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Nature’s Anti-Aging Secret Ecologists are finding animals and plants that defy aging.


A dozen years ago, Daniel Doak began crawling around the Alaskan tundra carrying a container of colorful party toothpicks. He was there on the chilly North Slope at the top of the continent to study moss campion, a low, flat plant that explodes with pink flowers in early summer.

Moss campion seedlings are “the size of the head of a pushpin,” Doak says, and 20 years can pass before they grow much bigger. Nonetheless, Doak, an ecologist at the University of Colorado, dutifully identified, mapped and measured the plants, using the toothpicks to mark the location of the smallest ones.


Moss campion in bloom.

Tracy Feldman

Every summer he returns, and after all those years of strained eyes and bruised knees, he now has data on 2,500 plants in the Arctic and thousands more at sites across the globe, from the Rocky Mountains to the Pyrenees. (Moss campion grows across a wide swath of the world’s high latitudes and elevations.) That information led Doak and his collaborator, Duke University ecologist William Morris, to a surprising find: The plants live for centuries. And that insight is helping to shape an emerging field: the science of how nature ages.

Initially, Doak simply wanted to understand how organisms respond to harsh environmental conditions, such as the frigid temperatures of an Alaskan winter. “How does a species make a living,” he wondered, “in a place where it’s tough to get established and tough to live?” So Doak and Morris recorded basic demographic data, measuring things like how fast the plants grow — and how long they live. “We do the equivalent of what the Census Bureau does,” says Doak. “We ask, ‘Are you alive? How big are you? How many children do you have?’ ”

By tracking the plants year after year, Doak has shown that moss campion follows a biological strategy known as negative senescence. Senescence is the scientific term for what we commonly think of as aging. All aging really signifies is time lived. To us, there’s no separating the passage of time from the process of decline. We see it in ourselves: gray hair, bad knees, flagging energy. But in negative senescence, the risk of death decreases as an organism grows older.

For years, biologists believed this strategy was largely impossible. Everything that survives for long enough, they thought, will eventually enter a deteriorating slide toward death. A combination of long-term data sets and new computational tools is painting a different picture: plants and animals that stay healthy, and even reproduce, for far longer than anyone would have predicted. Death may still be their ultimate fate, but it doesn’t represent the end point of decline. It arrives via catastrophe, or a whim of nature, or as a result of human-caused changes to the environment.

Doak and other scientists examining how various species age have discovered that in some cases, they simply don’t. Evolution may sometimes favor organisms that follow a different path. “Clearly there are ways for natural selection to dramatically change how senescence happens,” Doak says. “It doesn’t seem that hard to defeat senescence.”


Duke scientists William Morris (left) and Patrick Corcoran study tiny moss campion plants in Alaska’s Wrangell Mountains.

Rachel Mallon

Questions of Life and Death

Doak’s conclusion would have seemed heretical just a few years ago.

Why living things age is one of biology’s most vexing questions. For the past several decades, biologists have clung to a trio of theories, all of which hold that senescence is inescapable. One theory holds that organisms age because of built-up genetic mutations that aren’t weeded out by natural selection — a disease, say, that hits after your reproductive prime. Another maintains that aging occurs because some traits that make you better at reproducing may also cue your demise. And according to a third theory, as organisms age they deteriorate and must spend more energy to repair cell damage — to the detriment of other essential physical functions.


Toothpicks mark the smallest seedlings.

Daniel Doak

For years scientists have quibbled over which theory proved the best, but few doubted that, among the three, they explained the evolution of aging.

Now a new branch of the science of aging has sprouted, from a part of the world that, oddly, was excluded before: nature. And its early results suggest that those long-standing theories only tell part of the story. Until as recently as a decade ago, the mostly lab-based scientists who studied aging assumed that senescence wasn’t visible in nature. You wouldn’t see it in the wild, they believed, because the cruel realities of nature simply don’t allow anything to live long enough to decline. But years of data from long-term studies by Doak and other scientists examining plants, birds, mammals and fungi in the field are showing the flaws in these assumptions.

“There’s dogma in the literature — which is more oriented toward the cell biology of aging — that wild animals don’t actually senesce,” says Daniel Nussey, an evolutionary ecologist at the University of Edinburgh who studies aging in Soay sheep on a remote Scottish island. “That is absolutely wrong. This process can be seen, and it is shaped by evolution.”

