Humans no longer have ancient defence mechanism against viruses

Insects and plants have an important ancient defence mechanism that helps them to fight viruses. This is encoded in their DNA. Scientists have long assumed that vertebrates – including humans – also had this same mechanism. But researchers at KU Leuven have found that vertebrates lost this particular asset in the course of their evolution.

Credit: KU Leuven

The possibilities encoded in our DNA are expressed via RNA. Conversely, RNA interference (RNAi) can also suppress the expression of a specific gene. Insects and plants use this RNAi mechanism to defend themselves against viruses, among other things. With a little help, insects and plants can even be made resistant to certain diseases through this RNAi mechanism. Examples include so-called genetically modified crops.

It seems only logical to assume, then, that humans can be protected against specific diseases in a similar way. However, past experiments to this effect have proven to be a challenge. Researchers from the Animal Physiology and Neurobiology unit at KU Leuven have now shown why this is the case.

KU Leuven researcher Niels Wynant studied Argonaute proteins, which play an important role in the RNAi process. “In a first stage, we compared the DNA of more than 40 living organisms from various important animal groups. It’s the first time that such a diverse group was studied. It didn’t take us long to find the Argonaute proteins in these organisms. We also discovered the existence of three distinct types of Argonautes, each with a specific biological role,” Wynant explains.

Credit: KU Leuven

“Two out of these three types are especially important for our research: AGO1 and AGO2. The AGO1 family plays a role in regulating its own gene expression. These proteins help to determine which characteristics encoded in the DNA are actually expressed. The AGO2 family takes care of the defence against viruses. However, we didn’t find these AGO2 proteins in vertebrates."

The researchers also went back in time by examining the DNA of sponges and cnidarians, two ancient animal species. They found AGO2 proteins in the genome of these animals. Given that vertebrates and humans descend from these organisms, their common ancestor must have had the AGO2 type as well. "We suspect that the AGO2 proteins lost importance when vertebrates started developing a secondary immune system in which antibodies, interferons, and T-cells – rather than Argonaute proteins – fight viruses.”

In a second stage, the researchers examined the speed at which the Argonaute proteins evolved over time. “Argonautes that fight viruses have to be able to evolve very quickly because viruses are constantly adapting as well.” says Niels Wynant. "In invertebrates, we noticed that AGO2 proteins indeed evolved much faster than their AGO1 counterparts. We didn’t see this rapidly evolving group in the vertebrates.”

These findings, published in Scientific Reports, explain for the first time why RNAi is more efficient for fighting diseases in insects than in humans.

Author: Tine Danschutter | Source: KU Leuven [September 15, 2017]

Read More

Why we did not evolve to live forever: Unveiling the mystery of why we age

Researchers at the Institute of Molecular Biology (IMB) in Mainz have made a breakthrough in understanding the origin of the ageing process. They have identified that genes belonging to a process called autophagy – one of the cells most critical survival processes – promote health and fitness in young worms but drive the process of ageing later in life.

Researchers have made a breakthrough in understanding the origin of the ageing process [Credit: Pixabay]

This research published in the journal Genes & Development gives some of the first clear evidence for how the ageing process arises as a quirk of evolution. These findings may also have broader implications for the treatment of neurodegenerative disorders such as Alzheimer's, Parkinson's, and Huntington's disease where autophagy is implicated. The researchers show that by promoting longevity through shutting down autophagy in old worms there is a strong improvement in neuronal and subsequent whole body health.

Getting old, it's something that happens to everyone and nearly every species on this planet, but the question is, should it? In a recent publication in the journal Genes & Development titled "Neuronal inhibition of the autophagy nucleation complex extends lifespan in post-reproductive C. elegans,"  the laboratory of Dr. Holger Richly at IMB, has found some of the first genetic evidence that may put this question to rest.

