Number of fungal species has been greatly overestimated

The good news for the Estonian mycophile is that when it comes to mycorrhizal fungi, which include almost all edible and poisonous mushrooms, the forests of our climate zone are the richest in species.

A study led by the researchers of the University of Tartu Natural History Museum discovered that the most species-rich fungal communities are in tropical rainforests. The estimated global species richness of fungi, 1.5-5.1 million species, however, seems to be a vast overestimation, according to their data.

"Together with 35 research institutions we collected approximately 15,000 soil samples from various areas across the world. We then sequenced the DNA in the collected samples, using the new generation sequencing method. When analysing the soil samples, we found more than 45,000 fungal species. To our knowledge, this is the largest dataset of biodiversity studies published so far," said Leho Tedersoo, Senior Research Fellow of the University of Tartu Natural History Museum and the manager of the project.

"The coordination of the activities of all partners and obtaining all the required permits for getting the samples meant a lot of paperwork. In some countries we could not collect samples just because we could not get the permits. For generalisations, however, the amount of the collected material is more than enough," said Tedersoo.

As the main findings, the study concluded that the species richness patterns of fungi in general follow these of plants and animals -- i.e. the species richness is the highest in tropical rainforests and general rules of biogeography apply. In the past, it was commonly held that the latter do not apply to microorganisms -- that all forms are present everywhere depending on the substrate. The study found that the number of fungal species in the world has been greatly overestimated.

"We discovered that endemism -- the phenomenon that particular species live only in a rather limited area -- is also very common among fungi," explained Tedersoo. Tedersoo added that there are also many species that are spread across the world, such as mould and animal pathogens. "Although the spread of plant and animal species in the temperate climate zone of the northern hemisphere is limited to continents, many fungal species are equally spread in Asia, North America and Europe. This indicates that fungi have a more efficient spreading mechanism: microscopic spores," said Tedersoo.

"The research findings will not save the world, but help the researchers understand the global biological processes much better. As the species richness and spread of fungi mostly depend on precipitation, temperature and vegetation, it can be assumed that climate change strongly affects mycobiota in dry and cool regions. The good news for the Estonian mycophile is that when it comes to mycorrhizal fungi, which include almost all edible and poisonous mushrooms, the forests of our climate zone are the richest in species. The age-old Abruka limetree forest holds the record," said Tedersoo.

In the future, the working group of ecology of biological interactions is planning to focus on detecting functional difference in soil organisms in different ecosystems of the world, to show how these organisms have adapted to different climatic and soil-formation processes and to historical-biogeographical factors.

"Such analyses require computational power and cloud services, which are available in the PlutoF system and at the High Performance Computing Center of the University of Tartu," said Tedersoo. "Huge work has been done by my colleagues Mohammad Bahram, Sergei Põlme, Urmas Kõljalg and Kessy Abarenkov. These days, analyses of such scale cannot even be conducted by a single researcher or a small working group."

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Scientists question tropical protected areas' role under climate change

Prothoe franck (marked in pink to allow to its dispersal to be studied), is a forest dependent butterfly that may be at risk from climate change in lowland forest habitats.

New research led by University of York scientists highlights how poor connectivity of protected area (PA) networks in Southeast Asia may prevent lowland species from responding to climate change.

Tropical species are shifting to higher elevations in response to rising temperatures, but there has been only limited research into the effectiveness of current protected area networks in facilitating such movements in the face of climate change.

However, the new study, published in the journal Biological Conservation, focuses on the connectivity of the protected area network on the highly biologically diverse island of Borneo. The island is facing severe pressure due to deforestation and cultivation of oil palm plantations, resulting in an important biodiversity conservation role for protected areas in this region.

The research paper analyses future changes in the spatial distribution of climate within protected areas, and also uses population modelling to examine their connectivity. The results suggest that low elevation protected areas are particularly vulnerable to climate change, and that management to improve their linkage as terrain increases in elevation should be a conservation priority.

Lead author Sarah Scriven, a PhD student from the Department of Biology at York, said: "This study gave me an opportunity to learn valuable new skills such as the manipulation of land cover and climate data using GIS (geographic information system) software, as well as modelling the dispersal of species -- such as forest-dependant butterflies -- through fragmented landscapes. I will combine these new research skills with field-work in Sabah, Malaysian Borneo, to address the overall theme of my PhD -- which is to examine the resilience of biodiversity to climate change within tropical agricultural landscapes."

