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Study suggests new way to help the immune system fight off Trypanosoma parasite

Study suggests new way to help the immune system fight off Trypanosoma parasite | Amazing Science | Scoop.it
Some infectious diseases are particularly difficult to treat because of their ability to evade the immune system. One such illness, African sleeping sickness, is caused by the parasite Trypanosoma brucei, transmitted by the tsetse fly, and is fatal if left untreated. The trypanosome parasite is transmitted to mammals through fly bites and eventually invades major organs such as the brain, disrupting the sleep cycle, among other symptoms.

Trypanosomes exist in different forms. When inhabiting a fly, they are covered with proteins called procyclins. Upon entering the bloodstream of a mammal, they acquire a dense layer of glycoproteins that continually change, allowing the parasite to dodge an attack from the host's immune system.

Now, new research from postdoctoral scientists Danae Schulz and Erik Debler, working in the Papavasiliou and Blobel labs at Rockefeller University, reveals a method to manipulate trypanosomes in the mammalian bloodstream to acquire fly stage characteristics, a state that makes it easier for the host immune system to eliminate the invader. The findings suggest that inhibiting specific proteins that interact with chromatin--the mass of DNA and proteins that packages a cell's genetic information--can "trick" the parasite into differentiating to a different stage of its lifecycle. The study is publishing on December 8 in the Open Access journal PLOS Biology.

"By blocking these chromatin-interacting proteins, we have found a way to make the parasite visible to the immune system," says Nina Papavasiliou, head of the Laboratory of Lymphocyte Biology. "The bloodstream form of the parasite is constantly switching protein coats, so the immune system can't recognize and eliminate it. This new method makes the parasite think it's in the fly, where it doesn't need to worry about the immune system attacking it."
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Why mice have longer sperm than elephants

Why mice have longer sperm than elephants | Amazing Science | Scoop.it

In the animal world, if several males mate with the same female, their sperm compete to fertilize her limited supply of eggs. Longer sperm often seem to have a competitive advantage. However, a study conducted by researchers from the Universities of Zurich and Stockholm now reveals that the size of the animals also matters. The larger the animal, the more important the number of sperm is relative to sperm length. That's why elephants have smaller sperm than mice.


Based on their joint consideration of sperm size and number, and with the aid of new meta-analytical methods, the two researchers now reveal that species facing intense sperm competition invest more in their ejaculates on average than their monogamous counterparts. Moreover, they discovered that whether the length or the number of sperm is more important actually depends on the size of the animals. The bigger the animal, the greater the selection pressure on the overall investments in ejaculates and the more important the number of sperm becomes compared to sperm length. This is due to the more voluminous female reproductive tract, in which the sperm tend to get lost or become "diluted."

In larger species, sperm length or speed probably comes into effect only if a sufficient number of sperm manage to get near the egg. In smaller species, however, the distance for sperm to cover is shorter and the risk of loss much smaller, allowing the advantage of longer sperm to manifest itself. As a result, you tend to find the most complex sperm forms in small species, not in large ones. For instance, small fruit flies have the longest sperm ever described, not whales, whose sperm are less than a tenth of a millimeter long and almost a thousand times shorter than those of the flies.

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DNA Repair Protein BRCA1 Implicated in Cognitive Function and Dementia

DNA Repair Protein BRCA1 Implicated in Cognitive Function and Dementia | Amazing Science | Scoop.it

In dividing cells, BRCA1 helps repair a type of DNA damage known as double-strand breaks that can occur when cells are injured. In neurons, though, such breaks can occur even under normal circumstances, for example, after increased brain activity, as shown by the team of Gladstone scientists in an earlier study. The researchers speculated that in brain cells, cycles of DNA damage and repair facilitate learning and memory, whereas an imbalance between damage and repair disrupts these functions.


To test this idea, the scientists experimentally reduced BRCA1 levels in the neurons of mice. Reduction of the DNA repair factor led to an accumulation of DNA damage and to neuronal shrinkage. It also caused learning and memory deficits. Because Alzheimer’s disease is associated with similar neuronal and cognitive problems, the scientists wondered whether the problems might be mediated by depletion of BRCA1. They therefore analyzed neuronal BRCA1 levels in post-mortem brains of Alzheimer’s patients.


Compared with non-demented controls, neuronal BRCA1 levels in the patients were reduced by 65-75%. To determine the causes of this depletion, the investigators treated neurons grown in cell culture with amyloid-beta proteins, which accumulate in Alzheimer brains. These proteins depleted BRCA1 in the cultured neurons, suggesting that they may be an important cause of the faulty DNA repair seen in Alzheimer brains. Further supporting this conclusion, the researchers demonstrated that accumulation of amyloid-beta in the brains of mice also reduced neuronal BRCA1 levels. They are now testing whether increasing BRCA1 levels in these mouse models can prevent or reverse neurodegeneration and memory problems.


