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Newly discovered insect genus 'Supersonus' has 150kHz ultrasound mating call

Newly discovered insect genus 'Supersonus' has 150kHz ultrasound mating call | Amazing Science |
In the rainforests of South America, scientists have discovered a new genus and three new species of insect with the highest ultrasonic calling songs ever recorded in the animal kingdom. The insects have lost the ability of flight due to their reduced wing size, so the adoption of extreme ultrasonic frequencies might play a role in avoiding predators, such as bats.

Katydids (or bushcrickets) are insects known for their acoustic communication, with the male producing sound by rubbing its wings together (stridulation) to attract distant females for mating.

Scientists from the universities of Lincoln, Strathclyde and Toronto located a new genus with three new species of katydid in the rainforests of Colombia and Ecuador. These insects were found to produce the highest ultrasonic calling songs known in nature, with males reaching 150 kHz. The calling frequencies used by most katydids range between 5 kHz and 30 kHz. The nominal human hearing range ends at around 20 kHz. For this reason, the new genus has been named Supersonus.

Dr Fernando Montealegre-Z, from the School of Life Sciences, University of Lincoln, UK, said: "To call distant females, male katydids produce songs by 'stridulation' where one wing (the scraper) rubs against a row of 'teeth' on the other wing. The scraper is next to a vibrating drum that acts like a speaker. The forewings and drums are unusually reduced in size in the Supersonus species, yet they still manage to be highly ultrasonic and very loud."

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Cancer-resistant blind mole rat gets its genome sequenced

Cancer-resistant blind mole rat gets its genome sequenced | Amazing Science |

Scientists have sequenced the genome of the blind mole rat, a mammal that digs with its teeth, has skin over its eyes and lives for more than 20 years. It is also resistant to cancer, like its distant cousin the naked mole rat.

Among the results were what the researchers believe are the genetic signatures of the mole rat's complete loss of vision and its impressive tolerance of low oxygen (or "hypoxia"). They also discovered how its special cancer-fighting mechanism might have evolved.

One of the study's lead authors, Prof Eviatar Nevo from the University of Haifa in Israel, has studied blind mole rats for more than 50 years. In all of that time, a spontaneous tumour has never been discovered.

Even when treated with carcinogenic chemicals, these remarkable rodents were incredibly resistant to cancer.

Most animals rely on cells detecting a cancerous malfunction and shutting themselves down (programmed cell death or "apoptosis"), but the blind mole rat's immune system attacks tumours and causes "necrosis" instead. The new study reports that genes involved in this immune defence have been favoured by evolution, and some have been expanded or duplicated.

All this may have happened because one of the key mediators of the normal cell-shutdown defence, a protein called p53, is mutated in the mole rats as part of their adaptation to low oxygen.

The mole rat spends its entire life under the ground, where oxygen is scarce. In other animals this would send p53 into overdrive. "When there is low oxygen, in other species, normal p53 would mean that some cells would die from apoptosis - but not in blind mole rats, because that would be a disaster," said Dr Denis Larkin from the Royal Veterinary College in London, one of the study's authors.

So the mole rats have evolved a unique trade-off, weakening p53 and boosting the immune system's necrotic defence, which "the cancer doesn't know how to deal with," Dr Larkin. 

The blind mole rat (the newly sequenced species is Spalax galili) is only distantly related to the naked mole rat (Heterocephalus glaber), another unusual, subterranean critter with remarkable cancer resistance.

Their evolutionary histories diverged over 70 million years ago, according to calculations in the new study, and the two mole rats adapted completely separately to life underground.

The new work, published in the journal Nature Communications, will help unpick those secrets and the wider adaptation of animals to difficult environments.

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Single nucleotide mutation in c-KIT ligand gene is responsible for blond hair trait

Single nucleotide mutation in c-KIT ligand gene is responsible for blond hair trait | Amazing Science |
HHMI researchers find that a single-letter change in the genetic code is enough to generate blond hair in humans.

Genomic surveys by other groups had revealed that the gene – Kit ligand – is indeed evolutionarily significant among humans. “The very same gene that we found controlling skin color in fish showed one of the strongest signatures of selection in different human populations around the world,” Kingsley says. His team went on to show that in humans, different versions of Kit ligand were associated with differences in skin color.

Furthermore, in both fish and humans, the genetic changes associated with pigmentation differences were distant from the DNA that encodes the Kit ligand protein, in regions of the genome where regulatory elements lie. “It looked like regulatory mutations in both fish and humans were changing pigment,” Kingsley says.

Kingsley's subsequent stickleback studies have shown that when new traits evolve in different fish populations, changes in regulatory DNA are responsible about 85 percent of the time. Genome-wide association studies have linked many human traits to changes in regulatory DNA, as well. Tracking down specific regulatory elements in the vast expanse of the genome can be challenging, however.

“We have to be kind of choosy about which regulatory elements we decide to zoom in on,” Kingsley says. “We thought human hair color was at least as interesting as stickleback skin color.” So his team focused its efforts on a human pigmentation trait that has long attracted attention in history, art, and popular culture.

Kit ligand encodes a protein that aids the development of pigment-producing cells, so it made sense that changing its activity could affect hair or skin color. But the Kit ligand protein also plays a host of other roles throughout the body, influencing the behavior of blood stem cells, sperm or egg precursors, and neurons in the intestine. Kingsley wanted to know how alterations to the DNA surrounding this essential gene could drive changes in coloration without comprising Kit ligand's other functions.

Catherine Guenther, an HHMI research specialist in Kingsley's lab, began experiments to search for regulatory switches that might specifically control hair color. She snipped out segments of human DNA from the region implicated in previous blond genetic association studies, and linked each piece to a reporter gene that produces a telltale blue color when it is switched on. When she introduced these into mice, she found that one piece of DNA switched on gene activity only in developing hair follicles.

“When we found the hair follicle switch, we could then ask what's different between blonds and brunettes in northern Europe,” Kingsley said. Examining the DNA in that regulatory segment, they found a single letter of genetic code that differed between individuals with different hair colors.

Their next step was to test each version's effect on the activity of the Kit ligand gene. Their preliminary experiments, conducted in cultured cells, indicated that placing the gene under the control of the “blond” switch reduced its activity by about 20 percent, as compared to the "brunette" version of the switch. The change seemed slight, but Kingsley and Guenther suspected they had identified the critical point in the DNA sequence.