The study shows that analogue climates will shift out of more than 61 per cent of protected areas resulting in many species needing to move to cooler areas if they are to track climate changes. The study also reveals that many low-lying protected areas are isolated and not well connected to cooler forested areas at higher elevation.

Co-author Dr Colin McClean, from the Environment Department at York, said: "We show that the majority of PAs on Borneo will fail to retain analogue climate conditions in future, and these PAs are primarily located in lowland areas. This is worrying because there has been huge expansion of oil palm plantations in tropical lowlands in recent decades, not just in Borneo, but all over Southeast Asia."

Co-author Dr Jenny Hodgson, now of the University of Liverpool but formerly in the Department of Biology at York, who developed the population model used in the study, said: "Our results are concerning because biodiversity is known to peak in low-lying forests, and in Borneo these forests contain exceptionally high numbers of endemic species. Large-scale oil palm plantations will likely act as barriers to species moving between PAs."

Project leader Professor Jane Hill, Sarah Scriven's PhD supervisor, added: "Our new research highlights the isolation of low-lying PAs on Borneo. Management to improve linkage of PAs along elevation gradients should be a conservation priority."

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Female mice do not avoid mating with unhealthy males

Mating choice is not based solely on odor.

Female mice are attracted more strongly to the odour of healthy males than unhealthy males. This had already been shown in an earlier study by researchers from the Konrad Lorenz Institute of Ethology at the Vetmeduni Vienna. Now the team of behavioural scientists went one step further -- and tested a common assumption that more attractive males have better mating success than other males.

Females also mate with unhealthy males

Sarah Zala and Dustin Penn investigated whether females would also choose to mate with healthy over infected male if given a choice. In the laboratory and in large enclosures, the females were allowed to freely choose between two males, one healthy and another challenged with a mild infection, which they previously found to alter male odour.

The majority of females, about 86 percent, were initially more attracted to the healthy males. However, unhealthy males were also chosen as mating partners. "That surprised us. We assumed that the females would opt for the healthy males. Not only would this minimise the chance of becoming infected themselves, but choosing a healthy, disease-resistant partner would also be advantageous for their offspring," first author Zala explains.

Polyandry not unusual for female mice

A genetic analysis of the offspring revealed that about 30 percent of the litters had two fathers, the healthy male and the unhealthy one.

"Many females apparently mate with both males, whether these are healthy or not," Zala says. "We suspect that the females do this to protect their young. A male that was rejected as a mating partner may commit infanticide in order to get another chance at siring offspring."

"The females recognise whether males are healthy or unhealthy. We saw this quite clearly. But why they still mate with the unhealthy male remains unclear," says Dustin Penn.

In the future, Zala and Penn intend to study more closely the effect of an infection on the odour of the animals.

Odour preference seems irrelevant for mate choice

"Until now, scientists generally assumed that females choose their mates depending on their males' scent or other secondary sexual traits. Our study shows that this isn't necessarily the case," says Zala. The situation could be different in the wild. As females recognise healthy males quite well based on odour, and are more attracted to them, they may be more likely to find healthy males in the wild. In the end, odour preference could still be an important factor determining sexual selection.

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Hidden meaning and 'speed limits' found within genetic code

Case Western Reserve scientists have discovered that speed matters when it comes to how messenger RNA (mRNA) deciphers critical information within the genetic code -- the complex chain of instructions critical to sustaining life. The investigators' findings, which appear in the March 12 journal Cell, give scientists critical new information in determining how best to engage cells to treat illness -- and, ultimately, keep them from emerging in the first place.

"Our discovery is that the genetic code is more complex than we knew," said senior researcher Jeff Coller, PhD, associate professor, Division of General Medical Sciences, and associate director, The Center for RNA Molecular Biology, Case Western Reserve University School of Medicine. "With this information, researchers can manipulate the genetic code to achieve more predictable outcomes in an exquisite fashion."

The genetic code is a system of instructions embedded within DNA. The code tells a cell how to generate proteins that control cellular functions. mRNA transmits the instructions from DNA to ribosomes. Ribosomes translate the information contained within the mRNA and produce the instructed protein. The genetic code comprises 61 words, called "codons," and a single codon, a sequence of three nucleotides, instructs the ribosome how to build proteins.

The code not only dictates what amino acids are incorporated into proteins, it also tells the cell how fast they should be incorporated. With this information, researchers can manipulate the genetic code to achieve predictable protein levels in an exquisite fashion."