In fact, signs of nature aging are all around us. Nussey’s wild sheep shed several pounds the year before they die; alpine ibex older than 8 or 9 can’t tolerate harsh weather; some plants lose their ability to survive drought. Elderly albatross seek out food in different areas than they did in their youth. Why organisms age differently — the comparative biology of aging — is a growing fascination for scientists. “We’re trying to understand what it is that drives variation in this process,” Nussey says.

That variation, it turns out, includes species that simply don’t follow the established rules. Back in 2004, a team of scientists looked at the emerging evidence from ecology and proposed that aging isn’t inevitable at all. In a controversial paper published in the journal Theoretical Population Biology, they wrote that “some, and perhaps many, species show negative senescence” — a situation in which death rates actually fall as the years pass.


Bristlecone pines, like this one in California’s White Mountains, can live for thousands of years.

Neil Lucas/Nature Picture Library

Live Slow, Die Old

Since then, evidence of negative senescence has been stacking up.

In the case of moss campion, the plant has evolved a strategy of slow, deliberate growth. Doak believes it spends much of its early energy building an extremely long tap root that helps ensure water and nutrients later on, but slows the plant’s above-ground growth in the meantime. In the moss campion’s tundra home, “it’s very hard to get established,” says Doak. But once it is, its chances of surviving and eventually reproducing are high. There’s not much that will kill moss campion. The plant is so flat and low to the ground, and its leaves so tiny (less than half an inch long), that caribou and Dall sheep have a hard time eating it.

To Doak, it makes sense that natural selection would, in this case, act against aging. “Random catastrophes aren’t going to kill you, and it’s worth your while to put your investment in yourself rather than just in putting out offspring,” he says. Rather than “live fast, die young,” the campion strategy is more “live slow, die old.” Really, really old.

With some organisms, really old can mean millennia. High in the White Mountains near the California-Nevada border live some of the oldest trees in the world. Their trunks thick and gnarled, their oldest needles, born when JFK was president, still hanging on, these bristlecone pines are nearly 5,000 years old. Living five millennia is quite a feat, but what’s even more surprising is that these trees show no sign of decline. They are more likely to survive environmental stress than their younger cohorts, and they continue to reproduce at a steady rate. Their measured growth allows them to build extra-durable wood that resists rot, drought and lightning. In other words, in this case, natural selection appears to favor avoiding senescence entirely.

But plants are hardly the only organisms defying the aging process. Studies of turtles and lizards have also turned up negative senescence. One long-term study of three-toed box turtles in Missouri found that the animals were still reproducing well into their 70s.

In the mammal world, naked mole rats are the longest-living rodents. They can reach nearly 30 years of age in captivity. Scientists have found that breeding females “show no decline in fertility even well into their third decade of life,” according to a 2008 study published in the Journal of Comparative Physiology B. That makes sense, says Doak: “They live underground, in a resource-poor environment. They live cooperatively, meaning that your only chance to reproduce is after you’ve lived for a while and moved up the social strata.” Natural selection in this scenario favors individuals that live longer.

A New Threat

Doak’s moss campion research has lately turned up more than just evidence for negative senescence. He’s also found signs that global warming may be exerting a tangible influence on death’s odds. Close monitoring of the Alaskan moss campion plants over the years reveals that what’s most likely to kill the plants today is climate. “In winters when it’s quite cold but there are warm periods, the plants lose the blanket of snow that covers them,” Doak explains. They come down with the equivalent of freezer burn; ultimately, they die from being freeze-dried. “We’ve been seeing more and more of that over the course of our study,” he says.

While global warming represents a hurdle for the plants, Doak himself faces a more existential challenge. “It’s very difficult,” he admits, “to show that senescence doesn’t ever occur.” To prove conclusively that something doesn’t age would itself require human immortality. And, unfortunately, negative senescence in humans remains elusive.


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Strangest Genitals In The Animal Kingdom


Here at IFLS, we love many things. But we relish the opportunity to talk about two of our favorite subjects- animals, and genitals. So we thought we would dedicate an entire article on wacky willies and quirky nether regions. Because who doesn’t love to learn about four headed penises and musical privates? You can thank us afterwards for this enlightening genital journey.