The scientists next engineered mice with a Kit ligand gene placed under the control of the brunette or the blond hair enhancer. Using technology developed by Liqun Luo, who is also an HHMI investigator at Stanford, they were able to ensure that each gene was inserted in precisely the same way, so that a pair of mice differed only by the single letter in the hair follicle switch—one carrying the ancestral version, the other carrying the blond version.

“Sure enough, when you look at them, that one base pair is enough to lighten the hair color of the animals, even though it is only a 20 percent difference in gene expression,” Kingsley says. “This is a good example of how fine-tuned regulatory differences may be to produce different traits. The genetic mechanism that controls blond hair doesn't alter the biology of any other part of the body. It's a good example of a trait that's skin deep—and only skin deep.”

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The crab-castrating parasite that zombifies its prey

The crab-castrating parasite that zombifies its prey | Amazing Science |
Meet Sacculina carcini – a barnacle that makes a living as a real-life body-snatcher of crabs. Unlike most barnacles that are happy to simply stick themselves to a rock and filter food from the water, Sacculina and its kin have evolved to be parasitic, and they are horrifyingly good at it.

The microscopic larva of Sacculina seeks out an unsuspecting crab using specialised sensory organs. It then settles on a part of the crab where its armours is most vulnerable, usually on the membrane at the base of one of the crab's hair (called a setae).

The larvae then transforms itself into a kind of living hypodermic syringe (called a kentrogon). This syringe stabs the base of the crab's hair and injects the next stage of the parasite – a microscopic blob called the vermigon – into the crab's bloodstream. This blob will eventually grow into a parasite that takes over the crab's entire body.

The body of the fully mature Sacculina is unrecognisable as a barnacle (or any animal for that matter) – it consists of a part called the interna which looks more like the roots of a plant than any animal. Its tendrils spread throughout the crab's insides and the only part of the parasite which is visible on the outside is the externa – the female reproductive organ which protrudes from the crab's abdomen.

Sacculina takes over the host in both body and mind – it castrates the crab, then turns it into a doting babysitter that grooms and aerates the barnacle's brood, tending the next generation of baby-snatchers as if they were its own babies. Lest you think Sacculina is alone in its nightmarish ways, it is just one genus in an entire order of barnacles called Rhizocephala (the "root head").

recent study found the effects these parasites have on the host's behaviour also affect the rest of the ecosystem. On the coast of South Carolina lives the flatback mud crab (Eurypanopeus depressus), where it is infected with a species of rhizocephalan call Loxothylacus panopei. Usually, the mud crab has an omnivorous diet and sometimes feeds on mussels, using their claws to pry open the shells. But crabs that are infected with L. panopei lose their appetite for such fare.

When confronted with a pile of mussels, uninfected crabs treat it as an all-you-can-eat seafood buffet, and eat as much as they can without hesitation. The more mussels they are presented with, the more they eat. But no matter how many mussels you offered to crabs infected with L. panopei, they simply eat one and call it a day. The parasitised crabs also took longer to get their act together and this seems to be related to the size of the parasite – the larger the parasite has grown, the longer the crab takes to start digging into a mussel.

Based on a field survey of the estuary where the study took place, the researchers concluded that about a fifth of the crab at that location were infected with L. panopei. Given the effects that L. panopei has on a crab's appetite for shellfish, it seems that the mussels might have an unlikely ally in the form a parasitic barnacle. The finding of this study share some parallels with a species of muscle-wasting parasite that curbs the appetite of an otherwise ravenous freshwater shrimp which has become invasive in parts of Europe and the UK.

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Species disappearing at least 1,000 times faster than they did before humans arrived

Species disappearing at least 1,000 times faster than they did before humans arrived | Amazing Science |

A new study looks at past and present rates of extinction and finds a lower rate in the past than scientists had thought. Species are now disappearing from Earth about 10 times faster than biologists had believed, said study lead author noted biologist Stuart Pimm of Duke University. Species of plants and animals are becoming extinct at least 1,000 times faster than they did before humans arrived on the scene, and the world is on the brink of a sixth great extinction, the new study says.

"We are on the verge of the sixth extinction," Pimm said from research at the Dry Tortugas. "Whether we avoid it or not will depend on our actions."

The work, published Thursday by the journal Science, was hailed as a landmark study by outside experts.

Numerous factors are combining to make species disappear much faster than before, said Pimm and co-author Clinton Jenkins of the Institute of Ecological Research in Brazil. But the No. 1 issue is habitat loss. Species are finding no place to live as more places are built up and altered by humans. Add to that invasive species crowding out native species, climate change affecting where species can survive, and overfishing, Pimm said.

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Wasp uses zinc-tip drill to lay eggs

Wasp uses zinc-tip drill to lay eggs | Amazing Science |

Video footage captured by scientists has revealed the power of a parasitic wasp, which has evolved a zinc-tipped drill to bore into fruit. The wasps penetrate the fruit in order to lay their eggs inside. A team from the Indian Institute of Science in Bangalore found that wasps' fruit-drilling and egg-laying tool - which is thinner than a human hair - has teeth enriched with zinc. The researchers' study is published in the Journal of Experimental Biology.

The female parasitic fig wasp bores its way through a tough, unripe fig to find the larvae of other pollinating insects already developing inside. Its own offspring will then feed on these larvae as they develop within the safety of the fig.

Taking measurements from this tiny drill bit, Dr. Gundiah, member of the research team, said, revealed the presence of zinc, and that it "was only at these teeth-like structures. "So we think the zinc is there to harden the tips."

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Mice with MS-like condition walk again after neural stem-cell treatment

Mice with MS-like condition walk again after neural stem-cell treatment | Amazing Science |

When scientists transplanted human neural stem cells into mice with multiple sclerosis (MS), within a remarkably short period of time, 10 to 14 days, the mice had regained motor skills.

Six months later, they showed no signs of slowing down.

Results from the study demonstrate that the mice experience at least a partial reversal of symptoms. Immune attacks are blunted, and the damaged myelin is repaired, explaining their dramatic recovery.