The most significant breakthrough in the Case Western Reserve work is that all of the words, or codons, in the genetic code are deciphered at different rates; some are deciphered rapidly while others are deciphered slowly. The speed of how mRNA decodes its information is the sum of all the codons it contains. This imposed speed limit then ultimately affects the amount of protein produced. Sometimes faster is better to express a high level of protein. Sometimes slower is better to limit the amount protein. Importantly, codons are redundant -- many of these words mean the same thing.

Coller and colleagues found that each of the codons is recognized differently by a ribosome. Some codons are recognized faster than others, but these differences in speed are tiny. Over the entire span of an mRNA, however, each tiny difference in speed is powerfully additive.

"Many codons mean the same thing, but they influence decoding rate differently. Because of this, we can change an mRNA without changing its protein sequence and cause it to be highly expressed or poorly expressed and anywhere in between," he said. "We can literally dial up or down protein levels any way we want now that we know this information."

During their research, investigators measured the mRNA decay rate for every transcript within the cell. They were seeking answers for why different RNAs had different stabilities. With statistical analysis, investigators compared the half-lives of mRNAs to the codons used within these messages. A strong correlation emerged between codon identity and mRNA message stability. They ultimately linked these observations back to the process of mRNA translation.

"mRNA translation and mRNA decay are intimately connected. This can be very beneficial to scientists. If you would like a gene to be expressed really well, you simply change the protein sequence to be derived by all optimal codons. This will both stabilize the mRNA and cause it to be translated more efficiently," Coller said. "If you need an mRNA to express at a low level, you fill it with non-optimal codons. The mRNA will be poorly translated and thus unstable. Evolution has used codon optimization to shape the expression of the proteome. Genes of similar function use similar codons; therefore, they are expressed at similar levels."

His discovery has a variety of practical implications for medicine. From a bioengineering perspective, molecular biology techniques can be applied to manipulate the gene to contain ideal codons and obtain the gene expression pattern that is most beneficial to the application. From a human physiological standpoint, it's possible to learn the speed limit for each and every mRNA and then determine if this changes in specific pathologies such as cancer. Currently, it is unknown whether codons convey different speeds in disease states. A future direction for research will be to link codon speeds to specific illnesses. The potential is also there to develop drugs that can manipulate higher or lower gene expression by changing the decoding rate.

Codon activity also may also provide important clues about the source of many illnesses that have not been linked to specific gene mutations. Altering codon-dependent translation rates has the potential to change protein function profoundly, and no primary mutation will be detected. Rather the problem is not the gene itself, but the factors that influence decoding rates. Codon-dependent speed limits may underlie the cause of whole classes of disease states. For example, a recent study suggests that in more than 450 different cancer samples, factors influencing codon-dependent speed limits might be changing.

"The sky is the limit," Coller said. "Since this finding is so new, we have no idea what the potential is. The next step is to determine if changes in decoding speed can be an underlying mechanism that alters gene expression in human disease."

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Nature's inbuilt immune defense could protect industrial bacteria from viruses

Findings from a new study that set out to investigate the evolution of immune defences could boost the development of industrial bacteria that are immune to specific viral infections. The study is published today in the journal Current Biology.

Bacteria have many industrial uses including the production of cheese and yoghurt, paper making, biogas and the synthetic production of hormones like insulin. Viral infections of these bacterial cultures can halt production processes resulting in significant financial cost.

Dr Edze Westra from the Environment and Sustainability Institute at the University of Exeter's Penryn Campus in Cornwall said: "Our study indicates that it is the risk of infection that determines the type of immune defence used. This naturally occurring mechanism can be used to our advantage to equip industrial bacteria with immunity against viral attack."

In a series of experiments researchers from the University of Exeter exposed bacteria to phages -- viruses that infect bacteria. They discovered that when the bacteria were exposed to high numbers of the same strain of phage they evolved a permanent immune response by modifying their cell walls. This was an irreversible defence mechanism that had a negative impact on the long term health of the bacteria.

When the bacteria were exposed to low numbers of the same phage, a temporary defence was induced that used an immune response known as a CRISPR. Although costly when in use, in the absence of viruses the CRISPR response can lie dormant until required. The low overhead cost of this immune response has little impact on the long term health of the bacteria making it ideal for use in commercial applications.

Working in a similar way to a vaccine, bacteria could be 'pre-loaded' with CRISPR immune responses for multiple different phages. This is better for the health of the bacteria and results in higher product yields as well as protecting the culture in the event of infection with a range of viruses.

