A melting snow patch in Greenland has revealed what could be the oldest fossilized evidence of life on Earth. The 3.7-billion-year-old structures may help scientists retrace the rise of the first organisms relatively soon after Earth’s formation around 4.5 billion years ago (SN: 2/8/14, p. 16), the discoverers report online August 31 in Nature.
Unlike dinosaur bones, the new fossils are not preserved bits of an ancient critter. The Greenland fossils are mounds of minerals a few centimeters tall that may have been deposited by clusters of microbes several hundred million years after Earth formed. The shape and chemical composition of the mounds, called stromatolites, match those formed by modern bacterial communities living in shallow seawater, says a team led by geologist Allen Nutman of the University of Wollongong in Australia.
If confirmed, the fossils demonstrate that sophisticated, mound-building microbial life appeared early on in Earth’s history. That early start backs up previous genetic and chemical studies that place the advent of basic life on Earth before 4 billion years ago (SN Online: 10/19/15).
Hawaiian honeycreepers are a marvel of evolution. Millions of years ago, some finches arrived on the Hawaiian Islands and began to diversify. As the Pacific Plate moved over the Hawaiian hotspot and new islands formed and others shriveled away, these colorful songbirds evolved into more than 50 species that differed so much in what they ate, where they lived and how they looked that it took scientists quite a while to figure out that they were all related.
More than half of those species are now gone. “Many extinctions took place when the islands were first settled by Polynesian people,” notes Helen James, who, as curator of birds at Smithsonian’s National Museum of Natural History, has studied the birds’ evolutionary history. Then Westerners arrived and bird populations started to disappear more quickly due to a combination of threats, including habitat loss, introduction of invasive species and the arrival of diseases such as avian malaria.
Bird populations on Hawaii’s oldest island, Kauai, have been hit especially hard. Kauai lost at least eight species of honeycreepers — as well as several other “marvelous species” of birds, James notes — before people began keeping good records of the island’s fauna. And now a new study warns that the birds’ situation will get worse — and soon. The honeycreepers that are left on the island are declining fast, and some species could disappear in as little as a decade.
Eben Paxton of the U.S. Geological Survey Pacific Islands Ecosystems Research Center at Hawaii Volcanoes National Park and colleagues looked at population trends for seven species of native forest birds living on Kauai’s Alakai Plateau, the eroded crater of a long-extinct volcano. On other Hawaiian islands, only high-elevation areas have generally been cool enough to keep out the mosquitoes that spread avian diseases. But on lower-lying Kauai, its forests have tended to be cooler than similar-elevation regions on the other islands, so spots such as the Alakai Plateau have been disease-free refuges for native birds. Or, they were. A 2014 study found that disease prevalence in birds had more than doubled there between 1994-1997 and 2007-2013. Climate change had warmed the plateau enough that disease-laden mosquitoes could spread. In the new study, Paxton and his colleagues found that six of seven native forest birds surveyed (an eighth proved too wily for scientists to accurately count) are rapidly disappearing and their ranges contracting. All six are honeycreepers, and four are now found only in small, remote parts of the plateau. Fewer than 1,000 Akekee and fewer than 500 Akikiki remain, the team reports September 2 in Science Advances.
“If native species linearly decline at a rate similar to or greater than that of the past decade, then multiple extinctions are likely in the next decade,” the team writes.
James says that she hopes the new findings will be a call to action. “Their data show alarming declines in population and geographic ranges of endemic Hawaiian honeycreepers on the island of Kauai,” she says. The birds’ extinction “would be a tremendous loss.”
Even without avian diseases and climate change, the honeycreepers still face threats from habitat loss, introduced predators and competition with non-native birds (some of whom, such as the Japanese bush-warbler, are thriving on the plateau, the study finds). Reducing those threats could buy the honeycreepers some time to adapt to the growing threat of disease. Scientists can also help by developing genetically modified mosquitoes and figuring out why honeycreepers are so susceptible to avian malaria — and how to protect them from it, James notes.
