The study shows that although fish may be exposed to endocrine disruptors early in life, those changes may not harm them forever. “That was part of the surprise — [that] adult fish could recover,” says Servos. He doesn’t know whether other species of fish would respond the same way. He suspects many would.

Chris Metcalfe is an environmental toxicologist at Canada’s Trent University in Peterborough, Ontario. He studies materials that can act as poisons in the environment. Metcalfe cautions that not all endocrine disruptors behave the same way. Just because one type can be removed from wastewater doesn’t mean all others will, too.

He also points out that not all urban areas have good water treatment. Some have none; they just spew polluted wastes directly into rivers. And outside of cities, many people rely on underground septic tanks to store water from toilets and showers. Septic tanks filter and capture many pollutants. If people don’t take good care of these systems,  wastes can leak from these tanks into groundwater. From there, pollutants can enter downstream rivers, lakes or the ocean.

What the new work shows is that hormone mimics can hurt fish populations, but that good water-cleansing techniques can limit the risk that this happens.

Bacteria genes offer new strategy for sterilizing mosquitoes

Bacteria genes offer new strategy for sterilizing mosquitoes

A pair of bacterial genes may enable genetic engineering strategies for curbing populations of virus-transmitting mosquitoes.

Bacteria that make the insects effectively sterile have been used to reduce mosquito populations. Now, two research teams have identified genes in those bacteria that may be responsible for the sterility, the groups report online February 27 in Nature and Nature Microbiology.

“I think it’s a great advance,” says Scott O’Neill, a biologist with the Institute of Vector-Borne Disease at Monash University in Melbourne, Australia. People have been trying for years to understand how the bacteria manipulate insects, he says.

Wolbachia bacteria “sterilize” male mosquitoes through a mechanism called cytoplasmic incompatibility, which affects sperm and eggs. When an infected male breeds with an uninfected female, his modified sperm kill the eggs after fertilization. When he mates with a likewise infected female, however, her eggs remove the sperm modification and develop normally.

Researchers from Vanderbilt University in Nashville pinpointed a pair of genes, called cifA and cifB,connected to the sterility mechanism of Wolbachia. The genes are located not in the DNA of the bacterium itself, but in a virus embedded in its chromosome.

When the researchers took two genes from the Wolbachia strain found in fruit flies and inserted the pair into uninfected male Drosophila melanogaster, the flies could no longer reproduce with healthy females,says Seth Bordenstein, a coauthor of the study published in Nature. But modified uninfected male flies could successfully reproduce with Wolbachia-infected females, perfectly mimicking how the sterility mechanism functions naturally.

The ability of infected females to “rescue” the modified sperm reminded researchers at the Yale School of Medicine of an antidote’s reaction to a toxin.

They theorized that the gene pair consisted of a toxin gene, cidB, and an antidote gene, cidA. The researchers inserted the toxin gene into yeast, activated it, and saw that the yeast was killed. But when both genes were present and active, the yeast survived, says Mark Hochstrasser, a coauthor of the study in Nature Microbiology.

Disease control

Scientists could insert the bacteria genes into either mosquitoes not infected with Wolbachia (left) or into the bacteria in infected insects (right) to help control the spread of Zika and dengue.

Hochstrasser’s team also created transgenic flies, but used the strain of Wolbachia that infects common Culex pipiens mosquitoes.

Inserting the two genes into males could be used to control populations of Aedes aegypti mosquitoes, which can carry diseases such as Zika and dengue.

The sterility effect from Wolbachia doesn’t always kill 100 percent of the eggs, says Bordenstein. Adding additional pairs of the genes to the bacteria could make the sterilization more potent, creating a “super Wolbachia.

You could also avoid infecting the mosquitoes altogether, says Bordenstein. By inserting the two genes into uninfected males and releasing them into populations of wild mosquitoes, you could “essentially crash the population,” he says.

Hochstrasser notes that the second method is safer in case Wolbachia have any long-term negative effects.

O’Neill, who directs a research program called Eliminate Dengue that releases Wolbachia-infected mosquitoes, cautions against mosquito population control through genetic engineering because of public concerns about the technology. “We think it’s better that we focus on a natural alternative,” he says.

World’s tallest corn towers nearly 14 meters

World’s tallest corn towers nearly 14 meters

Western New York is getting its own kind of rural skyscraper: giant corn stalks. A researcher there in Allegany now reports growing corn nearly 14 meters (45 feet) high. That makes it about as tall as a four-story building. They appear to be the tallest corn plants ever recorded.

A corn stalk typically grows to about 2.5 meters (8 feet). One strain from Mexico is taller, sometimes 3.4 meters or more. But when the nights are short and the days are long, corn has more time to tap growth-fostering sunlight. Then it can grow even more, sometimes taller than 6 meters (20 feet). Raising it in a greenhouse can add another 3 meters. And tweaking a gene called Leafy1 can up its height yet another 3 meters. Put them together and such factors can cause this strain to ascend nearly 14 meters, notes Jason Karl. He is an agricultural scientist who helped turn some corn plants into such giants.

The Mexican name for corn is maize. That’s also the common term for this plant outside the United States. The unusually tall maize type is called Chiapas 234. Usually “people try to make maize shorter, not taller,” Karl notes. “So it is plainly funny even to consider adding Leafy1 to the tallest strain.”

Corn is the most widely grown food crop in the United States. Most scientists who study corn want to make it better for harvesting. So why would farmers prize shorter corn? Shorter stalks flower earlier in the season. That allows the ears of grain (containing the ymmy kernels that we eat) to mature sooner.