“Therapeutic manipulation of repair factors such as BRCA1 may ultimately be used to prevent neuronal damage and cognitive decline in patients with Alzheimer’s disease or in people at risk for the disease,” says senior authorLennart Mucke, MD, director of the Gladstone Institute of Neurological Disease. “By normalizing the levels or function of BRCA1, it may be possible to protect neurons from excessive DNA damage and prevent the many detrimental processes it can set in motion.”

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Tarantulas have evolved cobalt blue color at least eight times during evolution

Tarantulas have evolved cobalt blue color at least eight times during evolution | Amazing Science | Scoop.it

A study finds that tarantulas evolved almost exactly the same shade of vibrant blue at least eight separate times. That is the conclusion of a study by US biologists, exploring how the colour is created in different tarantula species. The hue is caused by tiny structures inside the animals' hairs, but those shapes vary across the family tree.


This suggests, the researchers say, that the striking blue is not driven by sexual selection - unlike many other bright colors in the animal kingdom. This argument is also supported by the fact that tarantulas have poor color vision, and do not appear to show off their hairy blue body parts during courtship.


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Ancient viral molecules essential for human embryonic development

Ancient viral molecules essential for human embryonic development | Amazing Science | Scoop.it
Genetic residue from ancient viral infections has been repurposed to play a vital role in acquiring pluripotency, the developmental state that allows a fertilized human egg to become all the cells in the body.


Genetic material from ancient viral infections is critical to human development, according to researchers at the Stanford University School of MedicineThey’ve identified several noncoding RNA molecules of viral origins that are necessary for a fertilized human egg to acquire the ability in early development to become all the cells and tissues of the body. Blocking the production of this RNA molecule stops development in its tracks, they found.


The discovery comes on the heels of a Stanford study earlier this year showing that early human embryos are packed full of what appear to be viral particles arising from similar left-behind genetic material. “We’re starting to accumulate evidence that these viral sequences, which originally may have threatened the survival of our species, were co-opted by our genomes for their own benefit,” said Vittorio Sebastiano, PhD, an assistant professor of obstetrics and gynecology. “In this manner, they may even have contributed species-specific characteristics and fundamental cell processes, even in humans.”


Sebastiano is a co-lead and co-senior author of the study, published online Nov. 23 in Nature Genetics.Postdoctoral scholar Jens Durruthy-Durruthy, PhD, is the other lead author. The other senior author of the paper is Renee Reijo Pera, PhD, a former professor of obstetrics and gynecology at Stanford who is now on the faculty of Montana State University.


Sebastiano and his colleagues were interested in learning how cells become pluripotent, or able to become any tissue in the body. A human egg becomes pluripotent after fertilization, for example. And scientists have learned how to induce other, fully developed human cells to become pluripotent by exposing them to proteins known to be present in the very early human embryo. But the nitty-gritty molecular details of this transformative process are not well understood in either case.


The researchers knew that a type of RNA molecules called long-intergenic noncoding, or lincRNAs, have been implicated in many important biological processes, including the acquisition of pluripotency. These molecules are made from DNA in the genome, but they don’t go on to make proteins. Instead they function as RNA molecules to affect the expression of other genes. 


Sebastiano and Durruthy-Durruthy used recently developed RNA sequencing techniques to examine which lincRNAs are highly expressed in human embryonic stem cells. Previously, this type of analysis was stymied by the fact that many of the molecules contain highly similar, very repetitive regions that are difficult to sequence accurately.


They identified more than 2,000 previously unknown RNA sequences, and found that 146 are specifically expressed in embryonic stem cells. They homed in on the 23 most highly expressed sequences, which they termed HPAT1-23, for further study. Thirteen of these, they found, were made up almost entirely of genetic material left behind after an eons-ago infection by a virus called HERV-H.


HERV-H is what’s known as a retrovirus. These viruses spread by inserting their genetic material into the genome of an infected cell. In this way, the virus can use the cell’s protein-making machinery to generate viral proteins for assembly into a new viral particle. That particle then goes on to infect other cells. If the infected cell is a sperm or an egg, the retroviral sequence can also be passed to future generations.


HIV is one common retrovirus that currently causes disease in humans. But our genomes are also littered with sequences left behind from long-ago retroviral infections. Unlike HIV, which can go on to infect new cells, these retroviral sequences are thought to be relatively inert; millions of years of evolution and accumulated mutations mean that few maintain the capacity to give instructions for functional proteins.


After identifying HPAT1-23 in embryonic stem cells, Sebastiano and his colleagues studied their expression in human blastocysts — the hollow clump of cells that arises from the egg in the first days after fertilization. They found that HPAT2, HPAT3 and HPAT5 were expressed only in the inner cell mass of the blastocyst, which becomes the developing fetus. Blocking their expression in one cell of a two-celled embryo stopped the affected cell from contributing to the embryo’s inner cell mass. Further studies showed that the expression of the three genes is also required for efficient reprogramming of adult cells into induced pluripotent stem cells.