The finding, which uncovers potential new avenues for treating MS, was published May 15, 2014 in the journal Stem Cell Reports (open access).

How they did it: Ronald Coleman (a graduate student of Jeanne Loring, Ph.D., co-senior author and director of the Center for Regenerative Medicine at The Scripps Research Institute and co-first author on the publication) changed the normal protocol and grew the neural stem cells so they were less crowded on a Petri dish than usual.

That yielded a human neural stem cell type that turned out to be extremely potent. The experiments have since been successfully repeated with cells produced under the same conditions, but by different laboratories.

The human neural stem cells send chemical signals that instruct the mouse’s own cells to repair the damage caused by MS. Experiments by Lane’s team suggest that TGF-beta proteins comprise one type of signal, but there are likely others. This realization has important implications for translating the work to clinical trials in the future.

“Rather than having to engraft stem cells into a patient, which can be challenging from a medical standpoint, we might be able to develop a drug that can be used to deliver the therapy much more easily,” said Tom Lane, Ph.D., a professor of pathology at the University of Utah.

With clinical trials as the long-term goal, the next steps are to assess the durability and safety of the stem cell therapy in mice. “We want to try to move as quickly and carefully as possible,” he said. “I would love to see something that could promote repair and ease the burden that patients with MS have.”

“The aspect I am most interested is to define what is being secreted from the human cells that influence demyelination,” Lane told KurzweilAI in an email interview. “Other studies have shown either effects on neuroinflammation or demyelination; ours is one of a select few to show that stem cells influence both.”

However, it is too soon to say when can we expect this innovation to be available for MS patients, Lane added.

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New Details on Microtubules and How the Anti-Cancer Drug Taxol Works

New Details on Microtubules and How the Anti-Cancer Drug Taxol Works | Amazing Science |

A pathway to the design of even more effective versions of the powerful anti-cancer drug Taxol has been opened with the most detailed look ever at the assembly and disassembly of microtubules, tiny fibers of tubulin protein that form the cytoskeletons of living cells and play a crucial role in mitosis. Through a combination of high-resolution cryo-electron microscopy (cryo-EM) and new methodology for image analysis and structure interpretation, researchers with the Lawrence Berkeley National Laboratory (Berkeley Lab) and the University of California (UC) Berkeley have produced images of microtubule assembly and disassembly at the unprecedented resolution of 5 angstroms (Å). Among other insights, these observations provide the first explanation of Taxol’s success as a cancer chemotherapy agent.

“This is the first experimental demonstration of the link between nucleotide state and tubulin conformation within the microtubules and, by extension, the relationship between tubulin conformation and the transition from assembled to disassembled microtubule structure,” says Eva Nogales, a biophysicist with Berkeley Lab’s Life Sciences Division who led this research. “We now have a clear understanding of how hydrolysis of guanosine triphosphate (GTP) leads to microtubule destabilization and how Taxol works to inhibit this activity.”

During mitosis, the process by which a dividing cell duplicates its chromosomes and distributes them between two daughter cells, microtubules disassemble and reform into spindles across which the duplicate sets of chromosomes migrate. For chromosome migration to occur, the microtubules attached to them must disassemble, carrying the chromosomes in the process. The crucial ability of microtubules to transition from a rigid polymerized or “assembled” state to a flexible depolymerized or “disassembled” state – called “dynamic instability” – is driven by GTP hydrolysis in the microtubule lattice. Taxol prevents or dramatically slows down the unchecked cell division that is cancer by binding to a microtubule in such a manner as to block the effects of hydrolysis. However, until now the atomic details as to how microtubules transition from polymerized to depolymerized structures and the role that Taxol can play have been sketchy.

The tubulin protein is a heterodimer consisting of alpha (α) and beta (β) monomer subunits. It features two guanine nucleotide binding sites, an “N-site” on the α-tubulin that is buried, and an “E-site” on the β-tubulin that is exposed when the tubulin is depolymerized. Previous microtubule reconstruction studies were unable to distinguish the highly similar α-tubulin and β-tubulin from each other.

Nogales and her colleagues found that GTP hydrolysis and the release of the phosphate (GTP becomes GDP) leads to a compaction of the E-site and a rearrangement of the α-tubulin monomer that generates a strain on the microtubule that destabilizes its structure. Taxol binding leads to a reversal of this E-site compaction and α-tubulin rearrangement that restores structural stabilization.

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Immunocamouflage lets donor blood cells go undetected

Immunocamouflage lets donor blood cells go undetected | Amazing Science |

A bio-inspired approach to creating universal red blood cells. 

Chinese scientists are developing a new approach to create “universal” blood: red blood cells (RBCs) that can be transfused into any patient, regardless of the patient's or recipient's blood group.

Blood groups are characterised by the presence (or absence) of various proteins known as antigens on the surface of RBCs, the most well-known of which form the ABO system and the Rhesus D (RhD) system. One consequence of the existence of these groups is that blood mismatching can occur when an incompatible blood group is used for transfusion. The recipient’s antibodies recognise the antigens on the donor RBCs as being foreign and attack the cells – with potentially fatal results.

Several approaches have been investigated in the past to strip RBCs of their antigen identity, such as chemical cleavage of the antigens, disruption of antigen–antibody binding by grafted poly(ethylene glycol) molecules or ex vivo production of universal RBCs from genetically engineered hematopoitic stem cells, but each of these methods has its downfalls. Ruikang Tang and co-workers, from Zheijiang University, have used a simple method to mask the ABO group antigens by chemically modifying the RBC surface with polydopamine (PDA), a mimic of the bioadhesive produced by the mussel Mytilus edulis.

‘The concept is very clever because the coatings can be performed in situ using dopamine as a precursor molecule,’ says Christopher Bettinger, a biomaterials researcher from Carnegie Mellon University in the US. ‘The resulting polydopamine coating is therefore composed of materials that already exist in the human body.’

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Thousands of bacteria have hitchhiked to Mars on the Curiosity Rover

Thousands of bacteria have hitchhiked to Mars on the Curiosity Rover | Amazing Science |

Bacteria found on the Curiosity rover reveal the types of microorganisms that spacecrafts carry.

Dozens of microbial species may have accompanied the Curiosity rover to Mars, where it landed in August 2012. The stowaways withstood spacecraft cleaning methods before the rover's launch, although no one knows for sure whether the bacteria survived the inter-planetary ride.