CRISPR functions by integrating genetic information from the virus into the bacterial DNA, forming a genetic database of viral sequences that is used as a memory to identify viruses during infection. If a viral infection then threatens the bacterial cell, the CRISPR immune system can thwart the attack by destroying the genome of the invading virus.

The research indicates that parasite exposure is likely to be a key factor in driving the evolution of permanent versus inducible -- or temporary -- defences in nature. This suggests that organisms living together in large populations, or parasite-rich conditions, are more likely to evolve permanent defences, whereas low parasite conditions select for inducible defences.

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'Warhead' molecule to hunt down deadly bacteria

Targeting deadly, drug-resistant bacteria poses a serious challenge to researchers looking for antibiotics that can kill pathogens without causing collateral damage in human cells. A team of Boston College chemists details a new approach using a "warhead" molecule to attack bacteria -- and spare healthy human cells -- by targeting a pair of lipids found on the surface of deadly germs, according to a report today in the journal Nature Communications.

The new strategy required the researchers to develop a novel type of "warhead molecule" capable of selectively targeting bacteria, overcoming biological conditions that interfere with bonding to pathogens and avoiding healthy human cells, said Boston College Associate Professor of Chemistry Jianmin Gao, the lead author of the report.

The BC team found answers to those challenges in the covalent chemistry of lipids, Gao said.

"In contrast to other efforts focused on the charge-to-charge attraction between molecules, we are using a completely different mechanism to target bacterial cells," said Gao. "Our method exploits the covalent chemistry of lipids -- where the lipids react with synthetic molecules to form new chemical structures based on the formation of new covalent bonds."

Pathogenic bacteria that are resistant to conventional antibiotics pose increasingly serious threats to public health. Researchers in medicinal chemistry, particularly those who seek to develop new antibiotics, are constantly looking for new ways to identify and differentiate bacterial pathogens from host cells within the human body.

Gao said bacterial cells are known to display a different set of lipids in their membranes. Prior research has focused on the use of positively charged peptides to target negatively charged lipids on the surface of bacterial cells. The approach has seen limited success as the charge-charge attraction between the attacking molecules and bacteria is prone to weakening by the presence of salt and other molecules, said Gao.

The researchers developed a novel, unnatural amino acid that serves as a suitable molecular warhead to target bacterial pathogens. Gao and his group sent the warhead molecule after bacterial lipids known as amine-presenting lipids -- specifically phosphatidylethanolamine (PE) and lysyl phosphatidylglycerol (Lys-PG) -- which can be selectively derivatized to form iminoboronates, a covalent bond forming process that allows the selective recognition and labeling of bacterial cells.

In addition, because amine-presenting lipids are scarce on the surface of mammalian cells, they are able to seek out and label bacterial cells with a high degree of selectivity, Gao said. Furthermore, iminoboronate formation can be reversed under physiologic conditions, giving the new method a high degree of control and allowing the warhead molecules to self-correct if unintended targets are reached.

Gao said a large number of bacterial species present PE and Lys-PG on their surfaces, making the covalent labeling strategy applicable to many applications in the diagnosis of bacterial infections and the delivery of antibiotic therapies.

"For the short term, we hope this work will inspire other people to consider using covalent chemistry for interrogating biological systems," Gao said. "Going into the future, we are excited to explore the potential of our chemistry for imaging bacterial infections. We are also working hard to apply our current findings to facilitate the targeted delivery of potent antibiotics to bacterial cells only."

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Why do cells rush to heal a wound? Mysteries of wound healing unlocked

These are leader cells, shown fluorescing green in this photomicrograph, pull follower cells in their wake as they move to cover and heal a wound.

Researchers at the University of Arizona have discovered what causes and regulates collective cell migration, one of the most universal but least understood biological processes in all living organisms.

The findings, published in the March 13, 2015, edition of Nature Communications, shed light on the mechanisms of cell migration, particularly in the wound-healing process. The results represent a major advancement for regenerative medicine, in which biomedical engineers and other researchers manipulate cells' form and function to create new tissues, and even organs, to repair, restore or replace those damaged by injury or disease.

"The results significantly increase our understanding of how tissue regeneration is regulated and advance our ability to guide these processes," said Pak Kin Wong, UA associate professor of mechanical and aerospace engineering and lead investigator of the research.

"In recent years, researchers have gained a better understanding of the molecular machinery of cell migration, but not what directs it to happen in the first place," he said. "What, exactly, is orchestrating this system common to all living organisms?"

Leaders of the Pack

The answer, it turns out, involves delicate interactions between biomechanical stress, or force, which living cells exert on one another, and biochemical signaling.