As Charles Darwin explained, natural selection results in the fittest individuals for a given environment surviving to breed and pass on their genes to the next generation. The more fruitful a trait is at promoting reproductive success, the stronger the selection for that trait will be. In theory, this should give rise to individuals with traits which prevent ageing as their genes could be passed on nearly continuously. Thus, despite the obvious facts to the contrary, from the point of evolution ageing should never have happened.

This evolutionary contradiction has been debated and theorised on since the 1800s. It was only in 1953 with his hypothesis of antagonistic pleiotropy (AP) that George C. Williams gave us a rational explanation for how ageing can arise in a population through evolution. Williams proposed that natural selection enriches genes promoting reproductive success but consequently ignores their negative effects on longevity. Importantly, this is only true when those negative effects occur after the onset of reproduction. Essentially, if a gene mutation results in more offspring but shortens life that's fine. This is because there can be more descendants carrying on the parent's genes in a shorter time to compensate.

Accordingly, over time, these pro-fitness, pro-ageing mutations are actively selected for and the ageing process becomes hard-wired into our DNA. While this theory has been proven mathematically and its implications demonstrated in the real world, actual evidence for genes behaving in such as fashion has been lacking.

This evidence has now arrived according to the co-lead author of the paper Jonathan Byrne, "The evolutionary theory of ageing just explains everything so nicely but it lacked real evidence that it was happening in nature. Evolution becomes blind to the effects of mutations that promote ageing as long as those effects only kick in after reproduction has started. Really, ageing is an evolutionary oversight." Jonathan continues "These AP genes haven't been found before because it's incredibly difficult to work with already old animals, we were the first to figure out how to do this on a large scale." He explains further "From a relatively small screen, we found a surprisingly large number of genes [30] that seem to operate in an antagonistic fashion." Previous studies had found genes that encourage ageing while still being essential for development, but these 30 genes represent some of the first found promoting ageing specifically only in old worms. "Considering we tested only 0.05% of all the genes in a worm this suggests there could be many more of these genes out there to find," says Byrne.

The evidence for ageing driven by evolution was not the only surprise the paper had in store, according to Thomas Wilhelm, the other co-lead author on the paper. "What was most surprising was what processes those genes were involved in." Not content to provide just the missing evidence for a 60-year-old puzzle, Wilhelm and his colleagues went on to describe what a subset of these genes do in C. elegans and how they might be driving the ageing process. "This is where the results really get fascinating," says Dr. Holger Richly, the principal investigator of the study. "We found a series of genes involved in regulating autophagy, which accelerate the ageing process." These results are surprising indeed, the process of autophagy is a critical recycling process in the cell, and is usually required to live a normal full lifetime.

Autophagy is known to become slower with age and the authors of this paper show that it appears to completely deteriorate in older worms. They demonstrate that shutting down key genes in the initiation of the process allows the worms to live longer compared with leaving it running crippled. "This could force us to rethink our ideas about one of the most fundamental processes that exist in a cell," Richly explains. "Autophagy is nearly always thought of as beneficial even if it's barely working. We instead show that there are severe negative consequences when it breaks down and then you are better off bypassing it all together. It's classic AP. In young worms, autophagy is working properly and is essential to reach maturity but after reproduction, it starts to malfunction causing the worms to age,” he continues.

In a final revelation, Richly and his team were able to track the source of the pro longevity signals to a specific tissue, namely the neurons. By inactivating autophagy in the neurons of old worms they were not only able to prolong the worms life but they increased the total health of the worms dramatically. "Imagine reaching the halfway point in your life and getting a drug that leaves you as fit and mobile as someone half your age who you then live longer than, that's what it's like for the worms," says Thomas Wilhelm. "We turn autophagy off only in one tissue and the whole animal gets a boost. The neurons are much healthier in the treated worms and we think this is what keeps the muscles and the rest of the body in good shape. The net result is a 50% extension of life."

While the authors do not yet know the exact mechanism causing the neurons to stay healthier for longer, this finding could have real world implications. "There are many neuronal diseases associated with dysfunctional autophagy such as Alzheimer's, Parkinson's, and Huntington's disease, it is possible that these autophagy genes could represent a good way to help preserve neuronal integrity in these cases," elaborates Thomas Wilhelm. While any such a treatment would be a long way off, assuming such findings could be recapitulated in humans, it does offer a tantalising hope; prevent disease and get younger and healthier while doing it.