A study that identified 377 strains found that a surprising number resist extreme temperatures and damage caused by ultraviolet-C radiation, the most potentially harmful type. The results, presented today at the annual meeting of the American Society for Microbiology, are a first step towards elucidating how certain bacteria might survive decontamination and space flight.

The work tells scientists a lot “about the kind of microbes that could be space explorers”, says evolutionary ecologist John Rummel of East Carolina University in Greenville, North Carolina, who was not involved in the research.

Swabs of Curiosity’s surfaces before it was launched, including its heat shield and flight system, revealed 65 species of bacteria. Most were related to the genus Bacillus. In the lab, scientists exposed the microbes to desiccation, UV exposure, cold and pH extremes. Nearly 11% of the 377 strains survived more than one of these severe conditions. Thirty-one per cent of the resistant bacteria did not form tough, protective spore coats; the researchers suspect that they used other biochemical means of protection, such as metabolic changes.

“When we embarked on these studies there wasn’t anything known about the organisms in this collection,” says microbiologist Stephanie Smith of the University of Idaho in Moscow, who is the lead author on the work. The group now plans to study how the most resilient of the identified bacteria survive in extreme environments.

Identifying resilient microbial species helps to gauge actual levels of contamination on such spacecraft. Planetary scientists worry that hitchhiking microbes could, in principle, contaminate Mars soil, or possibly taint rock samples collected as part of future missions — hence providing false signs of life on the red planet.

Although spacecraft go through multiple cleaning steps to ensure that they bear no biological contaminants, previous reports suggest that Curiosity project developers did not follow these planetary protection protocols to the letter. The regulations are a safeguard; whether microbes can tolerate conditions on the surface of Mars is still unknown.

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Hotter climate could turn sea turtles all female

Hotter climate could turn sea turtles all female | Amazing Science |

Sea turtles are likely to be beneficiaries of a warming climate as hotter incubation conditions trigger a rising share of female hatchlings that could lift natural rates of population growth, new research to be published in Nature Climate Change on Monday shows.

But gains will be temporary if temperatures keep rising and nudge populations towards becoming all female, or exceed levels at which developing embryos die, the study found. ''There'll be a bit of a breathing space … but down the track it'll be serious,'' said Graeme Hays from Deakin University, one of the report's authors.

It has been known for decades that reptile reproduction is highly sensitive to temperature, with the ratio of male to female offspring varying. For species of sea-turtles, the pivotal temperature is an oddly uniform 29 degrees for incubation, beyond which more females emerge from the eggs.

At about 30.5 degrees, populations become fully female. As remaining males die off, ''it will be end of story without human intervention'', Professor Hays said. At higher than 33 degrees, embryos do not survive.

The study focused on a globally important loggerhead turtle rookery on the Cape Verde Islands in the Atlantic but its results also apply to species elsewhere, including the Pacific. It found light-coloured sandy beaches already produce 70.1 per cent females, while beaches with darker sands are at 93.5 per cent.

The findings should help steer conservation efforts to make a priority of protecting lighter-coloured sandy beaches or planting more vegetation near dark ones to ameliorate the warming, Professor Hays said. 

Since breeding populations are likely to swell in coming decades, sea turtle adult populations are ''unlikely to be dire in the next 150 years'', the paper said.

Professor Hays said any near-term increase in turtles would be modest compared with past populations. Green turtles in the Caribbean, for instance, are ''a fraction of 1 per cent'' of their original numbers.

Other changes linked to global warming, including effects on food sources, will also likely offset some of the benefits of having more breeding females, he said.

''Rising sea levels resulting in the loss of nesting beaches through erosion could push local turtle populations over the brink unless new suitable nesting beaches are found,'' the paper said.

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Science explains why octopus arms don't stick together

Science explains why octopus arms don't stick together | Amazing Science |

Octopus arms can grab onto just about any smooth surface with ease and, for the most part, they do so without communicating their location to the brain. This ability has turned them into darlings of the robotics industry, which has made numerous attempts to reproduce their underwater grasping abilities. Yet, despite all the work that has gone into deciphering the mechanics of octopus suckers, researchers have never asked one seemingly glaring question: how do octopuses avoid getting their suckers stuck to their own skin if they have no idea where their arms are most of the time?

According to a new study published today in Current Biology, the answer is chemical. Through a series of experiments, researchers were able to figure out that octopuses produce molecules in their skin that prevent their arms from getting tangled. Moreover, under certain conditions, these animals are able to stop those molecules from doing their thing in order to grasp other octopuses. "Everybody knew the lack of knowledge in octopus arms, but nobody wanted to investigate this," says Guy Levy, a neuroscientist at the Hebrew University of Jerusalem and a co-author of the study. "Now we know that they have a built-in mechanism that prevents them from grabbing octopus skin."

To study this phenomenon, the researchers came up with a number of novel experiments, most of which involved watching amputated octopus arms grab various objects. "An octopus arm is lively for more than an hour after amputation," Levy says, and they retain the ability to attach to "just about anything" during that period. But even when separated from the rest of its body, octopus arms are still unable to grasp fresh octopus skin — whether it's attached to an octopus or not. "We thought that the reason might be electrical," Levy says, but the amputated arms had no trouble grabbing onto skinned octopus arms, so an electrical mechanism seemed unlikely.

In another experiment, the researchers demonstrated that the mechanism wasn't texture or electricity related because the amputated arms couldn't grab "reconstructed skin" that had been broken down to its constituent molecules and embedded in a gel. Thus, only one possibility remained: a chemical one. Unfortunately, there's still a lot that the researchers don't know. "We do not know which molecules are involved," Levy says, "but we do know that molecules in the skin are sensed in the suckers and this inhibits the attachment behavior." This, the researchers think, is a "built-in program" that stays on after the arms are amputated. When an arm is still attached to its owner, however, "the brain can decide to cancel the program and force the arm to grab the skin."