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Scientists describe detailed make-up of deadly toxin for the first time

Scientists describe detailed make-up of deadly toxin for the first time | Amazing Science | Scoop.it
Scientists from the University of Leicester have for the first time created a detailed image of a toxin - called pneumolysin - associated with deadly infections such as bacterial pneumonia, meningitis and septicaemia.


he three-year study involving four research groups from across the University has been described as an exciting advance because it points to the possibility of creating therapeutics that block assembly of pneumolysin pores to treat people with pneumococcal disease. The University has recently set up a company Axendos Therapeutics to pursue this aim.


Using a technique called X-ray crystallography at Diamond Light Source, the UK's national synchrotron science facility, the Leicester team was able to see the individual atoms of the toxin. The structure not only reveals what the toxin looks like, but also shows how it assembles on the surface of cells to form lethal pores.


Professor Wallis said: "Our research is about a toxin called pneumolysin produced by a bacterium called pneumococcus (aka Streptococcus pneumoniae). Pneumococcal infections are the leading cause of bacterial pneumonia as well as the cause of a range of other life-threatening diseases such as meningitis and septicaemia. Pneumolysin is instrumental in the ability of pneumococcus to cause disease. The World Health Organization (WHO) estimated that more than 1.6 million people die every year from pneumococcal infections, including more than 800,000 children under 5 years old.


"The aim of the research was to find out how pneumolysin kills our cells, thereby causing tissue damage and contributing to disease. In particular we wanted to find out how multiple copies of the toxin assemble on the surface of cells. "We managed to determine the structure of pneumolysin using a technique called X-ray crystallography, which enables us to see the individual atoms of the toxin. The structure not only reveals what the toxin looks like, but also shows how it assembles to form lethal pores.


"Ours is the first detailed structure of pneumolysin. This level of detail is important and useful because it enables us to begin to understand how the toxin works. For example, we can see which parts of the toxin come together during pore assembly. When we disrupt these contacts, the toxin becomes inactivated so can no longer kill cells. "The mode of action of pneumolysin action revealed by our work appears to be conserved in related toxins from other disease-causing bacteria e.g. toxins produced by pathogenic species of Listeria."

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Cheap DNA sequencing is here, writing DNA inexpensively is next

Cheap DNA sequencing is here, writing DNA inexpensively is next | Amazing Science | Scoop.it

Twist Bioscience dramatically scaled down the equipment for synthesizing DNA in a lab, making the process cheaper and faster. The stamp-sized wafers contain 100 microwells. Each of these contains 100 nanowells in which DNA can be synthesized.


AT TWIST BIOSCIENCE’S office in San Francisco, CEO Emily Leproust pulled out of her tote bag two things she carries around everywhere: a standard 96-well plastic plate ubiquitous in biology labs and her company’s invention, a silicon wafer studded with a similar number of nanowells.


Twist’s pitch is that it has dramatically scaled down the equipment for synthesizing DNA in a lab, making the process cheaper and faster. As Leproust gave her spiel, I looked from the jankety plastic plate, the size of two decks of cards side by side, to the sleek stamp-sized silicon wafer and politely nodded along. Then she handed me a magnifying lens to look down the wafer’s nanowells. Inside each nanowell was another 100 microscope holes.


That’s when I actually got it. The 96-well plate was not equivalent to the wafer, the entire plate was equivalent toone nanowell on the wafer. To put a number on it, traditional DNA synthesis machines can make one gene per 96-well plate; Twist’s machine can make 10,000 genes on a silicon wafer set the same size as the plate.


But who wants to order 10,000 genes? Until recently, that question might have been met with silence. “It was a lonely time,” says Leproust of her early fundraising efforts for Twist. Fast forward a couple years, though, and Twist has just signed a deal to sell at least 100 million letters of DNA—equivalent to tens of thousands of genes—to Ginkgo Bioworks, a synthetic biology outfit that inserts genes into yeast to make scents like rose oil or flavors like vanillin. Ginkgo is at the forefront of a wave of synthetic biology companies, bolstered by new gene-editing technologies like Crispr and investor interest.


“We’re Intel and Ginkgo is Microsoft,” says Leproust, which sounds exactly the kind of rhetoric you hear all the time in startupland. But her words reveal Twist’s specific ambition to be the driver behind synthetic biology innovations. Synthesizing genes in a lab allows biologists to design—down to the letter—the ones they want to test. Companies out there are already tinkering with DNA in various cells to create spider silk, cancer treatments, biodegradable plastic, diesel fuel—and Twist’s founders thinks the company can become the driving technology behind that new world.


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Mantis shrimp uses polarized light message for communication

Mantis shrimp uses polarized light message for communication | Amazing Science | Scoop.it

QBI researchers have uncovered an entirely new form of secret light communication used by mantis shrimp.