“The Hawaiian honeycreepers are a classic example of adaptive radiation in animals, second only to Darwin’s finches,” she says. Losing Kauai’s endemic honeycreepers “would definitely cost us in terms of our opportunities to study, understand and appreciate nature.”
Aneil Agrawal, his rangy frame at ease on a black metal street bench, is staring into some midair memory and speaking about disgust.
“I was first exposed to the idea of theoretical biology as an undergraduate and I actually hated it,” he says. “I loved biology and I liked math — it was like two different food types that you like but the two of them together are going to be terrible.”
Since then, he has remained a fan of the two foods, and his distaste for combining them has turned into enthusiasm strong enough to build a career on. Agrawal, now a 41-year-old evolutionary geneticist at the University of Toronto, both builds mathematical descriptions of biological processes and leads what he describes as “insanely laborious” experiments with fruit flies, duckweed and microscopic aquatic animals called rotifers. Often experimentalists venturing into theory “dabble and do some stuff, but it’s not very good,” says evolutionary biologist Mark Kirkpatrick of the University of Texas at Austin. Agrawal, however, is “one of the few people who’s doing really good theory and really good experimental work.”
Two of the themes Agrawal works on — the evolution of sex and the buildup over time of harmful mutations — are “very deep and important problems in evolutionary biology,” Kirkpatrick says. Agrawal and colleagues have made a case for a once-fringe idea: that an abundance of harmful mutations can invite even more harmful mutations. Agrawal’s work has also provided rare data to support the idea that the need to adapt to new circumstances has favored sexual over asexual reproduction. Why sexual reproduction is much more common among complex life-forms has been a long-standing puzzle in biology. Life’s complexity appealed to Agrawal from childhood; he remembers days playing among the backyard bugs and frogs in suburban Vancouver. At first, he imagined his grown-up life out in the field, “living in a David Attenborough show.” As he grew older though, he discovered he was a lab animal: “I was more interested in being able to ask more precise questions under more controlled circumstances.”
Sally Otto, now president-elect of the Society for the Study of Evolution, met Agrawal in the 1990s when he was an undergraduate at the University of British Columbia in Vancouver. He returned to Vancouver in 2003, after earning his Ph.D., to do experimental work and “beef up his ability to do theory,” she says. She cosupervised his postdoctoral effort. Agrawal “picks up theory very quickly,” Otto says. Knowing a huge amount of math to begin with is less important than having insight into what math to learn. The first alluring ideas about how to approach a puzzle often don’t work out, she says, so “there’s a certain doggedness — you have to really keep at it.”
Agrawal needed some time before he came around to theoretical biology. It disgusted him, he says, because he expected it to take the rich variety out of biology. “The reason many people, including me, were attracted to biology was because it’s not boxes and triangles,” he says. “It’s complicated and interesting.” At first he thought modeling a biological process mathematically “sterilized it.” But he eventually found that mathematical description could “help to clarify our thinking about the wonderful mess of diversity that’s out there.” At the street bench, Agrawal muses about how he tends to “think quantitatively.” His father has a Ph.D. in engineering, but “we weren’t the kind of family that had to do math problems at the dinner table.” He laughs. “Though I do that to my own kids.” His success so far is mixed, depending in part on whether he catches his two sons, ages 10 and 7, in the right mood. Agrawal also thinks intensely, possibly another secret to his success — he has received more than half a dozen awards and prizes, including the 2015 Steacie Prize for Natural Sciences. The bench where we’ve settled is only half a block from the conference center in Austin, where Evolution 2016, the field’s biggest meeting of the year, has hit day four of its five-day marathon. Agrawal gave one of the first talks, a smooth, perfectly timed zoom through a recent fly experiment. He is a coauthor on five more presentations, along with chairing one of the frenetic sessions where talks are compressed into five minutes. By this point, many of the 1,800 or so attendees are showing strain — wearing name tags wrong side frontward, snoring open-mouthed in hallway chairs or flailing their arms in conversations fueled by way too much caffeine. Agrawal, however, seems relaxed, listening quietly, staring off in thought, speaking in quiet bursts. This guy can focus.