“Singing” Genitals

Who wants a musical penis?! Don’t lie, of course you do. Water boatmen (Micronecta scholtzi) are tiny freshwater insects that you’ll find throughout Europe. They might not look like much, but they’re actually the loudest animal relative to body size. They can create noises of up to 99 decibels, which is roughly equivalent to listening to an orchestra from the front row. How do they do it? With their penises, of course. Similar to how a cricket will produce sound by rubbing body parts together, water boatmen rub their penis along their ribbed abdomen, kind of like a Guiro, only much more amusing. This is called stridulation.

Image credit: BBC Nature

Four Headed Penises?!

Like the platypus, echidnas are monotremes, or egg-laying mammals. There are four extant species of echidna that you can find in New Guinea and Australia. Alongside looking like a platypus/hedgehog hybrid, echidnas have various other odd features. Their tongues are extremely long, reaching around 7 inches in length. And then there’s the penis. Their penises actually have four heads. Yes, you read that correctly. If it’s any consolation, only one is active at a time; they actually rotate (in the line of duty, not physically like an exorcist penis), because obviously we don’t want one getting all the action. But it doesn’t end there. Females will mate with lots of males, and to ensure the best chance of reproductive success the sperm bundle together like a comet in order to swim more efficiently. Super sperm.

Image credit: Gordon Grigg, University of Queensland


There isn’t a great deal to say about the genitals of the elasmobranchs (sharks, rays and skates), except just to point out that they have a pointy double penis. These reproductive organs, called claspers, are used to deposit sperm into the female’s cloaca. This would perhaps be a good time to mention that cloacas are equally weird- they are the singular opening found in some animals that are used for urination, mating and defecation. Nice.

Image credit: Jean-Lou Justine, via Wikimedia Commons

Willy Wars

Good sir, I challenge you to a dual of… Penis cuffs? Hmm… Flatworms are hermaphrodites, meaning that they have both male and female reproductive organs. Producing eggs is more costly than producing sperm, so when two flatworms come together to mate they fight over who gets to wear the trousers in the relationship. During the penis crusade, the flatworms will fence, sometimes quite violently, in an attempt to impregnate the other without getting pregnant themselves.

Image credit: Yeowatzup, via Wikimedia Commons


Snakes and lizards, which are collectively known as squamates, have some rather funky genitals. Their male sexual organ is called a hemipenis; individual males have two hemipenes which they alternate between when mating with females. Some are even embellished with sharp spines to stop the male from slipping out of the female’s cloaca. Lovely.

Rattlesnake hemipenis. Image credit: Tess Thornton, via Wikimedia Commons.

Giant Genitals

Relative to their body size, barnacles have the largest penises in the animal kingdom; they can be up to 40 times the length of their body. I think that would be a tad difficult to tuck away if that were the case for humans. Barnacles are sessile organisms, i.e. fixed and immobile. They are therefore equipped with these giant genitals in order to seek out females that could be some distance away. Some other sessile organisms have evolved a slightly different approach by just shooting their load into the environment so the sperm may cross paths with an egg.

Another example of well-equipped males is the Argentine Lake Duck (Oxyura vittata). A report back in 2011 in Nature described this animal as having the longest bird penis on record, reaching a whopping 42.5 centimeters. Most birds don’t actually have penises and they instead mate by touching openings. This finding was therefore a bit of a surprise, and scientists aren’t entirely sure as to why it is quite so long. Some speculate that the brush-like tip of the penis may serve to remove sperm from other males that has already been deposited in the female’s cloaca.

Image Credit: K McCracken/ Nature

Detachable Penises

Argonauts, which are a type of octopus, don’t bother getting cozy and cuddly with their mates during the deed since they pack their sperm into a detachable tentacle called a hectocotylus. This then goes on its merry way and swims into the female to fertilize her. Females can actually store several of these from different males so that she can become fertilized more than once over a period of a few days. No post-coitus snuggles for Argonauts, then.


So I’ve had enough talk of actual penises for one day, sorry. It’s time for females to be in the spotlight. Female hyenas produce a lot of testosterone, meaning that they develop pseudo-penises. These are actually just enlarged clitorises, but they can reach up to 7 inches long! The poor hyenas actually have to give birth through these appendages, and unfortunately a lot of the offspring die of suffocation during the process. Copulation is also tricky business since the male has to somehow get his penis inside her lady penis. Sounds… Interesting…

Swapping Genitals

Earlier this year, a report in Current Biology described insects of the newly discovered genus Neotrogla which have apparently swapped genitals. The female dons a large, penis-like appendage called a gynosome which is inserted into the male’s opening. The gynosomes are adorned with spines so that the male can’t get away, and copulation can last between 40 and 70 hours! Wow.