The UA researchers discovered that when mechanical force disappears -- for example at a wound site where cells have been destroyed, leaving empty, cell-free space -- a protein molecule, known as DII4, coordinates nearby cells to migrate to a wound site and collectively cover it with new tissue. What's more, they found, this process causes identical cells to specialize into leader and follower cells. Researchers had previously assumed leader cells formed randomly.

Wong's team observed that when cells collectively migrate toward a wound, leader cells expressing a form of messenger RNA, or mRNA, genetic code specific to the DII4 protein emerge at the front of the pack, or migrating tip. The leader cells, in turn, send signals to follower cells, which do not express the genetic messenger. This elaborate autoregulatory system remains activated until new tissue has covered a wound.

The same migration processes for wound healing and tissue development also apply to cancer spreading, the researchers noted. The combination of mechanical force and genetic signaling stimulates cancer cells to collectively migrate and invade healthy tissue.

Biologists have known of the existence of leader cells and the DII4 protein for some years and have suspected they might be important in collective cell migration. But precisely how leader cells formed, what controlled their behavior, and their genetic makeup were all mysteries -- until now.


Broad Medical Applications

"Knowing the genetic makeup of leader cells and understanding their formation and behavior gives us the ability to alter cell migration," Wong said.

With this new knowledge, researchers can re-create, at the cellular and molecular levels, the chain of events that brings about the formation of human tissue. Bioengineers now have the information they need to direct normal cells to heal damaged tissue, or prevent cancer cells from invading healthy tissue.

The UA team's findings have major implications for people with a variety of diseases and conditions. For example, the discoveries may lead to better treatments for non-healing diabetic wounds, the No. 1 cause of lower limb amputations in the United States; for plaque buildup in arteries, a major cause of heart disease; and for slowing or even stopping the spread of cancer, which is what makes it so deadly.

The research also has the potential to speed up development of bioengineered tissues and organs that can be successfully transplanted in humans.

About the Study

In the UA Systematic Bioengineering Laboratory, which Wong directs, researchers used a combination of single-cell gene expression analysis, computational modeling and time-lapse microscopy to track leader cell formation and behavior in vitro in human breast cancer cells and in vivo in mice epithelial cells under a confocal microscope.

Their work included manipulating leader cells through pharmacological, laser and other means to see how they would react.

"Amazingly, when we directed a laser at individual leader cells and destroyed them, new ones quickly emerged at the migrating tip to take their place," said Wong, who likened the mysteries of cell migration and leader cell formation to the processes in nature that cause geese to fly in V-formation or ants to build a colony.

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Giant sea creature hints at early arthropod evolution

Artist's rendering of Aegirocassis benmoulae. (Screenshot from video available at: 

 

 

 

http://youtu.be/vzvCH2td-AM

Newly discovered fossils of a giant, extinct sea creature show it had modified legs, gills on its back, and a filter system for feeding -- providing key evidence about the early evolution of arthropods.

The new animal, named Aegirocassis benmoulae in honor of its discoverer, Mohamed Ben Moula, attained a size of at least seven feet, ranking it among the biggest arthropods that ever lived. It was found in southeastern Morocco and dates back some 480 million years.

"Aegirocassis is a truly remarkable looking creature," said Yale University paleontologist Derek Briggs, co-author of a Nature paper describing the animal. "We were excited to discover that it shows features that have not been observed in older Cambrian anomalocaridids -- not one but two sets of swimming flaps along the trunk, representing a stage in the evolution of the two-branched limb, characteristic of modern arthropods such as shrimps."

Briggs is the G. Evelyn Hutchinson Professor of Geology and Geophysics at Yale and curator of invertebrate paleontology at the Yale Peabody Museum of Natural History. First author Peter Van Roy, an associate research scientist at Yale, led the research; Allison Daley of the University of Oxford is co-author.

Since their first appearance in the fossil record 530 million years ago, arthropods have been the most species-rich and morphologically diverse animal group on Earth. They include such familiar creatures as horseshoe crabs, scorpions, spiders, lobsters, butterflies, ants, and beetles. Their success is due in large part to the way their bodies are constructed: They have a hard exoskeleton that is molted during growth, and their bodies and legs are made up of multiple segments. Each segment can be modified separately for different purposes, allowing arthropods to adapt to every environment and mode of life.

Modern arthropod legs, in their most basic form, have two branches. Each is highly modified to cater to a specific function on that leg, such as locomotion, sensing its surroundings, respiration, or copulation; or it has been lost altogether. Understanding how these double-branched limbs evolved has been a major question for scientists.