Source: Johannes Gutenberg Universitaet Mainz [September 15, 2017]

Read More

Scientists create alternate evolutionary histories in a test tube

Scientists at the University of Chicago studied a massive set of genetic variants of an ancient protein, discovering a myriad of other ways that evolution could have turned out, and revealing a central role for chance in evolutionary history.

University of Chicago graduate student Tyler Starr holds a vial of yeast cells engineered with a library of proteins 
comprising millions of possible evolutionary paths from our ancient ancestor to its modern function 
[Credit: Matt Wood, University of Chicago]

The study, published this week in Nature by UChicago graduate student Tyler Starr and Prof. Joseph Thornton, is the first to subject reconstructed ancestral proteins to deep mutational scanning—a state-of-the-art technique for characterizing massive libraries of protein variants. The authors’ strategy allowed them to compare the path that evolution actually took in the deep past to the millions of alternative routes that could have been taken, but were not.

Starting with a resurrected version of an ancient protein that evolved a new function some 500 million years ago—a function critical to human biology today—the researchers synthesized a massive library of genetic variants and used deep mutational scanning to analyze their functions. They found more than 800 different ways that the protein could have evolved to carry out the new function as well, or better than, the one that evolved historically.

The researchers showed that chance mutations early in the protein’s history played a key role in determining which ones could occur later. As a result, the specific outcome of evolution depended critically on the way a serial chain of chance events unfolded.

“By comparing what happened in history to all the other paths that could have produced the same result, we saw how idiosyncratic evolution is,” said Tyler Starr, a graduate student in biochemistry and molecular biology, who performed the paper’s experiments. “People often assume that everything in biology is perfectly adapted for its function. We found that what evolved was just one possibility out of many that were just as good, or even better, functionally than what we happened to end up with today.”

Molecular time travel

Over the last 15 years, Thornton, senior author on the new study and a professor in ecology and evolution and human genetics, led research that pioneered “molecular time travel” using ancestral protein reconstruction. In 2013, his team resurrected and analyzed the functions of the ancestors of a family of proteins called steroid hormone receptors, which mediate the effects of hormones like testosterone and estrogen on sexual reproduction, development, physiology and cancer. The body’s various receptors recognize different hormones and, in turn, activate the expression of different target genes, which they accomplish by binding specifically to DNA sequences called response elements near those targets.

Thornton’s group inferred the genetic sequences of ancient receptor proteins by statistically working their way back down the tree of life from a database of hundreds of present-day receptor sequences. They synthesized genes corresponding to these ancient proteins, expressed them in the lab and measured their functions.

They found that the ancestor of the family behaved like an estrogen receptor—recognizing only estrogens and binding to estrogen response elements—but during one specific interval of history, they evolved into a descendant group capable of recognizing other steroid hormones and binding to a new class of response elements. The researchers found that three key mutations before the emergence of vertebrate animals caused the ancestral receptor to evolve its ability to bind to the new target sequences.

That work set the stage for the current study. Knowing precisely how evolution played out in the past, Thornton’s group asked: Was this the only evolutionary path to evolving the new function? Was it the most effective one, or the easiest to achieve? Or was it simply one of many possibilities?

Alternate histories

Starr began working on the project during his first year as a graduate student, developing the technique to assess massive numbers of variants of the ancestral receptor for their ability to bind the new response element. First, he engineered strains of yeast in which the ancestral or new response elements drive expression of a fluorescent reporter gene. He then synthesized a library of ancestral proteins containing all possible combinations of amino acids at the four key sites in the receptor that recognize DNA—160,000 in all, comprising all possible evolutionary paths that this critical part of the protein could have followed—and introduced this library into the engineered yeast. He sorted hundreds of millions of yeast cells by their fluorescence using a laser-driven device, and then used high-throughput sequencing to associate each receptor variant with its ability to carry out the ancestral function and the new function.