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How to reset a cell – Washing a cell with acid can turn it into any other type of cell the body may need

Researchers report a surprisingly easy method to change a specialized cell, such as muscle or bone, into becoming a universal stem cell. Stem cells are immature cells that can be coaxed into becoming specialized cells — and they hold a lot of potential for treating sickness and disease

The body needs many different types of stem cells to replace sick, aging or dying cells in its many different tissues. An embryo, a ball of unspecialized cells that will grow into an animal with a backbone, is different. Scientists describe its stem cells as universal “blank slates,” because each can mature into any type of tissue. Now researchers have found a way to create stem cells that mimic the universal role of embryonic cells.

Their method is simple: Just dip the specialized cell briefly in acid. This doesn’t work all of the time. But it did work for 7 to 9 percent of cells taken from newborn mice. And that success rate has surprised a large number of scientists.

Haruko Obokata and her coworkers showed that other ways of stressing a baby mouse’s cells, such as squeezing them, also worked like a reset button. Obokata is a stem-cell biologist at the RIKEN Center for Developmental Biology in Kobe, Japan. She also works at Harvard Medical School in Boston, Mass.

She and her coworkers described the stem-cell making experiments in two papers in the Jan. 30 issue of Nature.

“It’s fascinating. It’s perplexing. It’s potentially profound, but leaves a lot of reasons to scratch my head,” George Daley toldScience News. He studies stem cells at Boston Children’s Hospital and Harvard Medical School. The new findings are “begging to be replicated,” he says. Replication is when other scientists perform the same experiment to see if they get the same results. Daley’s team is working on that now.

Other ways exist to turn ordinary cells into stem cells. These methods tend to be much more complicated, however. One requires removing cells from embryos. Another requires removing the nucleus from a specialized cell and inserting it into an egg cell. In yet another method, scientists turn on certain genes to reset cells into stem cells.

Finding an easy way to turn specialized cells into stem cells could provide advances in many areas of medicine. Easy-to-make stem cells could be used to replace cells in diseased organs.

This might one day help people with such brain diseases as Parkinson’s or Alzheimer’s. It might also help replace diseased cells in the pancreas (seen in diabetes) or the liver cells damaged by hepatitis. Because scientists could use the new stem cells to make any tissue in a test tube, they might have an easier time studying certain diseases and treatments. The new stem cells might one day even be useful in overcoming some conditions that prevent a woman from becoming pregnant or from successfully carrying a baby until it’s ready to be born.

Called STAP cells, the new stem cells can change into more types of cells than other lab-made stem cells. The stem cells in an embryo, for example, are pluripotent. That means they can grow into any type of tissue. STAP cells can do this, too, but also make a placenta. This organ nurtures a fetus in the womb. Other stem cells have a hard time growing into a placenta.

In its new study, Obokata’s team bathed blood, skin, brain, muscle, fat, bone marrow, lung and liver cells from newborn mice in an acid solution. The technique also worked on cells from older mice, but not as well. Now, they’ve started testing the method on human cells.

Many biologists have a hard time believing the new findings. Dieter Egli is one. He’s a stem cell researcher at the New York Stem Cell Foundation. He says he can’t imagine how squeezing or acid-dipping a cell resets it.

“If I were to describe this over a coffee break to one of my colleagues,” he told Science News, “they’d say, ‘You must be kidding.’”

Cells in the body undergo stress all the time. So if this is all it takes to reset a cell into a pluripotent form, then it’s hard to imagine how the body keeps its cells in line, Egli says.

However, if the new method does work as well in people as it seems to do in mice, then it offers an exciting new way to create stem cells. More studies will be needed to confirm that the new method also can reliably engineer stem cells as effectively as current techniques.

In the July 3 Nature, authors of the stem-cell papers (reported above) owned up to substantial problems with their January claims. They said that mistakes in their initial work now make these researchers doubt that the phenomenon they had reported is real. As a result, the authors are retracting their papers — pulling them from Nature. (In a sense, it’s now as if the journal had never published them. One difference: The journal will keep the papers on its website, marked as retracted).