A long-extinct group of arthropods, the anomalocaridids, is considered central to the answer. The youngest known anomalocaridids are 480 million years old, and all of them looked quite alien: They had a head with a pair of grasping appendages and a circular mouth surrounded by toothed plates. Their elongate, segmented bodies carried lateral flaps that they used for swimming. Until now, it was believed that anomalocaridids had only one set of flaps per trunk segment, and that they may have lost their walking legs completely.

But the recent discovery of Aegirocassis benmoulae tells another story. The new animal shows that anomalocaridids in fact had two separate sets of flaps per segment. The upper flaps were equivalent to the upper limb branch of modern arthropods, while the lower flaps represent modified walking limbs, adapted for swimming. Furthermore, a re-examination of older anomalocaridids showed that these flaps also were present in other species, but had been overlooked. These findings show that anomalocaridids represent a stage before the fusion of the upper and lower branches into the double-branched limb of modern arthopods.

"It was while cleaning the fossil that I noticed the second, dorsal set of flaps," said Van Roy, who spent hundreds of hours working on the specimens. "It's fair to say I was in shock at the discovery, and its implications. It once and for all resolves the debate on where anomalocaridids belong in the arthropod tree, and clears up one of the most problematic aspects of their anatomy."

Aegirocassis benmoulae is also remarkable from an ecological standpoint, note the researchers. While almost all other anomalocaridids were active predators that grabbed their prey with their spiny head limbs, the Moroccan fossil has head appendages that are modified into an intricate filter-feeding apparatus. This means that the animal could harvest plankton from the oceans.

"Giant filter-feeding sharks and whales arose at the time of a major plankton radiation, and Aegirocassis represents a much, much older example of this -- apparently overarching -- trend," Van Roy said.

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Some Genes 'Foreign' in Origin and Not from Our Ancestors

Abstract illustration depicting DNA (stock image).

Many animals, including humans, acquired essential 'foreign' genes from microorganisms co-habiting their environment in ancient times, according to research published in the open access journal Genome Biology. The study challenges conventional views that animal evolution relies solely on genes passed down through ancestral lines, suggesting that, at least in some lineages, the process is still ongoing.

The transfer of genes between organisms living in the same environment is known as horizontal gene transfer (HGT). It is well known in single-celled organisms and thought to be an important process that explains how quickly bacteria evolve, for example, resistance to antibiotics.

HGT is thought to play an important role in the evolution of some animals, including nematode worms which have acquired genes from microorganisms and plants, and some beetles that gained bacterial genes to produce enzymes for digesting coffee berries. However, the idea that HGT occurs in more complex animals, such as humans, rather than them solely gaining genes directly from ancestors, has been widely debated and contested.

Lead author Alastair Crisp from the University of Cambridge, UK, said: "This is the first study to show how widely horizontal gene transfer (HGT) occurs in animals, including humans, giving rise to tens or hundreds of active 'foreign' genes. Surprisingly, far from being a rare occurrence, it appears that HGT has contributed to the evolution of many, perhaps all, animals and that the process is ongoing, meaning that we may need to re-evaluate how we think about evolution."

The researchers studied the genomes of 12 species of Drosophila or fruit fly, four species of nematode worm, and 10 species of primate, including humans. They calculated how well each of their genes aligns to similar genes in other species to estimate how likely they were to be foreign in origin. By comparing with other groups of species, they were able to estimate how long ago the genes were likely to have been acquired.

A number of genes, including the ABO blood group gene, were confirmed as having been acquired by vertebrates through HGT. The majority of the other genes were related to enzymes involved in metabolism.

In humans, they confirmed 17 previously-reported genes acquired from HGT, and identified 128 additional foreign genes in the human genome that have not previously been reported.

Some of those genes were involved in lipid metabolism, including the breakdown of fatty acids and the formation of glycolipids. Others were involved in immune responses, including the inflammatory response, immune cell signalling, and antimicrobial responses, while further gene categories include amino-acid metabolism, protein modification and antioxidant activities.

The team were able to identify the likely class of organisms the transferred genes came from. Bacteria and protists, another class of microorganisms, were the most common donors in all species studied. They also identified HGT from viruses, which was responsible for up to 50 more foreign genes in primates.

Some genes were identified as having originated from fungi. This explains why some previous studies, which only focused on bacteria as the source of HGT, originally rejected the idea that these genes were 'foreign' in origin.