One of his early theory papers studied mutation accumulation. Previous work had suggested that microbes in stressful environments, compared with microbes lapped in luxury, are more likely to make mistakes in copying genes that then get passed on to the next generation. Agrawal wondered whether cells that are stressed for another reason — an already heavy burden of harmful mutations — would likewise be more inclined to build up additional mutations. He calls this scenario “a spiral of doom.”
The idea intrigued him because he suspected that sexual reproduction would do a better job of purging these mutations than asexual reproduction. “What I found in doing the theory was that I was exactly wrong,” he says. The sexual populations would end up with more, not fewer, mutations.
Though the theory part of the paper turned out well, the journal Genetics rejected it — there was hardly any experimental evidence that the scenario would arise in the real world.
Agrawal published the paper elsewhere in 2002 and, when he began setting up his own lab at the University of Toronto, he returned to the idea. In the years since, he and colleagues have published a string of papers adding evidence to the argument. They have found, for example, that fruit flies burdened with misbegotten genes lag in growth and struggle to keep their DNA in good repair. The idea is no longer airy speculation, says Charles Baer, who’s checking for mutation accumulation in nematodes at the University of Florida in Gainesville.
Chrissy Spencer, a postdoc during the early years of Agrawal’s mutation studies, points out that a vital skill of a good experimentalist is just knowing intuitively whether a species is right for a certain kind of test. Agrawal has that knack, for better and for worse. For some studies on the evolution of sex, Agrawal eventually turned to rotifers. The stubby little cylinders with a circlet of hairy projections around their mouths can reproduce either sexually or asexually, so they’re great for testing what factors favor one over the other. Rotifers, however, are also “finicky,” he says. His students have cared for them, sometimes for months, only to have them all die for no discernible reason, sometimes before generating any data.
Having the practitioner’s inside view of experiments and theory may help Agrawal, but it also has its costs. “There are better theoreticians out there and there are better experimentalists,” he says, and he wishes at times that he was more solidly in one camp or the other. He pauses and then, a biologist to the core, says: “That’s my niche.”
DENVER — Life on Earth got into the shell game more than 200 million years earlier than previously thought.
Fossilized eukaryotes — complex life-forms that include animals and plants — discovered in Canada are decked out in armorlike layers of mineral plates, paleobiologist Phoebe Cohen said September 27 at the Geological Society of America’s annual meeting. At about 809 million years old, the find is the oldest evidence of organisms controlling the formation of minerals, a process called biomineralization. This new origin of biomineralization coincides with major changes that mark the end of a period known as the “boring billion” (SN: 11/14/15, p. 18), said Stanford University paleontologist Erik Sperling, who was not involved in the discovery. “There were big things going on with ocean chemistry,” he said. “It’s interesting to see the biological response.”
These ancient eukaryotes built their exoskeletons using a very different process from most modern shell-making microbes. That uniqueness offers insights into how the mineral-making ability first evolved, said Cohen, who studies ancient ecosystems at Williams College in Williamstown, Mass.
“We have been able to identify specific conditions that facilitated the evolution of the first eukaryote to biomineralize in Earth’s history,” she said. “It paints a beautiful picture of the ecology and evolution and environmental conditions that led to this dramatic innovation.”
Donning an exoskeleton of minerals protects microbes from predators and forms a crucial stage in the modern carbon cycle. The shells make marine microbes such as certain phytoplankton species sink faster after they die, removing carbon from the upper ocean. Previous clear evidence of eukaryote biomineralization dates back to around 560 million years ago in early corallike animals.
Odd fossils discovered in the late 1970s and covered in mineral plates shaped like circles, squares and “Honeycomb cereal” (as Cohen described them) hinted that the skill evolved much earlier, but the discovery raised many questions. Dating techniques then put the age of the fossils somewhere within a 100-million-year range from about 811 million to 717 million years ago, and scientists couldn’t rule out that the fossils’ scalelike minerals formed after the organisms died. Cohen and colleagues revisited these curious fossils. By accurately dating the organic-rich shale a few meters below the fossils in the rock record, the researchers pegged the fossils’ age at 809 million years old, give or take a few million years. An electron microscope let researchers see that each plate is a weave of elongated mineral fibers. This intricate, orderly design had to have been purposefully built by life manipulating mineral formation, Cohen said.