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A single female-specific piRNA is the primary determiner of sex in the silkworm

A single female-specific piRNA is the primary determiner of sex in the silkworm | Amazing Science |

The silkworm Bombyx mori uses a WZ sex determination system that is analogous to the one found in birds and some reptiles. In this system, males have two Z sex chromosomes, whereas females have Z and W sex chromosomes. The silkworm W chromosome has a dominant role in female determination12, suggesting the existence of a dominant feminizing gene in this chromosome. However, the W chromosome is almost fully occupied by transposable element sequences345, and no functional protein-coding gene has been identified so far. Female-enriched PIWI-interacting RNAs (piRNAs) are the only known transcripts that are produced from the sex-determining region of the W chromosome6, but the function(s) of these piRNAs are unknown. A team of scientists now show that a W-chromosome-derived, female-specific piRNA is the feminizing factor of B. mori. This piRNA is produced from a piRNA precursor which was named FemInhibition of Fem-derived piRNA-mediated signalling in female embryos led to the production of the male-specific splice variants of B. mori doublesex (Bmdsx), a gene which acts at the downstream end of the sex differentiation cascade78. A target gene of Fem-derived piRNA was identified on the Z chromosome of B. mori. This gene, named Masc, encodes a CCCH-type zinc finger protein. The research team was able to show that the silencing of Masc messenger RNA by Fem piRNA is required for the production of female-specific isoforms of Bmdsx in female embryos, and that Masc protein controls both dosage compensation and masculinization in male embryos. This study demonstrates that a single small RNA that is responsible for primary sex determination in the WZ sex determination system.

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Cellular traffic control system mapped for the first time

Cellular traffic control system mapped for the first time | Amazing Science |

Cells regulate the uptake of nutrients and messenger cargos and their transport within the cell. This process is known as endocytosis and membrane traffic. Different cargos dock onto substrate specific receptors on the cell membrane. Special proteins such as kinases, GTPases and coats, activate specific entry routes and trigger the uptake of the receptors into the cell. For their uptake, the receptors and docked cargos become enclosed by the cell membrane. In the next steps, the membrane invaginates and becomes constricted. The resulting vesicle is guided via several distinct stations, cellular organelles, to its final destination in the cell.

For her study, Dr. Prisca Liberali, senior scientist in the team of Professor Lucas Pelkmans, sequentially switched off 1200 human genes. Using automated high-throughput light microscopy and computer vision, she could monitor and compare 13 distinct transport paths involving distinct receptors and cellular organelles. Precise quantifications of thousands of single cells identified the genes required for the different transport routes. Surprisingly, sets of transport routes are co-regulated and coordinated in specific ways by different programs of regulatory control.

Subsequently, Dr. Liberali calculated the hierarchical order within the genetic network and thereby identified the regulatory topology of cellular transport. "The transport into the cell and within the cells proceeds analogously to the cargo transport within a city" describes the scientist. "Like in a city, the traffic on the routes within a cell and their intersections is tightly regulated by traffic lights and signs to guide the cargo flow."

Thanks to this unique quantitative map, the fine regulatory details of transport paths and processes within a cells could be mapped for the first time. Particularly the genes that encode for these traffic lights and switches are often de-regulated in disease. With this map, it is now possible to predict how this leads to traffic jams in the cells, causing the disease phenotype. Alternatively, since many drugs have been developed to target these traffic lights and switches, the map can be used to come up with possible drug combinations to target unwanted traffic, such as viruses, to the waste disposal system of the cell.

ComplexInsight's curator insight, June 9, 11:44 PM

Mapping the fine regulatory details of transport paths and processes within cells is key to understanding gene and protein functions, cancer, viral interactions and potential treatments.  Interesting read.

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Spiders know the meaning of "web music" made by vibrations of entangled prey, wind and mates

Spiders know the meaning of "web music" made by vibrations of entangled prey, wind and mates | Amazing Science |
Spider silk transmits vibrations across a wide range of frequencies so that, when plucked like a guitar string, its sound carries information about prey, mates, and even the structural integrity of a web.

The discovery was made by researchers from the Universities of Oxford, Strathclyde, and Sheffield who fired bullets and lasers at spider silk to study how it vibrates. They found that, uniquely, when compared to other materials, spider silk can be tuned to a wide range of harmonics. The findings, to be reported in the journal Advanced Materials, not only reveal more about spiders but could also inspire a wide range of new technologies, such as tiny light-weight sensors.

'Most spiders have poor eyesight and rely almost exclusively on the vibration of the silk in their web for sensory information,' said Beth Mortimer of the Oxford Silk Group at Oxford University, who led the research. 'The sound of silk can tell them what type of meal is entangled in their net and about the intentions and quality of a prospective mate. By plucking the silk like a guitar string and listening to the ‘echoes’ the spider can also assess the condition of its web.' 

This quality is used by the spider in its web by 'tuning' the silk: controlling and adjusting both the inherent properties of the silk, and the tensions and interconnectivities of the silk threads that make up the web. To study the sonic properties of the spider's gossamer threads the researchers used ultra-high-speed cameras to film the threads as they responded to the impact of bullets. In addition, lasers were used to make detailed measurements of even the smallest vibration.

'The fact that spiders can receive these nanometre vibrations with organs on each of their legs, called slit sensillae, really exemplifies the impact of our research about silk properties found in our study,' said Dr Shira Gordon of the University of Strathclyde, an author involved in this research.

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How to erase a memory –- and restore it: Researchers reactivate memories in rats

How to erase a memory –- and restore it: Researchers reactivate memories in rats | Amazing Science |
Researchers have erased and reactivated memories in rats, profoundly altering the animals’ reaction to past events. The study is the first to show the ability to selectively remove a memory and predictably reactivate it by stimulating nerves in the brain at frequencies that are known to weaken and strengthen the connections between nerve cells, called synapses.

Researchers at the University of California, San Diego School of Medicine have erased and reactivated memories in rats, profoundly altering the animals' reaction to past events.

The study, published in the June 1 advanced online issue of the journal Nature, is the first to show the ability to selectively remove a memory and predictably reactivate it by stimulating nerves in the brain at frequencies that are known to weaken and strengthen the connections between nerve cells, called synapses.

"We can form a memory, erase that memory and we can reactivate it, at will, by applying a stimulus that selectively strengthens or weakens synaptic connections," said Roberto Malinow, MD, PhD, professor of neurosciences and senior author of the study.