Most of the variants failed to function at all, and some maintained the ancestral function. But Starr found 828 new versions of the protein that could carry out the new function as well, or better than, the one that evolved during history. Remarkably, evolution could have accessed many of these even more easily than the historical “solution,” but it happened not to, apparently wandering around the space of possible mutations until it arrived at the version of the protein in our bodies today.

“We all share the same gene sequence for this protein, so it might seem like evolutionary destiny, as if we’ve arrived at the best possible version. But there are hundreds of other directions that evolution could just as well have taken,” Thornton said. “There’s nothing special about the history that happened, except that a few chance steps brought us to this singular chance outcome.”

Thornton said that deep mutational scanning will be a powerful tool for evolutionary biologists, geneticists and biochemists, and he looks forward to using the approach on successive ancestors at different points in history to see how the set of possible outcomes changed through time.

“We have a molecular time machine to go back to the past, and once we’re there, we can simultaneously follow every alternate history that could possibly have played out,” Thornton said. “It’s a molecular version of every evolutionary biologist’s dream.”

Author: Matt Wood | Source: University of Chicago Medical Center [September 13, 2017]

Read More

Rising CO2 leading to changes in land plant photosynthesis

Researchers led by Scripps Institution of Oceanography at the University of California San Diego have determined that major changes in plant behavior have occurred over the past 40 years, using measurements of subtle changes in the carbon dioxide (CO2) currently found in the atmosphere.

Photo: MistikaS/iStock

The two main isotopes, or atomic forms, of carbon are carbon-12 (12C) and carbon-13 (13C). As CO2 has risen since the late 19th century, the ratio of 13C to 12C in atmospheric CO2 has decreased. That's in part because the CO2 produced by the combustion of fossil fuels has a low 13C/12C ratio. There are other factors in nature as well, however, that have influenced the rate of decrease in the isotopic ratio. The measured rate of decrease in the isotopic ratio turns out to be different than what scientists previously expected.

The Scripps-led team updated the record of CO2 isotopic ratios that has been made at Scripps since 1978 using air samples collected at Hawaii's Mauna Loa and the South Pole. The researchers confirmed that the discrepancy exists and considered several reasons for it. They concluded that no combination of factors could plausibly explain the changes in the CO2 isotopic ratio unless plant behavior was changing in a way that influences how much water plants need for growth.

The work helps to understand the details of how leaves are responding to changes in CO2. Prior to this study, it was already clear that plants behave differently when they are exposed to higher atmospheric CO2 levels because CO2 influences the behavior of stomata, the microscopic holes in leaves that allow a leaf to take up CO2. These holes also allow water to evaporate from the leaf, which must be replenished by water supplied to the roots to avoid drying out. With more CO2 in the atmosphere, a plant can afford to have smaller or fewer stomata, thus allowing more photosynthesis for the same amount of water.

But measuring exactly how much more efficient plants have become at using water has not been easy. This study provides a new method for measuring this effect, because as a leaf becomes more efficient at using water, this also influences how it takes up the different carbon isotopes in CO2. When that factor is included as a variable, the ratio of the two forms of CO2 conforms much more closely to expectations. The National Science Foundation, the Department of Energy, NASA, and the Eric and Wendy Schmidt Fund for Strategic Innovation supported the study, "Atmospheric evidence for a global secular increase in carbon isotopic discrimination of land photosynthesis," which appears in the journal Proceedings of the National Academy of Sciences.

The research supports a long-standing hypothesis introduced by plant biologists, that posits plants will achieve an optimum response to rising CO2 levels in the atmosphere.

"This optimal model predicts nearly proportional scaling between water-use efficiency and CO2 itself," said study lead author and Scripps scientist Ralph Keeling, who also maintains the internationally renowned Keeling Curve data set measuring atmospheric CO2 since 1958. "Optimal or near optimal behavior has been found in smaller studies on individual plants, but this paper is the first to show that it may be evident at the scale of the entire planet."