The findings may have applications in satellite remote sensing, biomedical imaging, cancer detection, and computer data storage.


Dr Yakir Gagnon, Professor Justin Marshall and colleagues previously showed that mantis shrimp (Gonodactylaceus falcatus) can reflect and detect circular polarising light, an ability extremely rare in nature. Until now, no-one has known what they use it for.


The new study shows the shrimp use circular polarisation as a means to covertly advertise their presence to aggressive competitors. “In birds, colour is what we’re familiar with and in the ocean, reef fish display with colour – this is a form of communication we understand. What we’re now discovering is there’s a completely new language of communication,” said Professor Marshall.


Linear polarised light is seen only in one plane, whereas circular polarised light travels in a spiral – clockwise or anti-clockwise – direction. Humans cannot perceive polarised light without the help of special lenses, often found in sunglasses.


"We've determined that a mantis shrimp displays circular polarised patterns on its body, particularly on its legs, head and heavily armoured tail," he said. "These are the regions most visible when it curls up during conflict."


“These shrimps live in holes in the reef,” said Professor Marshall. “They like to hide away; they’re secretive and don’t like to be in the open.” They are also “very violent”, Professor Marshall adds. “They’re nasty animals. They’re called mantis shrimps because they have a pair of legs at the front used to catch their prey, but 40 times faster than the preying mantis. They can pack a punch like a .22 calibre bullet and can break aquarium glass. Other mantis shrimp know this and are very cautious on the reef.”


Researchers dropped a mantis shrimp into a tank with two burrows to hide in: one reflecting unpolarised light and the other, circular polarised light. The shrimps chose the unpolarised burrow 68 per cent of the time – suggesting the circular polarised burrow was perceived as being occupied by another mantis shrimp.


“If you essentially label holes with circular polarising light, by shining circular polarising light out of them, shrimps won’t go near it,” said Professor Marshall. “They know – or they think they know – there’s another shrimp there.

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Cameras capture super speedy tap dancing songbirds' courtship display

Cameras capture super speedy tap dancing songbirds' courtship display | Amazing Science | Scoop.it

High-speed cameras reveal that certain songbirds tap dance and sing so speedily that the fancy footwork is otherwise invisible to humans and other animals.


The discovery, published in the journal Scientific Reports, demonstrates how songbirds can flirt, woo, and otherwise communicate with each other completely under the radar of other animals' sensory perceptions. "The tap dancing is very fast and is completely invisible to the naked human eye," Associate Professor Masayo Soma of Hokkaido University said. "Even a normal digital video camera cannot capture their motion, as the tapping is quicker than one frame."


The scientists suspect the routines are intricate courtship displays designed to unite a male and female. "We predict that fine coordination or synchronisation of dancing should relate to long-term pair bonding," Dr Soma said. The routines even provide intriguing clues about the evolution of dancing in birds, as well as in humans and other animals.

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Lung Tumors' Spread Limited by Patrolling Monocytes, Study Shows

Lung Tumors' Spread Limited by Patrolling Monocytes, Study Shows | Amazing Science | Scoop.it

The immune system plays an important role in regulating tumor growth and metastasis. Classical monocytes promote tumorigenesis and cancer metastasis, but how nonclassical “patrolling” monocytes (PMo) interact with tumors is unknown. Scientists now show that PMo are enriched in the microvasculature of the lung and reduce tumor metastasis to lung in multiple mouse metastatic tumor models. Nr4a1-deficient mice, which specifically lack PMo, showed increased lung metastasis in vivo. Transfer of Nr4a1-proficient PMo into Nr4a1-deficient mice prevented tumor invasion in the lung. PMo established early interactions with metastasizing tumor cells, scavenged tumor material from the lung vasculature, and promoted natural killer cell recruitment and activation. Thus, PMo contribute to cancer immunosurveillance and may be targets for cancer immunotherapy.


The immune system has safeguarding mechanisms that identify and degrade harmful cells and cellular debris. Patrolling monocytes, a subpopulation of circulating white blood cells, is one type of immune cell serving as such a safeguard and is known to help counteract inflammation leading to atherosclerosis. Now, U.S. researchers have found that patrolling monocytes can also protect against lung tumor metastasis. Their study, entitled “Patrolling Monocytes Control Tumor Metastasis to the Lung” was published recently in Sciencemagazine.


The team used normal and Nr4a1 knockout mice, which do not produce patrolling monocytes, to investigate the role of patrolling monocytes in lung cancer metastasis. “No one had looked at how these cells might function in cancer. The knockout mouse gave us a model to test what they do,” Dr. Richard Hanna, from the La Jolla Institute for Allergy and Immunology and first author of the paper, said in a press release.