The mineral plates themselves are odd. Most modern microbes make shells out of calcium carbonate, but the ancient shells are made of calcium phosphate, the same crystal used in human teeth enamel. Today, phosphate is limited in the environment and most microbes avoid wasting it.
That may not have been as much of an issue in the marine basin where the eukaryotes lived, the researchers found. Analysis of rocks surrounding the fossils indicate that the amount of oxygen in the waters where the eukaryotes lived was inconsistent. Fluctuating oxygen levels pulled phosphate from underlying sediment into the water, where it was available for mineral making. These favorable conditions plus the need for protection from predation (SN: 11/28/15, p. 13) probably drove the first evolution of biomineralization, Cohen said. Eventually the environment changed, and these shell-making species died out.
ORLANDO, Fla. — Here’s another reason not to love car exhaust: The fumes may make it harder for honeybees to learn floral scents.
In lab tests, bees normally caught on quickly that a puff of floral scent meant a researcher would soon offer them a taste of sugar, Ryan James Leonard of the University of Sydney said September 30 at the International Congress of Entomology. After two sequences of puff-then-sugar, just a whiff of fragrance typically made the bees stick out their tongues. But when that floral scent was mixed with vehicle exhaust, it took the bees several more run-throughs to respond to the puff signal. Honeybees buzzing among roadside flowers must contend with vehicle pollution as they learn various foraging cues. Another lab reported in 2013 that diesel exhaust reacted with some of the chemical components of canola flowers, rendering them more difficult for bees to recognize.
Building on that concern, Leonard and colleagues found that it was easy for bees to learn the scent of linalool, a widespread ingredient in many flower fragrances, whether mixed with exhaust fumes or not. But exhaust made it take longer than two trials for bees to learn the scent ingredients myrcene (three trials), dipentene (four) and the full, multicomponent fragrance of geraniums (six).
Road ecologists have put a lot of effort into studying how vehicles kill animals. But Leonard hopes for more interest now in how chronic exposure to traffic affects living animals.
Language is a tricky thing to write about. You’re using it while dissecting it. That sort of recursion can trip you up. As a philosopher friend of mine once said, a zoologist studying tigers, while riding on the back of a tiger, should be very careful.
Of all the writers who’ve ever taken on the task of writing about language, nobody of any consequence has ever tripped himself up quite so much as Tom Wolfe. His new book, The Kingdom of Speech, has been widely denigrated (deservedly) by scientists who have encountered it. Wolfe has taken it upon himself to explain various aspects of science — having to do with biological evolution, linguistics, psychology and cognitive neuroscience — to scientists, in the process disparaging titans in their fields such as Charles Darwin and Noam Chomsky. It’s kind of like Brad Pitt or Angelina Jolie trashing George Washington and Abraham Lincoln. Wolfe pontificates about language without realizing that he’s riding on the back of a linguistic tiger.
It’s difficult to criticize him, though, without lapsing into the same sort of abominable adhominemism with which he assaults Darwin and Chomsky. It’s not enough just to assert disagreement with Darwin’s views on how language evolves or Chomsky’s theory that evolution endowed all human babies with a built-in hardwired “universal grammar.” Wolfe attacks their character.
He presents Chomsky as a demon, a bully, a knave. When criticizing another’s research, Chomsky “pulls out a boning knife and goes to work,” Wolfe writes; he refers to Chomsky’s “audacity” and accuses him of “double talk.” He calls him “an angry god raining fire and brimstone.” He lambastes Chomsky for attacking his critics as liars, charlatans and frauds. In short, Wolfe attacks Chomsky for using against others the same linguistic strategy that Wolfe uses against Chomsky. Riding on a tiger.