The increase in the efficiency of photosynthesis documented in this study has likely helped plants offset a portion of human-induced climate change by removing more CO2 from the atmosphere than they would have otherwise.

"The full implications are still far from clear, however, and any benefits may be more than offset by other negative changes, such as heat waves and extreme weather, biodiversity loss, sea level rise, and so on," said Keeling.

Source: University of California - San Diego [September 12, 2017]

Read More

The evolutionary origin of the gut

How did the gut, the skin and musculature evolve? This question concerns scientists for more than a century. Through the investigation of the embryonic development of sea anemones, a very old animal lineage, researchers from the University of Vienna have now come to conclusions which challenge the 150 year-old hypothesis of the homology (common evolutionary origin) of the germ layers that form all later organs and tissues.

Early embryonic stage of Nematostella vectensis [Credit: Sabrina Kaul-Strehlow, Patrick Steinmetz]

According to a 150 year-old hypothesis, all tissues and organs in our body derive from one of three germ layers that are established during early embryogenesis. This "germ layer hypothesis" states that skin and nervous system derive from the outer ectoderm layer, the gut and some inner organs, like the pancreas, derive from the inner endoderm layer, while muscles and gonads stem from the middle layer, the mesoderm. Early on, researchers noted a fundamental difference in the number of germ layers in different animal groups.

While most animals, like humans, insects and worms, develop from three germ layers, the cnidarians (corals, sea anemones or jellyfish) lack the intermediate layer and present only two cell layers during development and throughout life. The emergence of mesoderm as the third intermediate germ layer is considered a key event during the evolution of complex animals. So far, however, it was controversial how mesoderm has evolved, and how the two cnidarian germ layers relate to the three layers in most other animals. A new publication from the laboratory of Ulrich Technau at the Department for Molecular Evolution and Development of the University of Vienna presents a fundamentally new view of the evolution of germ layers.

The inner-most, gut-forming endoderm has always been considered as evolutionary related between cnidarians and other animals. In their study, Technau and colleagues have now tested this hypothesis by tracing the embryonic origin of digestive enzyme-producing cells as well as their developmental regulator genes typical of the gut and pancreas in a sea anemone. The authors show that in sea anemones, against all previous beliefs, digestive enzyme- and insulin-producing gland cells do not develop from endoderm but from the ectodermal part of the mouth, the pharynx. "I was puzzled when I first saw that all endoderm derivatives of sea anemones are totally devoid of digestive gland cells. That was not what is taught in biology textbooks" explains Patrick Steinmetz, who contributed most of the experiments and is now a group leader at the University of Bergen in Norway.

"The results completely change the way we think of the origin of germ layers. It means that 'endoderm' in sea anemones and vertebrates, although they are called the same, are actually not evolutionary related" adds Ulrich Technau. If the mouth ectoderm of the sea anemone and not the endoderm corresponds to the vertebrate gut and pancreas, then what is the vertebrate correlate of the sea anemone endoderm? When Steinmetz and Technau dwelled deeper into this question, they found strong similarities between the cnidarian endoderm and the intermediate mesoderm layer: both share a large number of regulatory genes, and both give rise to similar cell types such as muscle or gonad cells. The sea anemone thus shows a clear correlate of mesoderm, but not in an intermediate position as found in three-layered animals. Positioning, and not novel emergence, of tissue in-between the gut and skin was thus the key event that led to the evolution of three-layered animals.

"An overwhelming majority of animals nowadays develop three germ layers, and we have taken a big step towards the understanding of one of the most crucial events underlying this evolutionary success story" concludes Steinmetz.

The study is published in Nature Ecology & Evolution.

Source: University of Vienna [September 11, 2017]

Read More

Why it's difficult to predict evolutionary fate of a new trait

The phrase "survival of the fittest" makes the principle of evolution by natural selection easy to understand—individuals with a trait that adapts them well to their circumstances are more likely to pass that trait along. But as a new study explains, multiple factors make predicting the fate of a trait fiendishly difficult.