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Female Vampire Bats Donate Blood to Friends

Female Vampire Bats Donate Blood to Friends | Amazing Science | Scoop.it

Female vampire bats donate blood to friends to ensure their survival down the road—suggesting the animals' social lives are much more sophisticated than we thought, a new study says.


The findings shed further light on the often maligned species, which is native to the American tropics. Vampire bats eat only blood—taking small amounts without harming their hosts—and have amassed remarkable biological hardware to do so. They can sense body heat like a pit viper, run and jump surprisingly well, and urinate half of their blood meals’ water content within 30 minutes of eating.


They also live in tightly knit communities in which multiple unrelated females regularly band together, perhaps providing their pups—and each other—with body warmth and protection from predation. Vampire bats care for their their young for nine months—a long time relative to other bats, which usually become independent in about a month.


It doesn't end there. Female vampire bats also help out their friends by sharing regurgitated blood with bats unlucky enough to score a meal. Consider it an on-the-fly insurance policy: If a vampire bat misses two nightly meals in a row, it will starve.

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Uneven growth of identical monozygotic twins may begin shortly after conception

Uneven growth of identical monozygotic twins may begin shortly after conception | Amazing Science | Scoop.it

Unequal growth between genetically identical monozygotic (MZ) twins in the womb may be triggered in the earliest stages of human embryo development, according to a new study led by King’s College London.


Around 80% of MZ twins originate from monochorionic/diamniotic pregnancies, where they share the same placenta in the womb. MZ twins are recognized to be at greater risk of congenital anomalies. One of the most common complications is severe discordant growth, in which there is a 25% or greater difference in fetal or birth weight between the twins in the absence of twin-to-twin transfusion syndrome. Such severe discordant growth has been reported in 7% to 14% of all monochorionic/diamniotic pregnancies. Unequal placental sharing can explain about half of these pregnancies; the cause of the other half is largely unknown.


The case presented in the latest paper, published in the journal Stem Cell Reports, suggests that uneven growth of identical twins could start during the early stages of preimplantation development. An embryo donated for research revealed two inner cell masses (ICMs, internal cluster of cells at the embryonic pole of the blastocyst which develops into the body of the embryo), which is a sign of monochorionic/diamniotic pregnancy that will give rise to MZ twins. In this case, the two ICMs were not equal and high-resolution RNA sequencing indicated that they were at different stages of development; the smaller one was in the earliest stages of cell lineage commitment, while the bigger one had already differentiated to some extent. The differences in development would become negligible; however, the difference in size would be likely to continue throughout the pregnancy.


Laila Noli, first author and PhD student from King's College London said: 'Having two distinct ICMs within a single embryo of which one was bigger and more developmentally advanced than the other was an unexpected finding. Prevailing opinion would expect them to be absolutely identical at that stage, and that the cause of uneven growth of MZ twins would be due to their position in the womb or other unknown environmental circumstances at later stages of pregnancy.'


Dr Dusko Ilic, lead author from the Division of Women’s Health, King's College London, says: ‘Until now, the earliest report of uneven growth of MZ twins was at 12 weeks of pregnancy. We found that it can start virtually in the first few days after conception. The prevalence of such early stage uneven growth is not known and further case reports and studies are needed. We do not know whether the two ICMs within the same embryo may have originated from uneven splitting of a single “parental” ICM or whether the two ICMs formed independently. Either way, our case report suggests that cellular and molecular events may play a role in uneven growth of MZ twins from monochorionic/diamniotic pregnancies.’

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Transfer of immunity over two generations in pigeons without the direct use of deposited antibodies

Transfer of immunity over two generations in pigeons without the direct use of deposited antibodies | Amazing Science | Scoop.it

A team of researchers with Sorbonne Universités and Prédictive CEREEP-Ecotron Ile-De-France has found that grandmothers of pigeon chicks are somehow able to transfer immunity to a third generation, though the means is not apparent. In their paper published in the journal Biology Letters, the team describes how they injected three generations of pigeons with a protein to monitor their level of immunity response and what they found by doing so.


Suspecting that older generations were passing along immunity capabilities to more than just their own chicks, the researchers conducted a several year study of urban pigeons. They started by injecting 60 females with a protein called haemocyanin—it helps to transport oxygen in some invertebrates but does not do anything beneficial to pigeons. They also injected 60 additional female pigeons with a saline solution to serve as a control group. The team then injected the same protein into all of the offspring of the test pigeons, and then two years later, into all of the third generation of offspring as well. The purpose of the injections was to cause the birds to produce antibodies as a part of an immune response—after the birds were injected, blood tests were taken to see how strong of a response was triggered. They discovered that the immune response of the third generation was stronger for those chicks whose grandmothers had received haemocyanin than for those whose grandmothers had received the saline. This of course suggested that in reacting to the protein initially, the grandmother pigeons had developed an immune response that they had somehow passed down through their offspring, to their grand-chicks.