Wolfe gives the impression of being jealous of Chomsky’s fame, which seems odd for a writer so famous himself. As for Darwin, Wolfe presents the greatest biologist in history as a petty thief who stole credit for the theory of evolution by natural selection from Alfred Russell Wallace, who was (Wolfe alleges) screwed over by the British gentlemen’s club conspirators who rigged the system to give Darwin credit for priority. And then Wolfe ridicules Darwin for reporting observations on the behavior of his dog.
But the poverty of Wolfe’s intellectual rhetoric does not cement the case against him. Just as belittling Darwin and Chomsky personally does not really rebut their science, condemning Wolfe’s rhetorical juvenility does not confront the substance of his thesis — that humans invented speech (and subsequent forms of language derived from it) — and that evolution had nothing to do with it. And that speech, and speech virtually alone, makes humans superior to other animals.
Somehow Wolfe manages to claim that he and he alone has figured out what no one else (at least, “no licensed savant”) ever thought of, that speech is the “cardinal distinction between man and animal.” It did not evolve. “Man, man unaided, created language,” Wolfe says. Language is a system of mnemonics, based on sounds that represent meaning, enabling people to remember, think and plan. And humans invented that system. Yes, invented it!!! (That’s how Wolfe writes: his rhetoric would collapse if denied the use of italics and exclamation points.) In any case, the question is not whether Wolfe dismisses Darwin and Chomsky unfairly, but rather whether he marshals sufficient factual evidence to support his central claim. But facts are not Wolfe’s strong suit. On page 5, for instance, he announces that Watson and Crick discovered DNA. How unfair to Friedrich Mieschler, who discovered the molecule deoxyribonucleic acid in 1869. Watson and Crick discovered its double helix structure. Given such a weak grasp of such an elementary fact, Wolfe’s subsequent assertions on subtle points of evolutionary theory warrant suspicion.
There’s more. In one of his book’s most tweeted passages, he asserts that evolution fails all the tests of what makes “science”:
“Had anyone observed the phenomenon…? Could other scientists replicate it? Could any of them come up with a set of facts that, if true, would contradict the theory (Karl Popper’s ‘falsifiability’ test)? Could scientists make predictions based on it? Did it illuminate hitherto unknown or baffling areas of science?” To which questions Wolfe answers “no … no … no … no … and no.” But to which any long-time reader of Science News would have responded “yes, yes, yes, yes and yes” (as would any knowledgeable scientist, as biologist Jerry Coyne, among others, has pointed out).
Wolfe’s citing of Popper is especially lame; although in early writings Popper criticized natural selection, in his later years he assented that natural selection could be posed in testable terms (he even thought that it failed the test under certain circumstances).
Nonetheless it is true that ideas about the evolutionary origin of language are difficult to test. Wolfe, in fact, anchors his argument with two recent papers (2014), each with Chomsky as a coauthor, asserting that “the most fundamental questions about the origins and evolution of our linguistic capacity remain as mysterious as ever.” Evidence on this issue is either “inconclusive or irrelevant,” Chomsky and colleagues wrote in Frontiers in Psychology. Evidence of Neandertal ability to produce speech does not help trace the beginnings of language, he and collaborators wrote in PLOS Biology. Speech ability “is undoubtedly a necessary condition for the expression of vocally externalized language,” but “is not a sufficient one, and … is evidently no silver bullet for determining when human language originated.”
Others would disagree on how well the evidence illuminates language’s origins, just as some experts in linguistics have disagreements with Chomsky on many other points. But even if you acknowledge a lack of “conclusive” evidence, that’s not the same thing as saying there is “no evidence” — as Wolfe repeatedly alleges.
Of course, both papers clearly state that language did, in fact, evolve — it’s just that science can not yet say exactly how. And it’s true that the origin of speech is among the most stubborn of mysteries. So are the origin of the universe, the origin of life and the origin of baseball. Science has not yet fully understood the causes of Alzheimer’s disease, either (and certainly has found no cure); the logical conclusion is not that man just decided to get Alzheimer’s disease. Research continues on the premise that its biological basis might yet be discovered.