It’s an extreme move. A retraction of published research occurs only when reported data is found to be unreliable or unsupportable. Retraction of research can permanently tarnish a scientist’s reputation, especially if the reason for the retraction is fraud or some other serious misconduct.

RIKEN is the research institute in Japan where much of the now-retracted work had been done. It has been probing into the controversy. In April, it reported that the lead scientist (and possibly some others) had plagiarized material — copied passages without saying where the text originally came from. It also found that the scientists had improperly manipulated their data.

As a result, RIKEN concluded that the study’s lead author, Haruko Obokata, is guilty of misconduct. Obokata disputes that charge. But in the retraction notice, she and her co-authors describe five additional errors, including pictures of the same cells or embryos labeled as different cells or embryos.

Meanwhile, since January researchers in other labs have attempted to replicate the initial reported results. To date, none has been successful. RIKEN is giving Obokata five months to conduct experiments to show that her original findings are real. And all of her research will be videotaped. — Tina Saey

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How a Killer Parasite Evolved from Pond Scum

A genomic study of a corkscrew-shaped parasite living in the guts of insects shows how it originated from algae — just like another notorious killer, the malaria parasite. 
The transition to a parasitic lifestyle completely dependent on a host usually comes with genomic reduction — why keep genes that help you function and take care of yourself when you’re living off someone else at their expense? The most extreme of these transitions is from free-living algae making their own food (autotrophs) to obligate parasites. 
Helicosporidium parasiticum — which kills juvenile blackflies, caterpillars, beetles and mosquitoes — was first described about a century ago, but we still don’t know much about their origin. When a team led by Patrick Keeling from the University of British Columbia sequenced the genome of Helicosporidium, they found that the parasitic protist evolved from green algae. But surprisingly, the parasite kept most of its ancestral functions. Compared with the closely related green algae, Coccomyxa subellipsoidea and Chlorella variabilis, the parasite’s genome was hardly reduced at all.
There is, however, one major exception: It preserved virtually all of its genes except those needed for harvesting light and photosynthesis, which it doesn’t need as a parasite. “It’s as if photosynthesis has been surgically removed from its genome,” Keeling says in a news release
The researchers have previously shown that the malaria pathogen, Plasmodium, shares a common evolutionary lineage with the algae known for those toxic red tides. But unlike Helicosporidium, which lost nearly nothing, malaria reduced its genome dramatically and became dependent on its host for nutrients. “Both malaria and Helicosporidium started out as alga and ended up as intracellular parasites preying on animals, but they have done it in very different ways,” Keeling says.
By comparing how parasites evolve at the molecular level in these two distantly related lineages, the researchers hope to better understand their methods of infection. Maybe it could help control the population of pest-insect hosts.
The work was published in PLOS Genetics 

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Y Chromosome Is More Than a Sex Switch

Here to stay. The Y chromosome is small compared with the X, but is required to keep levels of some genes high enough for mammals to survive.

The small, stumpy Y chromosome—possessed by male mammals but not females, and often shrugged off as doing little more than determining the sex of a developing fetus—may impact human biology in a big way. Two independent studies have concluded that the sex chromosome, which shrank millions of years ago, retains the handful of genes that it does not by chance, but because they are key to our survival. The findings may also explain differences in disease susceptibility between men and women.

“The old textbook description says that once maleness is determined by a few Y chromosome genes and you have gonads, all other sex differences stem from there,” says geneticist Andrew Clark of Cornell University, who was not involved in either study. “These papers open up the door to a much richer and more complex way to think about the Y chromosome.”

The sex chromosomes of mammals have evolved over millions of years, originating from two identical chromosomes. Now, males possess one X and one Y chromosome and females have two Xs. The presence or absence of the Y chromosome is what determines sex—the Y chromosome contains several genes key to testes formation. But while the X chromosome has remained large throughout evolution, with about 2000 genes, the Y chromosome lost most of its genetic material early in its evolution; it now retains less than 100 of those original genes. That’s led some scientists to hypothesize that the chromosome is largely indispensable and could shrink away entirely.