Logic would suggest that the grandmother birds had somehow sent antibodies to their offspring to be wary of the haemocyanin protein—if so, there would be evidence of more antibodies in the eggs of their offspring. But, testing the eggs failed to find more antibodies, which left the researchers stumped as to how the grandmothers were passing on their immunological message. They suggest the immune system must be trained in some other way (via hormones, possibly, or nutrients), which means more studies need to be done to find the ultimate answer.

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Genomically unstable cancer genomes: Deciphering order from apparent chaos

Genomically unstable cancer genomes: Deciphering order from apparent chaos | Amazing Science | Scoop.it

Most cancer genomes are genomically unstable. Genomic instability (GI) accumulates through genomic aberrations at several levels, from single nucleotide changes (point mutations), large structural changes (losses, gains and translocations) of chromosome fragments, to gains and losses of whole chromosomes (aneuploidy).  GI is now considered a distinct cancer hallmark.


Recent large-scale whole-genome sequencing efforts by The Cancer Genome Atlas (TCGA), International Cancer Genome Consortium (ICGC) and others have identified high GI rates across multiple cancer types including breast, lung, gastric and colorectal. An important realisation that has come out from these studies is that GI is a major causal factor for cancer genesis and progression in several solid cancers. For example, limited amounts of GI in normal and pre-cancerous tissues can predispose to sporadic cancers during the lifetimes of individuals. GI promotes intratumoural heterogeneity by facilitating ‘clonal inventions’ in tumours, thus enabling adaptation of tumours to (micro)environmental stress. GI confers inherent and acquired resistance to therapies, and thus posses significant prognostic and therapeutic challenges.


However, most genomically unstable cancer genomes display apparently random accumulation of genomic aberrations at elevated rates. Consequently, to understand the causal nature of GI, it is crucial to answer some important questions: (i) how do we identify and track these dynamically accumulating aberrations?; (ii) how do we distinguish the causal (driver) aberrations from the background (passenger) ones?; and (iii) do these causal aberrations point to internal or external processes that give rise to these aberrations and which are thus responsible for tumorigenesis and tumour progression. In other words, can we make derive order from this apparent chaos of GI.


A few months ago, Cancer Research UK (CRUK) set out seven ‘biggest challenges‘ in cancer research, and among these is (challenge number 3): Can we prevent cancers by studying the ‘scars’ that carcinogens leave in our DNA? What this CRUK challenge means is as follows. The apparently random accumulation of genomic aberrations in cancer genomes in fact constitutes the “genomic history” the genomes. Each such aberration constitutes a ‘scar’ left by a ‘scarring process’ accumulated during this evolutionary history of the genome. Consequently, by careful analysis of these scars, it is possible to effectively reconstruct the evolutionary history of the cancer genome, and more importantly it is possible to identify distinct mutational processes that give rise to these scars.


These scarring mutational processes could be endogenous — i.e., internal cellular processes —e.g. aberrant DNA-damage repair mechanisms — or their products — e.g. reactive oxygen species and aldehydes — that are capable of damaging the DNA; or exogenous — i.e., external carcinogenic agents capable of damaging the DNA, for example, tobacco smoke and UV radiation. Each such mutational process produces a characteristic scar based on the manner in which the DNA is changed or damaged. Consequently, scars represent the footprints of these mutational processes, and by studying them it is possible to point to specific mutational processes, which if overcome or totally avoided may help to prevent cancers.


Each of these footprints could be associated to distinct endogenous or exogenous mutational processes — for example, signature 4 found mostly in lung cancers associated strongly with tobacco smoke, whereas signature 7 found mostly in melanoma associated strongly with UV radiations. Among the endogenous processes were aberrant DNA-damage repair mechanisms arising from BRCA1/2 mutations, which associated with signature 3 found mostly in breast, ovarian and pancreatic cancers.

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Mystery of how snakes lost their legs solved by reptile fossil

Mystery of how snakes lost their legs solved by reptile fossil | Amazing Science | Scoop.it
Fresh analysis of a reptile fossil is helping scientists solve an evolutionary puzzle -- how snakes lost their limbs. The findings show snakes did not lose their limbs in order to live in the sea, as was previously suggested.


The 90 million-year-old skull is giving researchers vital clues about how snakes evolved. Comparisons between CT scans of the fossil and modern reptiles indicate that snakes lost their legs when their ancestors evolved to live and hunt in burrows, which many snakes still do today.

The findings show snakes did not lose their limbs in order to live in the sea, as was previously suggested.


Scientists used CT scans to examine the bony inner ear of Dinilysia patagonica, a 2-meter long reptile closely linked to modern snakes. These bony canals and cavities, like those in the ears of modern burrowing snakes, controlled its hearing and balance. They built 3D virtual models to compare the inner ears of the fossils with those of modern lizards and snakes. Researchers found a distinctive structure within the inner ear of animals that actively burrow, which may help them detect prey and predators. This shape was not present in modern snakes that live in water or above ground.