Boiled down to its essentials, Wolfe’s case amounts to a fairly sparse syllogism: Science has not been able to establish how human language originated and evolved. Therefore, it did not evolve. And furthermore, I (Wolfe) know how it originated. Humans invented it.
Wolfe apparently doesn’t seem to care that his major premise is based on two papers that assert that language did in fact evolve. Or that his argument against language evolution hinges on a lack of testable evidence, while he declares that he knows how language originated — without any testable evidence. Tigers.
And Wolfe certainly missed the irony of one sentence in the paper in PLOS Biology he cites. “Evolutionary analysis of language is often plagued by popular, naïve, or antiquated conceptions of how evolution proceeds,” Chomsky and collaborators wrote. As in Wolfe’s book.
When small lies snowball into blizzards of deception, the brain becomes numb to dishonesty. As people tell more and bigger lies, certain brain areas respond less to the whoppers, scientists report online October 24 in Nature Neuroscience. The results might help explain how small transgressions can ultimately set pants aflame.
The findings “have big implications for how lying can develop,” says developmental psychologist Victoria Talwar of McGill University in Montreal, who studies how dishonest behavior develops in children. “It starts to give us some idea about how lying escalates from small lies to bigger ones.” During the experiment, researchers from University College London and Duke University showed 80 participants a crisp, big picture of a glass jar of pennies. They were told that they needed to send an estimate of how much money was in the jar to an unseen partner who saw a smaller picture of the same jar. Each participant was serving as a “well-informed financial adviser tasked with advising a client who is less informed about what investments to make,” study coauthor Neil Garrett of University College London said October 20 during a news briefing. Researchers gave people varying incentives to lie. In some cases, for instance, intentionally overestimating the jar’s contents was rewarded with a bigger cut of the money.
As the experiment wore on, the fibs started flying. People lied the most when the lie would benefit both themselves and their unseen partner. But these “financial advisers” still told self-serving lies even when it would hurt their partner.
Twenty-five participants underwent fMRI scans while lying. When a person had previously lied, brain activity lessened in certain areas of the brain, most notably in the amygdala. A pair of almond-shaped brain structures nestled deep in the brain, the amygdalae are tightly linked to emotions. This diminished amygdala activity could even predict whether a person would lie on the next trial, results that suggest that the reduced brain activity is actually influencing the decision to lie.
The study design gets around a problem that confounds other lying experiments, says neuroscientist Bernd Weber of the University of Bonn in Germany. Many experiments are based on lies that people have been instructed to say, a situation that “hardly resembles real-world behavior,” he says. Here, the participants were self-motivated liars.
Without any negative consequences from their lies, participants weren’t afraid of being caught. That impunity might affect activity in the amygdala, Weber says. Further experiments are needed to reveal the effects of such fear. From Ponzi schemes to current politics, case studies abound of small lies spiraling into much bigger deceits, study coauthor Tali Sharot of the University College London said in the news briefing. “There are many reasons why this might happen, societal reasons, but we suspected that there might be a basic biological principle of how our brain works that contributes to this phenomenon,” she said.
The principle she had in mind is called emotional adaptation — the same phenomenon that explains why the scent of strong perfume becomes less noticeable over time. The first time you cheat on your taxes, you’d probably feel quite bad about it, Sharot said. That bad feeling is good, because it curbs your dishonesty. “The next time you cheat, you have already adapted,” she said. “There’s less negative reaction to hold you back so you might be lying more.”
DNA in cancerous tissues of tobacco smokers shows mutation patterns that differ from those in cancerous tissues of nonsmokers, a new analysis finds. The new study, in the Nov. 4 Science, reveals how smoking contributes to different cancers, enhancing several kinds of DNA damage.