To determine which Y chromosome genes are shared across species, Daniel Winston Bellott, a biologist at the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts, and colleagues compared the Y chromosomes of eight mammals, including humans, chimpanzees, monkeys, mice, rats, bulls, and opossums. The overlap, they found, wasn’t just in those genes known to determine the sex of an embryo. Eighteen diverse genes stood out as being highly similar between the species. The genes had broad functions including controlling the expression of genes in many other areas of the genome. The fact that all the species have retained these genes, despite massive changes to the overall Y chromosome, hints that they’re vital to mammalian survival.

“The thing that really came home to us was that these ancestral Y chromosome genes—these real survivors of millions of years of evolution—are regulators of lots of different processes,” Bellott says.

Bellott and his colleagues looked closer at the properties of the ancestral Y chromosome genes and found that the majority of them were dosage-dependent—that is, they required two copies of the gene to function. (For many genes on the sex chromosomes, only one copy is needed; in females, the copy on the second X chromosome is turned off and in males, the gene is missing altogether.) But with these genes, the female has one on each X chromosome and the male has a copy on both the X and Y chromosomes. Thus, despite the disappearance of nearby genes, these genes have persisted on the Y chromosome, the team reports online today inNature.

“The Y chromosome doesn’t just say you’re a male; it doesn’t just say you’re a male and you’re fertile. It says that you’re a male, you’re fertile, and you’re going to survive,” Bellott explains. His group next plans to look in more detail at what the ancestral Y chromosome genes do, where they’re expressed in the body, and which are required for an organism’s survival.

In a second Nature paper, also published online today, another group of researchers used a different genetic sequencing approach, and a different set of mammals, to ask similar questions about the evolution of the Y chromosome. Like Bellott’s paper, the second study concluded thatone reason that the Y chromosome has remained stable over recent history is the dosage dependence of the remaining genes.

“Knowing now that the Y chromosome can have effects all over the genome, I think it becomes even more important to look at its implications on diseases,” Clark says. “The chromosome is clearly much more than a single trigger that determines maleness.” Because genes on the Y chromosome often vary slightly in sequence—and even function—from the corresponding genes on the X, males could have slightly different patterns of gene expression throughout the body compared with females, due to not only their hormone levels, but also their entire Y chromosome. These gene expression variances could explain the differences in disease risks, or disease symptoms, between males and females, Clark says.

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Why the Zebra Got Its Stripes

Scientists claim they’ve solved a centuries-old riddle, one that puzzled even Charles Darwin and Alfred Russel Wallace. And the answer was surprising: Zebras evolved their vivid stripes as bug repellent.
People often think that zebras have stripes for crypsis, or camouflage, reasons. For color-blind predators, the stripes could make them hard to see in tall grasses. Or, that their striking black-and-white stripes are a form of disruptive coloration, working to obscure the body contour or confuse predators and parasites through optical illusions or a distracting effect called motion dazzle when they run as a herd. (Check out some illusions here, here and here: where does one end and the other begin?) Still others have suggested that it has nothing to do with predator avoidance, that the stripes help manage heat by reducing thermal loads. Well those are all great hypotheses, but no one’s ever tested all of them together. 
So, pitting a bunch of ideas against each other, Tim Caro from the University of California, Davis, and colleagues examined the geographic distribution of current and extinct equid species (which include zebras, horses and asses). Among the seven species, and some subspecies, that were examined, there were both animals with stripes and without. Then they compared the geographic ranges with environmental variables, such as large predators, ectoparasite breeding conditions, and temperature. 
They found that the ranges of the most distinctively striped species (Equus burchelli, E. zebra, and E. grevyi) overlap remarkably with the areas where disease-carrying blood-suckers, like horseflies (tabanids) and tsetse flies (glossinids), are active and particularly annoying. This was consistent across different types of striping — facial, neck, flank, rump, belly, or leg stripes of varying intensity and thickness, as well as shadow striping — and different equid species and subspecies. 
“Again and again, there was greater striping on areas of the body in those parts of the world where there was more annoyance from biting flies,” Caro says in a press release.  After all, certain flies are known to avoid black and white surfaces, preferring uniformly colored ones (though why that’s the case is another mystery for another day). 
In contrast, they didn’t find consistent support across species for hypotheses about camouflage, predator avoidance, heat management, or some aspect of social interaction. But why zebras? According to the study, unlike other African hooved mammals living in the same areas, zebras have hair that’s shorter than the mouthpart length of biting flies, making them particularly susceptible to annoyance.