The findings help scientists fill gaps in the story of snake evolution, and confirm Dinilysia patagonica as the largest burrowing snake ever known. They also offer clues about a hypothetical ancestral species from which all modern snakes descended, which was likely a burrower.


Reference:

  1. H. Yi, M. A. Norell. The burrowing origin of modern snakesScience Advances, 2015; 1 (10): e1500743 DOI: 10.1126/sciadv.1500743


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Scientists Identify Two Genes (SERIN C5 and SERIN C3) that ‘Shut Down’ Infectivity of the HIV-1 Virus

Scientists Identify Two Genes (SERIN C5 and SERIN C3) that ‘Shut Down’ Infectivity of the HIV-1 Virus | Amazing Science | Scoop.it

In their two studies, the scientists found that host cell membrane proteins called SERINC5 and SERINC3 greatly reduce the virulence of HIV-1 by blocking the ability of the virus to infect new cells.


HIV-1 Nef, a protein important for the development of AIDS, counteracts the SERINCs. New drugs that target Nef would permit the SERINC proteins to inactivate the virus.


“It’s amazing, the magnitude of the effect that these proteins have on infectivity. The SERINC proteins reduce the infectivity of HIV-1 virions by more than 100-fold,” said Prof. Jeremy Luban from the University of Massachusetts Medical School.


“The ability of HIV to inhibit these SERINC proteins has a profound impact on its capacity to infect other cells,” said Prof. Heinrich Gottlinger, also from the University of Massachusetts Medical School.


“Disrupting this mechanism could be a very powerful strategy for treating HIV and similar viruses that express the Nef protein.”


The two studies used completely different, yet complementary, methodologies to unravel the complex interaction between the HIV-1 protein Nef and the cell surface membrane proteins SERINC5 and SERINC3, both of which are expressed in the immune system’s T cells.


The researchers performed parallel sequencing on 31 human cell lines that differed in terms of the magnitude of dependence on Nef for HIV-1 replication. They also approached the problem biochemically. Conducting proteomic analysis of purified virions, they were able to identify host cell proteins that Nef regulated.


“It has been known for more than 20 years that Nef is needed to make HIV-1 such a deadly virus. Our new studies may finally give us an important glimpse into how Nef might do this,” Prof. Luban said.

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Biologists induce flatworms to grow heads and brains of other species | KurzweilAI

Biologists induce flatworms to grow heads and brains of other species | KurzweilAI | Amazing Science | Scoop.it

Tufts University biologists have electrically modified flatworms to grow heads and brains characteristic of another species of flatworm — without altering their genomic sequence. This suggests bioelectrical networks as a new kind of epigenetics (information existing outside of a genomic sequence) to determine large-scale anatomy. Besides the overall shape of the head, the changes included the shape of the brain and the distribution of the worm’s adult stem cells.


The discovery could help improve understanding of birth defects and regeneration by revealing a new pathway for controlling complex pattern formation similar to how neural networks exploit bioelectric synapses to store and re-write information in the brain.


The findings are detailed in the open-access cover story of the November 2015 edition of the International Journal of Molecular Sciences, appearing online Nov. 24.


“These findings raise significant questions about how genes and bioelectric networks interact to build complex body structures,” said the paper’s senior author Michael Levin, Ph.D., who holds the Vannevar Bush Chair in biology and directs the Center for Regenerative and Developmental Biology in the School of Arts and Sciences at Tufts. Knowing how shape is determined and how to influence it is important because biologists could use that knowledge, for example, to fix birth defects or cause new biological structures to grow after an injury, he explained.


The researchers worked with Girardia dorotocephala — free-living planarian flatworms, which have remarkable regenerative capacity. They induced the development of different species-specific head shapes by interrupting gap junctions, which are protein channels that enable cells to communicate with each other by passing electrical signals back and forth.


The ease with which a particular shape could be coaxed from a Girardia dorotocephala worm was proportional to the proximity of the target worm on the evolutionary timeline. The closer the two species were related, the easier it was to effect the change. This observation strengthens the connection to evolutionary history, suggesting that modulation of physiological circuits may be one more tool exploited by evolution to alter animal body plans.


However, this shape change was only temporary. Weeks after the planaria completed regeneration to the other species’ head shapes, the worms once again began remodeling and re-acquired their original head morphology. Additional research is needed to determine how this occurs. The authors also presented a computational model that explains how changes in cell-to-cell communication can give rise to the diverse shape types.


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Spacefaring tardigrade (water bear) has largest contribution of foreign DNA in its genome

Spacefaring tardigrade (water bear) has largest contribution of foreign DNA in its genome | Amazing Science | Scoop.it

Sequencing reveals that the genome of the Tardigrade has been published, revealing approximately 6,000 genes of foreign origin.