“We are doing a sort of molecular archaeology,” says cancer geneticist Ludmil Alexandrov of Los Alamos National Laboratory in New Mexico, who led the analysis. While smoking’s link to cancer has been known for decades, “it’s always been a bit of a mystery why smoking increases the risk of cancers like bladder or kidney — tissues that aren’t exposed to smoke.” Mutations in DNA arise naturally in a person’s lifetime, but some genetic changes — such as those spurred by smoking — increase the risk of certain cancers. Scientists have identified several patterns of DNA mutations that consistently show up in tissues of some cancers. These patterns, which may appear over and over again in a stretch of tumor DNA, can serve as a signature of the underlying mechanism that led to the mutations, offering clues to how different cancers strike.
“When someone has a cancer, we only see what is now — we don’t know what happened 20 years ago when that cancer was only one cell,” says cancer biologist Gerd Pfeifer of the Van Andel Research Institute in Grand Rapids, Mich.
“These signatures give us a really good clue of what might have happened,” says Pfeifer, who was not involved with the study.
Alexandrov and an international team of researchers found several differences in the number of altered DNA signatures in tumors of smokers compared with those from nonsmokers with the same type of cancer. The research adds dismal specifics to what’s already known about smoking: It is really bad for you.
“Tobacco smoking leaves permanent mutations — it erodes the genetic material of most cells in your body,” says Alexandrov. “Even if you are a just a social smoker who occasionally has one or two or five cigarettes, there is still a cumulative effect.” Alexandrov and colleagues compiled data on DNA extracted from more than 5,000 human samples representing 17 cancers for which smoking is a known risk factor. About half of the samples were from smokers. The team then searched the DNA for various patterns of damage, or “mutational signatures.”
One suite of mutations, called signature 4, was consistently found in tissues exposed to tobacco smoke. While this signature also appeared in nonsmokers’ tumors, it occurred far less often. Smokers with lung squamous cancer, lung adenocarcinoma and larynx cancers had an especially high number of signature 4 mutations. Signature 4 signals damage to guanine (the structural component of DNA known as “G”). This signature also appears in the DNA of cells in a lab dish that are exposed to a chemical found in burnt products, including polluted air and the tar in cigarette smoke.
Signature 4 mutations also showed up in cancers of the oral cavity, pharynx and esophagus, but much less often. The researchers aren’t sure why these tissues, which are also directly exposed to smoke, don’t have as heavy a mutational load. Those tissues may metabolize smoke differently, the researchers speculate.
DNA damage in smokers also differed from that in nonsmokers for another suite of mutations, known as signature 5. This signature typically shows up in all cancers and across all tissue types. The cause of signature 5 remains unknown, but scientists do know that the number of signature 5 mutations is “clocklike” — it increases with age. The new analysis revealed that the signature 5 “clock” ticks faster in smokers. Depending how heavily a person smoked, the more signature 5 mutations were found.
In patients with lung adenocarcinoma, far more mutations associated with two other signatures, 2 and 13, had accumulated in smokers than in nonsmokers. There are hints that these mutations result from overactive DNA editing machinery. But because these signatures are found in many kinds of cancer, it isn’t clear why smoking ups the mutations load. Inflammation from smoke might be activating the cellular machinery that underlies the mutations.
When the researchers took into account the quantity smoked, they discovered that the number of mutations for some cancers was linked to the “pack years” smoked (a pack of cigarettes a day for one year). Breaking these data down into cancer types allowed the team to calculate the mutations caused by smoking for a particular tissue type: A pack a day for one year leads to 150 mutations in a lung cell, 97 in a larynx cell, 39 in the pharynx, 23 in the oral cavity, 18 in the bladder and six in a liver cell.
Narwhals use highly targeted beams of sound to scan their environment for threats and food. In fact, the so-called unicorns of the sea (for their iconic head tusks) may produce the most refined sonar of any living animal.
A team of researchers set up 16 underwater microphones to eavesdrop on narwhal click vocalizations at 11 ice pack sites in Greenland’s Baffin Bay in 2013. The recordings show that narwhal clicks are extremely intense and directional — meaning they can widen and narrow the beam of sound to find prey over long and short distances. It’s the most directional sonar signal measured in a living species, the researchers report November 9 in PLOS ONE.