Scientists optically stimulated a group of nerves in a rat's brain that had been genetically modified to make them sensitive to light, and simultaneously delivered an electrical shock to the animal's foot. The rats soon learned to associate the optical nerve stimulation with pain and displayed fear behaviors when these nerves were stimulated.

Analyses showed chemical changes within the optically stimulated nerve synapses, indicative of synaptic strengthening.

In the next stage of the experiment, the research team demonstrated the ability to weaken this circuitry by stimulating the same nerves with a memory-erasing, low-frequency train of optical pulses. These rats subsequently no longer responded to the original nerve stimulation with fear, suggesting the pain-association memory had been erased.

In what may be the study's most startlingly discovery, scientists found they could re-activate the lost memory by re-stimulating the same nerves with a memory-forming, high-frequency train of optical pulses. These re-conditioned rats once again responded to the original stimulation with fear, even though they had not had their feet re-shocked.

"We can cause an animal to have fear and then not have fear and then to have fear again by stimulating the nerves at frequencies that strengthen or weaken the synapses," said Sadegh Nabavi, a postdoctoral researcher in the Malinow lab and the study's lead author.


  1. Sadegh Nabavi, Rocky Fox, Christophe D. Proulx, John Y. Lin, Roger Y. Tsien and Roberto Malinow. Engineering a memory with LTD and LTPNature, 2014 DOI:10.1038/nature13294
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Amber discovery indicates Lyme disease is older than human race

Amber discovery indicates Lyme disease is older than human race | Amazing Science |
Lyme disease is a stealthy, often misdiagnosed disease that was only recognized about 40 years ago, but new discoveries of ticks fossilized in amber show that the bacteria which cause it may have been lurking around for 15 million years -- long before any humans walked on Earth. The findings were made by researchers who studied 15-20 million-year-old amber from the Dominican Republic that offer the oldest fossil evidence ever found of Borrelia, a type of spirochete-like bacteria that to this day causes Lyme disease.

"Ticks and the bacteria they carry are very opportunistic," said George Poinar, Jr., a professor emeritus in the Department of Integrative Biology of the OSU College of Science, and one of the world's leading experts on plant and animal life forms found preserved in amber. "They are very efficient at maintaining populations of microbes in their tissues, and can infect mammals, birds, reptiles and other animals.

"In the United States, Europe and Asia, ticks are a more important insect vector of disease than mosquitos," Poinar said. "They can carry bacteria that cause a wide range of diseases, affect many different animal species, and often are not even understood or recognized by doctors. "It's likely that many ailments in human history for which doctors had no explanation have been caused by tick-borne disease."

Lyme disease is a perfect example. It can cause problems with joints, the heart and central nervous system, but researchers didn't even know it existed until 1975. If recognized early and treated with antibiotics, it can be cured. But it's often mistaken for other health conditions. And surging deer populations in many areas are causing a rapid increase in Lyme disease -- the confirmed and probable cases of Lyme disease in Nova Scotia nearly tripled in 2013 over the previous year.

The new research shows these problems with tick-borne disease have been around for millions of years.

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The Hoosier Cavefish, a newly discovered cavefish from the caves of southern Indiana

The Hoosier Cavefish, a newly discovered cavefish from the caves of southern Indiana | Amazing Science |

A new eyeless cavefish is described from Indiana and named after the Indiana Hoosiers. It is the first new cavefish species described from the U.S. in 40 years. Notably, it has an anus right behind its head, and the females brood their young in their gill chamber. The new species was described in the open access journal ZooKeys.

The new speciesAmblyopsis hoosieri, is the closest relative of a species (A. spelaea) from the longest cave system in the world, Mammoth Cave in Kentucky. These two species are separated by the Ohio River, which also separates the states of Indiana and Kentucky.

The species from south of the Ohio River, A. spelaea, has a knockout mutation in the genetic sequence of rhodopsin, a gene important in vision. The new species, on the other hand, lacks this mutation and maintains a functional rhodopsin gene, despite lacking eyes and vision. The new species shows distinct morphological differences compared to its southern congener. It has a plumper, Bibendum-like body and shorter fins. It also has smaller mechanosensory neuromasts on papillae, which allow them to sense movement in the dark waters of the caves they are found in.

The authors decided to name the new species, A. hoosieri, the Hoosier Cavefish, not only after the Indiana Hoosiers team, but mainly to honor the proximity of the new species to Indiana University and several famed ichthyologists who worked there. "The senior author of the manuscript is a fervent fan of Indiana Hoosier basketball, but the first author is an alumni of the University of Michigan and is not. Also notable is that the middle author of the publication is currently an undergraduate at Louisiana State University." explain the authors.

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Molecular crowding: Simple nucleic acid and protein folding may be sped up by 400,000 percent inside cells

Molecular crowding: Simple nucleic acid and protein folding may be sped up by 400,000 percent inside cells | Amazing Science |

Crowding has notoriously negative effects at large size scales, blamed for everything from human disease and depression to community resource shortages. But relatively little is known about the influence of crowding at the cellular level. A new JILA study shows that a crowded environment has dramatic effects on individual biomolecules.

In the first data on the underlying dynamics (or kinetics)of crowded single biomolecules , reported in Proceedings of the National Academy of Sciences,* JILA researchers found that crowding leads to a 35-fold increase in the folding rate of RNA (ribonucleic acid), while the unfolding rate remains relatively stable.

RNA is a long chain-like molecule that contains genetic information, makes proteins and catalyzes biological reactions. It must fold into the correct 3D shape to function properly. The new results show that while RNA usually spends most of its time unfolded, in a crowded situation it folds much more often, although it remains folded for the usual period of time during each round.

"Cells are 25 to 35 percent filled with 'stuff'—proteins, nucleic acids, lipids, etc.—and the effect of crowding on simple reactions like folding of nucleic acids and proteins is not well understood," JILA/NIST Fellow David Nesbitt says. "Almost all detailed kinetic data comes from in vitro studies, that is, not in a living cell.

"But our work at the single-molecule level suggests that the rates and equilibrium constants (where folding and unfolding rates are equal) for simple nucleic acid folding processes may be shifted by up to 400,000 percent or more from what one might expect from such uncrowded solution studies."