The majority of HGT in primates was found to be ancient, occurring sometime between the common ancestor of Chordata and the common ancestor of the primates.

The authors say that their analysis probably underestimates the true extent of HGT in animals and that direct HGT between complex multicellular organisms is also plausible, and already known in some host-parasite relationships.

The study also has potential impacts on genome sequencing more generally. Genome projects frequently remove bacterial sequences from results on the assumption that they are contamination. While screening for contamination is necessary, the potential for bacterial sequences being a genuine part of an animal's genome originating from HGT should not be ignored, say the authors.

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Carnivorous plant packs big wonders into tiny genome

Light micrograph of the bladder of Utricularia gibba, the humped bladderwort plant (color added).

Great, wonderful, wacky things can come in small genomic packages.

That's one lesson to be learned from the carnivorous bladderwort, a plant whose tiny genome turns out to be a jewel box full of evolutionary treasures.

Called Utricularia gibba by scientists, the bladderwort is a marvel of nature. It lives in an aquatic environment. It has no recognizable roots. It boasts floating, thread-like branches, along with miniature traps that use vacuum pressure to capture prey.

A new study in the scientific journal Molecular Biology and Evolution breaks down the plant's genetic makeup, and finds a fascinating story.

According to the research, the bladderwort houses more genes than several well-known plant species, such as grape, coffee or papaya -- despite having a much smaller genome.

This incredibly compact architecture results from a history of "rampant" DNA deletion in which the plant added and then eliminated genetic material at a very fast pace, says University at Buffalo Professor of Biological Sciences Victor Albert, who led the study.

"The story is that we can see that throughout its history, the bladderwort has habitually gained and shed oodles of DNA," he says.

"With a shrunken genome," he adds, "we might expect to see what I would call a minimal DNA complement: a plant that has relatively few genes -- only the ones needed to make a simple plant. But that's not what we see."

A unique and elaborate genetic architecture

In contrast to the minimalist plant theory, Albert and his colleagues found that U. gibba has more genes than some plants with larger genomes, including grape, as already noted, and Arabidopsis, a commonly studied flower.

A comparison with the grape genome shows U. gibba's genetic opulence clearly: The bladderwort genome, holding roughly 80 million base pairs of DNA, is six times smaller than the grape's. And yet, the bladderwort is the species that has more genes: some 28,500 of them, compared to about 26,300 for the grape.

U. gibba is particularly rich in genes that may facilitate carnivory -- specifically, those that enable the plant to create enzymes similar to papain, which helps break down meat fibers. The bladderwort is also rich in genes linked to the biosynthesis of cell walls, an important task for aquatic species that must keep water at bay.

"When you have the kind of rampant DNA deletion that we see in the bladderwort, genes that are less important or redundant are easily lost," Albert says. "The genes that remain -- and their functions -- are the ones that were able to withstand this deletion pressure, so the selective advantage of having these genes must be pretty high.

"Accordingly, we found a number of genetic enhancements, like the meat-dissolving enzymes, that make Utricularia distinct from other species."

Much of the DNA the bladderwort deleted over time was noncoding "junk DNA" that contains no genes, Albert says.

High gene turnover

The study included partners from UB, the Universitat de Barcelona in Spain, the Laboratorio Nacional de Genómica para la Biodiversidad (LANGEBIO) in Mexico and the Instituto de Ecología in Mexico.

To determine how the bladderwort evolved its current genetic structure, the team compared the plant to four related species. What they uncovered was a pattern of rapid DNA alteration.

As Albert explains, "When you look at the bladderwort's history, it's shedding genes all the time, but it's also gaining them at an appreciable enough rate, permitting it to stay alive and produce appropriate adaptations for its unique environmental niche."

In the realm of DNA gain, the study found that U. gibba has undergone three duplication events in which its entire genome was replicated, giving it redundant copies of every gene.

This fast-paced gene gain was balanced out by swift deletion. Evidence for this phenomenon comes from the fact that the plant has a tiny genome despite its history of genetic duplication. In addition, the plant houses a high percentage of genes that don't have close relatives within the genome, which suggests the plant quickly deleted redundant DNA acquired through duplication events.

The study builds on the work of Albert and other team members, who reported in the journal Nature in 2013 that the bladderwort's genome was comprised almost entirely of useful, functional genes and their controlling elements, in contrast to species like humans, whose genomes are more than 90 percent "junk DNA."

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Retracing the roots of fungal symbioses

Mycorrhizal fungi include some of the most conspicuous forest mushrooms, such as the iconic fly agaric (Amanita muscaria), of the fungi sequenced for this project.