The sound beams are also asymmetrically narrow on top. That minimizes clutter from echoes bouncing off the sea surface or ice pack. Finally, narwhals scan vertically as they dive, which could help them find patches of open water where they can surface and breathe amid sea ice cover. All this means that narwhals employ pretty sophisticated sonar.
The audio data could help researchers tell the difference between narwhal vocalizations and those of neighboring beluga whales. It also provides a baseline for assessing the potential impact of noise pollution from increases in shipping traffic made possible by sea ice loss.
SAN DIEGO — Over the course of months, clumps of a protein implicated in Parkinson’s disease can travel from the gut into the brains of mice, scientists have found.
The results, reported November 14 at the annual meeting of the Society for Neuroscience, suggest that in some cases, Parkinson’s may get its start in the gut. That’s an intriguing concept, says neuroscientist John Cryan of the University College Cork in Ireland. The new study “shows how important gut health can be for brain health and behavior.” Collin Challis of Caltech and colleagues injected clumps of synthetic alpha-synuclein, a protein known to accumulate in the brains of people with Parkinson’s, into mice’s stomachs and intestines. The researchers then tracked alpha-synuclein with a technique called CLARITY, which makes parts of the mice’s bodies transparent.
Seven days after the injections, researchers saw alpha-synuclein clumps in the gut. Levels there peaked 21 days after the injections. These weren’t the same alpha-synuclein aggregates that were injected, though. These were new clumps, formed from naturally occurring alpha-synuclein, that researchers believe were coaxed into forming by the synthetic versions in their midst.
Also 21 days after the injections, alpha-synuclein clumps seemed to have spread to a part of the brain stem containing nerve cells that make up the vagus nerve, a neural highway that connects the gut to the brain. Sixty days after the injections, alpha-synuclein had accumulated in the midbrain, a region packed with nerve cells that make the chemical messenger dopamine. These are the nerve cells that die in people with Parkinson’s, a progressive brain disorder that affects movement.
After reaching the brain, alpha-synuclein spreads thanks in part to brain cells called astrocytes, a second study suggests. Experiments with cells in dishes showed that astrocytes can store up and spread alpha-synuclein among cells. That work was presented by Jinar Rostami of Uppsala University in Sweden at a news briefing on November 14.
The gradual accumulation and spread of alpha-synuclein caused trouble in the mice. As alpha-synuclein clumps slowly crept brainward, the mice began exhibiting gut and movement problems. Seven days after the injections, the mice’s stool was more plentiful than usual. Sixty and 90 days after the injections — after clumps of alpha-synuclein had reached the brain — the mice performed worse on some physical tests, including getting a sticker off their face and flipping around to shimmy down a pole headfirst. In many ways, the mice resembled other mice that have mutations that cause Parkinson’s-like symptoms, Challis says. An earlier study turned up evidence that clumps of alpha-synuclein can move from the gut to the brain stem in rats, but those experiments looked at shorter time scales, Challis says. And previous work monitored the movements of the injected alpha-synuclein, as opposed to the alpha-synuclein clumps that the mice produced themselves.
The idea that alpha-synuclein can spread from the gut to the brain is very new, says Alice Chen-Plotkin, a clinician and Parkinson’s researcher at the Hospital of the University of Pennsylvania. These new results and others have prompted scientists to start looking outside of the brain for the beginning stages of the disease, she says. “Increasingly, people are wondering if it starts earlier.”
Some evidence suggests that the gut is a good place to look. People with Parkinson’s disease often suffer from gut problems such as constipation. And in 2015, scientists reported that a group of Danish people who had their vagus nerves severed were less likely to develop Parkinson’s disease. Cut alpha-synuclein’s transit route from the gut to the brain, and the disease is less likely to take hold, that study hints.
It’s not clear why alpha-synuclein accumulates in the gut in the first place. “There are a lot of theories out there,” Challis says. Bacteria may produce compounds called curli that prompt alpha-synuclein to aggregate, a recent study suggests. Pesticides, acid reflux and inflammation are other possible culprits that could somehow increase alpha-synuclein clumps in the gut, Challis says.