The fitness of a genetic trait (an allele) may vary over time, rather than remain constant. In this simple model, 
populations with two different alleles (black or yellow) see-saw between advantage and disadvantage 
as their relative fitness changes over time (blue line below) [Credit: Weinreich et. al.]

Not only would improved predictive models help scientists better model how evolution works, but also they could aid in efforts to prevent infectious diseases. Every year, for example, vaccine makers, epidemiologists and physicians strive to predict where diseases such as influenza, Zika, HIV and Ebola may be headed next.

Fundamentally, the problem is that a trait conveyed by a gene variant, or allele, may be advantageous for one or a few generations, but provide no advantage or become a liability when circumstances change, said senior author Daniel Weinreich, a professor of ecology and evolutionary biology at Brown University. But most theoretical models of population genetics assume that fitness remains constant.

"We are articulating a number of different biological contexts in which the fitness of an allele might change over its 'lifetime' or lineage" in a population," Weinreich said. "We are convinced that the other contexts, where it is constant, are the exceptions, not the rule."

The new study in the Annual Review of Ecology, Evolution and Systematics provides an overview of what complicates predictive models and how scientists are trying to make progress, for the benefit of public health, among other areas.

"Infectious diseases experience constantly varying selective pressures as they spread within and between hosts and encounter drugs and host immune responses," said lead author Christopher Graves, who earned his Ph.D. from Brown and is now a researcher at Bayer. "Understanding how evolution proceeds in scenarios of highly variable selective pressures will increase our ability to predict drug resistance and disease outbreaks and ultimately lead to the creation and deployment of more clever drug and vaccine strategies."

Fitness can be fickle

Perhaps the most obvious way that the fitness of a trait can vary is that the environment can change, not only over time but also over space. Consider the population of a species of weed in a vacant lot. Some might carry an allele that helps them thrive in a hot sun and others might have an allele that conveys a relative advantage in cool shade. Not only could weather patterns change dramatically over timescales ranging from days to years, but also new buildings might go up or get torn down around the lot, creating new patches of shade or sun. A model projecting the fate of each allele becomes much more complicated along multiple dimensions.

Another dimension that can vary is the "social" life of alleles. Alleles that result in "cheating" are abundant in nature, but they are most effective when they are rare. Once everyone is cheating, it might no longer be an advantage, so the trait over time can become a victim of its own success. Moreover, genetic predispositions to cooperation doesn't just roll over. The paper cites cases in which "policing" behaviors have evolved, such as insects that preserve the supremacy of the queen by destroying the "selfishly" laid eggs of mere workers, or genes that produce a tumor-suppressing immune capacity to destroy cancer cells because they are growing too fast.

Conditions can even vary within a lineage because one allele might emerge that affects another. Weinreich has studied this in the emergence of antibiotic resistance in bacteria. He found that four mutations of a particular enzyme sometimes increased drug resistance and sometimes didn't, depending on what other mutations were present or absent.

Even more complications

That any of these circumstances can change over time adds yet another layer of complexity, Weinreich said, because the rate at which circumstances change matters. When circumstances change faster than the organism's rate of reproduction—for instance sunny or cloudy weather patterns that come and go over a few days—the sun- or shade-loving weeds each experience only minor influences on their reproductive success. But if circumstances vary more slowly—for instance a large new building shades the entire lot for decades—the sunny allele carriers could vanish from the lot and the shady allele will fully displace the other type. In this case, the sun-loving weeds may have gone extinct by the time the building is torn down again.

Indeed, Weinreich said, many models for predicting the fate of alleles have overlooked the possibility that traits can go completely extinct.

Meanwhile, the rate of environmental change is very similar to the rate at which natural selection acts, the math becomes especially tricky.