But Karl isn’t interested in corn that blooms quickly or is easy to harvest (because climbing an 12- to 14-meter ladder to pick their ears of corn would hardly be easy). Instead, he wants to know which genes and other factors, such as light, affect the stalk’s growth.

The Chiapas 234 strain was discovered in the 1940s in Mexico. Researchers stored seed from it in a freezer for nearly 30 years. Then, in a 1970 experiment, they grew up some of that seed in a greenhouse. To simulate summer nights, they gave the plants only short periods of darkness. The corn responded by growing more leafy segments, called internodes. Each internode is typically about 20 centimeters (8 inches) long. The corn that you might see on an American farm today has 15 to 20 internodes. The Chiapas 234 strain had 24. When grown with short nights, its stalks developed twice as many.

Karl read about the 1970s night-length study with Chiapas 234. He also knew about a mutation in the Leafy1 gene that could make maize taller. He decided to put them together. “The mutation makes common U.S. maize a good third taller. And I had seen synergy between mutations and the night-length reaction,” he says. And that, he recalls, was a “good omen for discovering new things via preposterously lofty maize.”

What the researchers did

For his experiment, Karl grew the Chiapas 234 in a greenhouse with artificially shortened nights. Materials in the greenhouse walls filtered out some types of light. This allowed more reddish — or longer wavelength — light to reach the plants. That red light increased the length of the internodes. This made the plant grow to nearly 11 meters (35 feet). Then, Karl bred the Leafy1 mutation into the stalks by controlling the pollen that landed on each plant. The result was a nearly 14-meter stalk with a whopping 90 internodes! That’s about five times as many as regular corn produces.

“The science done here makes lots of sense,” says Edward Buckler. He is a geneticist with the U.S. Department of Agriculture (USDA). He has a lab at Cornell University in Ithaca, N.Y. Buckler was not part of the new study but says Karl’s way of growing tall corn should make it grow nearly forever. “I have just never seen anyone try this in such a tall greenhouse,” he says.

Paul Scott also was not involved in the study. This USDA scientist studies the genetics of corn at Iowa State University in Ames. “Plant height is important because it is related to yield,” he says. “Bigger plants tend to produce more grain, but if they get too tall they tend to fall over.” He says the new work helps scientists better understand which genes and other factors affect corn growth.

The new giant corn stalks have trouble surpassing 12 meters (40 feet). That’s a result of the genetic mutation inserted into the corn, Karl says. He is now trying to tweak the corn’s genetics by inserting other mutations to see if this corrects the problem. If they do, Karl suspects he might be able to get even loftier corn.

Corn is incredibly diverse, Buckler notes. There are thousands of strains grown all over the world. This work can help scientists understand why plants may grow differently depending on their location (which would affect day length and light levels).

Ancient DNA shakes up the elephant family tree

Ancient DNA shakes up the elephant family tree

Fossil DNA may be rewriting the history of elephant evolution.

The first genetic analysis of DNA from fossils of straight-tusked elephants reveals that the extinct animals most closely resembled modern African forest elephants. This suggests that straight-tusked elephants were part of the African, not Asian, elephant lineage, scientists report online June 6 in eLife.

Straight-tusked elephants roamed Europe and Asia until about 30,000 years ago. Much like modern Asian elephants, they sported high foreheads and double-domed skulls. These features convinced scientists for decades that straight-tusked and Asian elephants were sister species, says Adrian Lister, a paleobiologist at the Natural History Museum in London who was not involved in the study.

For the new study, researchers extracted and decoded DNA from the bones of four straight-tusked elephants found in Germany. The fossils ranged from around 120,000 to 240,000 years old. The genetic material in most fossils more than 100,000 years old is too decayed to analyze. But the elephant fossils were unearthed in a lake basin and a quarry, where the bones would have been quickly covered with sediment that preserved them, says study author Michael Hofreiter of the University of Potsdam in Germany.

Hofreiter’s team compared the ancient animals’ DNA with the genomes of the three living elephant species — Asian, African savanna and African forest — and found that straight-tusked genetics were most similar to African forest elephants.

When the researchers told elephant experts what they’d found, “Everybody was like, ‘This can’t possibly be true!’” says study coauthor Beth Shapiro of the University of California, Santa Cruz. “Then it gradually became, ‘Oh yeah, I see.… The way we’ve been thinking about this is wrong.’”

If straight-tusked elephants were closely related to African forest elephants, then the African lineage wasn’t confined to Africa — where all elephant species originated — as paleontologists previously thought. It also raises questions about why straight-tusked elephants bore so little resemblance to today’s African elephants, which have low foreheads and single-domed skulls.

Family tree

This tree shows a revision to how scientists think straight-tusked elephants fit into elephant evolution: Straight-tusked elephants shared the most common ancestors with African forest elephants, rather than Asian elephants.

Accounting for this new finding may not be as simple as moving one branch on the elephant family tree, Lister says. It’s possible that straight-tusked elephants really were a sister species of Asian elephants, but they exhibit genetic similarities to African forest elephants from interbreeding before the straight-tusked species left Africa.

It’s also possible that a common ancestor of Asian, African and straight-tusked elephants had particular genetic traits that were, for some reason, only retained by African and straight-tusked elephants, he says.

Lister and colleagues are now reexamining data on straight-tusked skeletons to reconcile the species’ skeletal features with the new information on their DNA. “I will feel most comfortable if we can understand these genetic relationships in terms of the [physical] differences between all these species,” he says. “Then we’ll have a complete story.”