With apologies to the poet John Donne, and based on recent work from the U.S. Department of Energy Joint Genome Institute (DOE JGI), a DOE Office of Science user facility, it can be said that no plant is an island, entire of itself. Unseen by the human eye, plants interact with many species of fungi and other microbes in the surrounding environment, and these exchanges can impact the plant's health and tolerance to stressors such as drought or disease, as well as the global carbon cycle.

Mycorrhizal fungi live in the roots of host plants, where they exchange sugars that plants produce by photosynthesis for mineral nutrients that fungi absorb from the soil. They include some of the most conspicuous forest mushrooms, including the iconic, flaming red "fly agaric," Amanita muscaria, and are of interest to bioenergy researchers, because they play roles in maintaining the health of candidate feedstock crop trees. Recent studies indicate that mycorrhizal fungi also play a significant role in belowground carbon sequestration, which may mitigate the effects of anthropogenic CO2 emissions.

To understand the basis for fungal symbiotic relationships with plants, a team of DOE JGI researchers led by Igor Grigoriev and longtime collaborators at the French National Institute for Agricultural Research (INRA) and Clark University conducted the first broad, comparative phylogenomic analysis of mycorrhizal fungi, drawing on 49 fungal genomes, 18 of which were sequenced for this study. The 18 new fungal sequences included 13 mycorrhizal genomes, from ectomycorrhizal fungi that penetrate the host roots, and including species that comingle with orchid and heathland (which include blueberry, heather, and heath) plant roots. In the February 23, 2015 online edition of Nature Genetics, these researchers describe how the comparative analyses of these genomes allowed them to track the evolution of mycorrhizal fungi. The results help researchers understand how plants and fungi developed symbiotic relationships, and how the mutualistic association provides host plants with beneficial traits for environmental adaptation.

Starting with previously sequenced mycorrhizal fungi

"Mycorrhizal symbioses are highly complex, but analyses of the 49 genomes indicate that they have evolved independently in many fungal lineages," said INRA's Francis Martin, one of the study's senior authors. To understand the genetic shifts underlying the repeated origins of mycorrhizal lifestyles, the researchers focused on enzymes that degrade plant cell walls from 16 gene families associated with plant cell wall degradation. They took their cue from the first sequenced ectomycorrhizal fungus, Laccaria bicolor and the first sequenced arbuscular mycorrhizal fungus Rhizophagus irregularis- all work done at the DOE JGI-which illuminates the origins and evolution of these enzymes, knowledge to be applied in collaboration for improving biomass breakdown for biofuels production.

Through molecular clock analyses, which combine genome-scale molecular data with fossil calibrations, the team could work backwards to estimate when saprotrophic and mutualistic lineages last shared common ancestors based on the amount of divergence.

The analyses of the fungal genomes and fossils suggested that in comparison to brown rot fungi and white rot fungi that evolved over 300 million years ago, ectomycorrhizal fungi emerged fairly recently from several species and then spread out across lineages less than 200 million years ago. The team also found that up to 40 percent of the symbiosis-induced genes were restricted to a single mycorrhizal species.

Fungi evolving to break down plant cell walls

David Hibbett of Clark University, another of the study's senior authors, compared the work to a previous collaboration with the DOE JGI detailed in Science to trace the evolution of white rot fungi, which are capable of breaking down cellulose, hemicellulose and lignin in plants. Prior to the emergence of white rot fungi hundreds of millions of years ago, fungi were not capable of breaking down lignin, and the undecayed plant mass became the basis of large coal deposits.

"Together these studies tell a story about how mushroom-forming fungi evolved a complex mechanism for breakdown of plant cell walls in 'white rot' and then cast it aside following the evolution of mycorrhizal associations, as well as the alternative decay mechanism of 'brown rot,'" Hibbett said. "The other major part of the story is that in mycorrhizal lineages there is a huge turnover in genes that are upregulated in the symbiosis-many of these have no homologs in even closely related species, suggesting that the evolution of the symbiosis is associated with massive genetic innovation."

Martin chimed in: "Many of these genes are likely used to control plant immunity during the massive colonization of root tissues by the fungus."

DOE JGI's Igor Grigoriev also pointed out, "This first large-scale study of mycorrhizal genomics is also the first step in both broader and deeper exploration of mycorrhizal diversity, their interactions with host plans, and roles in forest ecosystems using genomics tools, which are the focus areas for the JGI Fungal Genomics Program."

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