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Flies pause while 200 neurons help with tough decisions

Flies pause while 200 neurons help with tough decisions | Amazing Science |

They spend more time choosing between a strong and a weak smell if the difference is small. The research links this deliberation to a particular gene, FoxP, and the activity of fewer than 200 neurons.

Mutations in FoxP, also associated with cognition and language in humans, made flies' decisions even slower without affecting which choice they made.

Gathering information before committing to a decision is a hallmark of intelligence. If the information is unclear, the choice is trickier and the decision takes more time. We do it, other primates do it, even rats and mice do it - but now it seems that flies do too.

"This is the clearest evidence yet of a cognitive process running in a very simple brain," said Prof Gero Miesenböck, whose team did the work at the University of Oxford's Centre for Circuits and Behaviour.

"People tended to think of insects as tiny robots that just respond reflexively to signals from the environment. Now we know that's not true."

After training fruit flies to avoid a new smell at a specific intensity, the researchers offered them a choice between that dangerous odour level and a weaker one. The flies did well when the safe option was four or five times weaker, but chose randomly if the difference was only 10%.

Crucially, as the differences became smaller and trickier to distinguish, the flies took more and more time to make a decision, waiting much longer in an intermediate zone between the two odour levels.

This is a pattern that psychologists have studied for many decades. "The same mathematical models that describe human decision-making also capture the flies' behaviour perfectly," said Prof. Miesenböck.

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The biomechanics behind the amazing strength of an ant

The biomechanics behind the amazing strength of an ant | Amazing Science |

How can an ant lift objects many times heavier than its own body? Engineers at The Ohio State University combined computational modeling at the Ohio Supercomputer Center (OSC) and lab experiments to find out.

They focused on the ant’s neck — the single joint of soft tissue that bridges the stiff exoskeleton of the ant’s head and thorax. When an ant carries food or any other object, the neck joint supports the full weight of the load.

The researchers reverse-engineered the biomechanics of the neck by developing 3-D models of the of the ant’s internal and external anatomy from X-ray cross-section images (microCT) of ant specimens and loading the data into a modeling program (ScanIPþFE) that assembled the segments and converted them into a mesh frame model of more than 6.5 million elements.

The model then was loaded into a finite element analysis program (Abaqus), an application that creates accurate simulations of complex geometries and forces, and the data was processed on the powerful Oakley Cluster, an array of 8,300 processor cores (Intel Xeon) at the Ohio Supercomputer Center.

The experiments, published in the Journal of Biomechanics, revealed that the neck joints could withstand loads of about 5,000 times the ant’s body weight, and that the ant’s neck-joint structure produced the highest strength when its head was aligned straight, as opposed to turned to either side.

“Loads are lifted with the mouthparts, transferred through the neck joint to the thorax, and distributed over six legs and tarsi that anchor to the supporting surface,” explainedCarlos Castro, assistant professor of mechanical and aerospace engineering at Ohio State.

“While previous research has explored attachment mechanisms of the tarsi (feet), little is known about the relation between the mechanical function and the structural design and material properties of the ant.”

“Our results accurately pinpoint the stress concentration that leads to neck failure and identify the soft-to-hard material interface at the neck-to-head transition as the location of failure,” said Castro.

“The design and structure of this interface is critical for the performance of the neck joint. The unique interface between hard and soft materials likely strengthens the adhesion and may be a key structural design feature that enables the large load capacity of the neck joint.”

The simulations confirmed the joint’s directional strength and, consistent with the experimental results, indicated that the critical point for failure of the neck joint is at the neck-to-head transition, where soft membrane meets the hard exoskeleton.

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When Trilobites Ruled the World

When Trilobites Ruled the World | Amazing Science |
The remains of trilobites, a diverse group of marine animals much older than dinosaurs, are remarkably well preserved, providing fresh insights of their anatomies and social behavior.

Trilobites may be the archetypal fossils, symbols of an archaic world long swept beneath the ruthless road grader of time. But we should all look so jaunty after half a billion years.

At the Smithsonian’s National Museum of Natural History, Brian T. Huber, chairman of paleobiology, points to a flawless specimen of Walliserops, a five-inch trilobite that swam the Devonian seas around what is now Morocco some 150 million years before the first dinosaurs hatched. With its elongated, triple-tined head horn and a bristle brush of spines encircling its lower body, the trilobite could be a kitchen utensil for Salvador Dalí. Nearby is the even older Boedaspis ensifer, its festive nimbus of spiny streamers pointing every which way like the ribbons of a Chinese dancer.

In most trilobites, each compound orb held hundreds of tiny calcite lenses, arranged in a tightknit honeycomb pattern, like the eye of a fly. But fairly late in trilobite evolution one group developed a different sort of eye, composed of a smaller number of larger, separated calcite lenses. As they described last spring in the journal Scientific ReportsBrigitte Schoenemann of the Universities of Cologne and Bonn in Germany and Euan N. K. Clarkson of the University of Edinburgh, used advanced scanning techniques, including synchrotron radiation, to examine specimens of these later, larger-lensed trilobite eyes. On the back of the lenses, the scientists were astonished to see traces of the sensory receptor cells that once linked the eyes to the brain. “It was extraordinary,” Dr. Schoenemann said. “As far as we know, these are the oldest receptor cells that have ever been seen in any fossil animal.”

Analyzing the microstructure of the receptor tracings, the researchers concluded that the eyes were designed to work optimally in lowlight, murky conditions, a sign that some trilobites were turning reclusive, descending to deeper waters or burrowing farther into the mud to escape the proliferation of toothy marine predators and new crustacean competitors. Toward the end of the Paleozoic Era, the once-thriving trilobite tribe had been reduced to a scattering of species. And they, too, vanished in the great Permian extinction 252 million years ago.

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Human Antibodies Given Sharklike Armor to Fight Disease

Human Antibodies Given Sharklike Armor to Fight Disease | Amazing Science |

Therapeutic antibodies are potent tools for cancer diagnosis and treatment. The trouble has been that human antibodies are rather delicate. When drug companies make them, a lot break apart. Shark antibodies, in contrast, are robust. Now chemists have figured out the sources of that strength–some extra features in the proteins that work like Super Glue to keep them together. Building upon our shared and ancient evolutionary heritage, scientists have engineered those shark features into human antibodies and made cells produce them. More intact antibodies come out of these cells, and those antibodies withstand more damage.