Pressing for progress

In their search for solutions, population geneticists have employed new approaches, Weinreich and Graves wrote. Among the most exciting, Weinreich said, are those in which they join forces with and borrow techniques from ecology and epidemiology—two fields in which modeling dynamic and complex change is central. This summer, for example, has featured a workshop, "Eco-Evolutionary Dynamics in Nature and the Lab" at the University of California at Santa Barbara's Kavli Institute for Theoretical Physics, that is dedicated to exploring such intersections.

Weinreich said he plans to delve deeper into the complexities of changes in fitness deriving from varying rates of change in social (e.g. cheaters), genetic (e.g. competing alleles) or environmental (e.g., weather) parameters.

"The overlap between ecological and evolutionary processes—that those two things speak to each other very intimately in a way that's been overlooked in many models—is the way forward," Weinreich said. "That's what's needed to make critical improvements to models."

Author: David Orenstein | Source: Brown University [September 08, 2017]

Read More

Hidden Inca treasure: Remarkable new tree genus discovered in the Andes

Hidden in plain sight -- that's how researchers describe their discovery of a new genus of large forest tree commonly found, yet previously scientifically unknown, in the tropical Andes. Researchers from the Smithsonian and Wake Forest University detailed their findings in a study just released in the journal PhytoKeys.

New canopy tree genus Incadendron esseri shown in this altitudinal transect of Manu National Park in Peru 
[Credit: Wake Forest University]

Named Incadendron esseri (literally "Esser's tree of the Inca"), the tree is a new genus and species commonly found along an ancient Inca path in Peru, the Trocha Union. Its association with the land of the Inca empire inspired its scientific name.

So how could a canopy tree stretching up to 100 feet tall and spanning nearly two feet in diameter go undetected until now?

"Incadendron tells us a lot about how little we understand life on our planet. Here is a tree that ranges from southern Peru to Ecuador, that is abundant on the landscape, and yet it was unknown. Finding this tree isn't like finding another species of oak or another species of hickory -- it's like finding oak or hickory in the first place," said Miles Silman, the Andrew Sabin Family Foundation Presidential Chair in Conservation Biology at Wake Forest.

"This tree perplexed researchers for several years before being named as new. It just goes to show that so much biodiversity is unknown and that obvious new species are awaiting discovery everywhere -- in remote ecological plots, as well as in our own backyards," said Kenneth Wurdack, a botanist with the Smithsonian's National Museum of Natural History.

Fruits and leaves of Incadendron esseri, new tree genus found in Peru and Ecuador 
[Credit: Jason Houston]

The tree belongs to the spurge family, Euphorbiaceae -- best known for rubber trees, cassava, and poinsettias -- and like many of its relatives, when damaged also bleeds white sap, known as latex, that serves to protect it from insects and diseases.

Its ecological success in a difficult environment suggests more study is needed to find the hidden secrets that are often inherent in newly discovered and poorly known biodiversity.

Currently the Incadendron is common in several research plots under intensive study as part of the Andes Biodiversity and Ecosystem Research Group, an international Andes-to-Amazon ecology program co-founded by Silman.

For nearly 25 years, Silman has worked to gain greater understanding of Andean species distributions, biodiversity, and the response of forest ecosystems to climate and land use changes over time.

Incadendron esseri branch [Credit: Wake Forest University]

"While Incadendron has a broad range along the Andes, it is susceptible to climate change because it lives in a narrow band of temperatures. As temperatures rise, the tree populations have to move up to cooler temperatures," said Silman.

One of the study's co-authors, William Farfan-Rios, is a Wake Forest graduate student researching tropical forest dynamics and responses to changing environments along the Andes-to-Amazon elevational gradient. Discovering the Incadendron hits particularly close to home for the Cusco, Peru-native. Not only is the new genus vulnerable to climate change, but it is also threatened by deforestation in nearby areas.

"It highlights the imperative role of parks and protected areas where it grows, such as Manu National Park and the Yanachaga-Chemillen National Park," he said. "Hopefully our ongoing study of the Incadendron and the intensive long-term forest monitoring will contribute to best practices in reforestation and forest management."

Source: Wake Forest University [September 07, 2017]

Read More