“We found that a lot more of these antibodies passed through the cell’s quality control checkpoints,“ says Linda Hendershot, a biologist at St. Jude Children’s Research Hospital in Tennessee and one of the scientists behind the new research, published online May 15 in the Proceedings of the National Academy of Sciences.

The shark-human connection first took shape at the Technical University of Munich, where chemists Matthias Feige, Johannes Buchner and several colleagues began exploring shark antibody durability. This strength was somewhat remarkable because while a shark swims in the sea, its antibodies are swimming in a sea of urea. Urea is a substance famous for breaking down proteins. Yet sharks need lots of it because the substance keeps shark cells from losing water and becoming dehydrated. So antibodies need to resist this necessary evil.

The way they resist breakdown turned out to be part of their structure. The antibodies, which are long chains, fold and twist. The researchers made molecular images of shark antibodies called immunoglobulin new antigen receptors, and learned the proteins have two regions that act like strong glue, holding different segments together.

One region, Hendershot says, is known as a “salt bridge,” and it has a positive electrical charge at one end and a negative at the other. The opposites attract, like magnets, keeping the antibody from unfolding. The other region, Feige says, is a large water-repellent group of amino acids called a core. As they move away from water outside the antibody and towards one another, the acids exert more force holding the antibody together.

The scientists also learned that, while the shark and human antibodies were made of different sequences of components, their overall shapes were very similar. Their chains both featured the same “V” or hinge. The similarities gave the researchers confidence to try adding the shark features to human antibodies.

Using genetic engineering, the scientists modified shark genes that make the bridge and the core and added them to genes that make human antibodies. First they got bacteria to produce the converted antibodies, and then coaxed mammalian cells to do the same. They found that when both features were included—one alone wasn’t good enough—the antibodies resisted urea as well as other sources of breakdown, like high heat.

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Cicades Inherit Microbes From Male’s Sperm

Cicades Inherit Microbes From Male’s Sperm | Amazing Science |

The green rice leafhopper is never alone. When a female’s egg and a male’s sperm fuse into a new cell, that cell is already infected with bacteria. As the newly conceived leafhopper grows from one cell into millions, its internal bacteria—its endosymbionts—go along for the ride. Right from the start, the leafhopper isn’t an individual in its own right, but a collection of animal and microbes that live together.

Many insects and other animals inherit endosymbionts from their parents, but almost all of them do so from their mothers. There’s good reason for this. An egg cell is big. Its central nucleus, which contains its DNA, is surrounded by a spacious and roomy cytoplasm, which can house lots of bacteria. But a sperm cell has no cytoplasm, and its tiny head is all nucleus. This streamlined shape is good for swimming, but it’s terrible for packaging bacterial heirlooms. That’s why males almost never pass on endosymbionts to their kids, while females often do. Sperm just isn’t very good packing material.

But try telling that to the green rice leafhopper. This small green bug is a serious pests of rice plants in East Asia, and its cells are filled with at least three species of bacteria. And one of them—Rickettsia—can infect the insect’s sperm.

Kenji Watanabe and Hiroaki Noda from the National Institute of Agrobiological Sciences in Japan found that almost every one of the leafhopper’s sperm cells contains several copies of Rickettsia, with up to 23 microbes per head. The team have no idea how the bacteria gain entry, or why their presence doesn’t seem to harm or disable the sperm in any way. But they do know that if these infected sperm fertilise eggs, they can pass their copies of Rickettsia into the next generation.

This unique ability to transmit microbes via sperm could completely change the usual relationship between the insects and the bacteria. These partnerships are fairly straightforward if microbes are only passed down the maternal line. Every individual inherits a single strain of microbe, and they co-evolve in neat tandem. Buchnera, for example, lives inside the cells of aphids, and has been co-evolving with them for over 150 million years. If you draw the family tree ofBuchnera strains, it would look almost identical to the family tree of their aphid hosts.

But in the leafhopper, both males and females can pass Rickettsia to their offspring, so each individual could end up with different bacterial strains. “Co-infections are likely to introduce more conflict with the host” as strains compete with each other, says Nancy Moran from the University of Texas in Austin. Conflicts between harmless bacteria can potentially harm their hosts, as the adaptations that allow one microbe to best another can sometimes allow them to cause disease. If that’s true here, Rickettsia may flip from being a harmless (or even beneficial) partner into an enemy.

Jack Werren from Rochester University, who studies Wolbachia, says that the Japanese team found irrefutable evidence for sperm transmission, but their study also raises many questions. How doesRickettsia function inside the nucleus? And with its host’s DNA within easy reach, could it be manipulating the leafhopper’s genes?

And what’s Rickettsia doing inside its host? Is it a benign parasite, or is it actually helpful? Many endosymbionts provide their hosts with nutrients or defend them against parasites and diseases. Aphids, for example, cannot survive without BuchneraRickettsia, however, seems to be dispensable. When Watanabe and Noda cured the leafhoppers of their infections, the adult insects seemed fine.

But as Werren points out, the team only studied small numbers of the insects in their laboratory. It’s possible that Rickettsia might help the leafhoppers by protecting them from parasites, or even by detoxifying pesticides in their environment—benefits that would only reveal themselves in the wild.

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The Prevalence of Species and Strains in the Human Microbiome: A Resource for Experimental Efforts

The Prevalence of Species and Strains in the Human Microbiome: A Resource for Experimental Efforts | Amazing Science |

Experimental efforts to characterize the human microbiota often use bacterial strains that were chosen for historical rather than biological reasons. A team of scientists report now an analysis of 380 whole-genome shotgun samples from 100 subjects from the NIH Human Microbiome Project. By mapping their reads to 1,751 reference genome sequences and analyzing the resulting relative strain abundance in each sample they present metrics and visualizations that can help identify strains of interest for experimentalists. They also show that approximately 14 strains of 10 species account for 80% of the mapped reads from a typical stool sample, indicating that the function of a community may not be irreducibly complex. Some of these strains account for >20% of the sequence reads in a subset of samples but are absent in others, a dichotomy that could underlie biological differences among subjects. These data should serve as an important strain selection resource for the community of researchers who take experimental approaches to studying the human microbiota.

Via Mel Melendrez-Vallard
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