The tardigrade, also known as the water bear, is renowned for many reasons. The nearly indestructible micro-organism is known to have the capacity to survive extreme temperatures (-272C to 151C), and is the only animal able to survive in the vacuum of space.


Today, with the publication of its genome in PNAS, the humble water bear can add another item to its exhaustive list of superlatives. Sequencing of the genome, performed by a team of researchers at the University of North Carolina at Chapel Hill, has revealed that a massive portion of the tiny organism’s genome is of foreign origin. Indeed, nearly 17.5% of the water bear’s genome is comprised of foreign DNA, translating to a genetic complement of approximately 6,000 genes. These genes are primarily of bacterial origin, though genes from fungi and plants have also been identified.


Horizontal gene transfer, defined as the shifting of genetic material materially (thus horizontally) between organisms is widespread in the microscopic world. In humans, however, the process does occur, but in a limited fashion, and via transposons and viruses. Other microscopic animals are also known to have large complements of foreign genes.


The authors of the newly published work have proposed a method by which this extremely extensive gene transfer may have occurred. Tardigrades have long been known to undergo, and survive, the process of desiccation (extreme drying out). The authors therefore postulated that during this drying out process and the subsequent rehydration, the tardigrade’s genome may have undergone significant sheering and breakage, resulting in a general loss of integrity and leakiness experienced by the water bear’s nucleus. In turn, this compromised nuclear integrity may have enabled foreign genetic material to readily integrate the genome, in much the same way as scientists perform gene transfer through the process of electroporation.


For now, the tardigrade has a dual claim to fame, being the only known animal to survive the vacuum of space, and being the animal with the largest genetic complement. Only with the study of other micro-organisms will we be able to validate if the humble tardigrade maintains its two, current, great claims to fame.


"Animals that can survive extreme stresses may be particularly prone to acquiring foreign genes—and bacterial genes might be better able to withstand stresses than animal ones," said Boothby, a postdoctoral fellow in Goldstein's lab. After all, bacteria have survived the Earth's most extreme environments for billions of years.


The team speculates that the DNA is getting into the genome randomly but what is being kept is what allows tardigrades to survive the harshest of environments, e.g. stick a tardigrade in a - 80 celsius freezer for a year or 10 and it starts running around in 20 minutes after thawing.


This is what the team thinks happens: when tardigrades are under conditions of extreme stress such as desiccation - or a state of extreme dryness—Boothby and Goldstein believe that the tardigrade's DNA breaks into tiny pieces. When the cell rehydrates, the cell's membrane and nucleus, where the DNA resides, becomes temporarily leaky and DNA and other large molecules can pass through easily. Tardigrades not only can repair their own damaged DNA as the cell rehydrates but also stitch in the foreign DNA in the process, creating a mosaic of genes that come from different species.

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Ants filmed building moving bridges from their live bodies

Ants filmed building moving bridges from their live bodies | Amazing Science | Scoop.it
Army ants build living bridges by linking their bodies to span gaps and create shortcuts across rainforests in Central and South America. An international team of researchers has now discovered these bridges can move from their original building point to span large gaps and change position as required.


The bridges stop moving when they become so long that the increasing costs incurred by locking workers into the structure outweigh the benefit that the colony gains from further shortening their trail. Bridges dismantle when the ants in the structure sense the traffic walking over them slows down below a critical threshold.


Co-lead author Dr Christopher Reid, a postdoctoral researcher at the University of Sydney's Insect Behaviour and Ecology Lab and formerly with the New Jersey Institute of Technology, said the findings could be applied to develop swarm robotics for exploration and rescue operations. By analysing how ants optimise utility, researchers may be able to create simple control algorithms to allow swarms of robots to behave in similar ways to an ant colony.


The team of researchers - from the Max Planck Institute for Ornithology (Konstanz, Germany), University of Konstanz, and the United States's New Jersey Institute of Technology, Princeton University and George Washington University - found the bridges can assemble and disassemble in seconds. They can also change their position in response to the immediate environment.


The dynamic nature of the bridges has been found to facilitate travel by the colony at maximum speed, across unknown and potentially dangerous terrains. Prior to the study it was assumed that, once they had been built, the bridges were relatively static structures.


The paper, 'Army ants dynamically adjust living bridges in response to a cost-benefit trade-off', is being published in the journal Proceedings of the National Academy of Sciences (PNAS).

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Genomics and Precision Agriculture: The Future of Farming

Genomics and Precision Agriculture: The Future of Farming | Amazing Science | Scoop.it

For nearly 400 years, Thanksgiving has been a time in North America when families come together to celebrate food and agriculture. As we reflect on yet another year, agricultural scientists at USDA continue to keep a wary eye on the future. At the end of what may be the hottest year on record, a period of drought has threatened the heart of one of the most important agricultural production zones in the United States. Water demands are increasing, and disease and pest pressures are continually evolving. This challenges our farmers’ ability to raise livestock and crops.  How are science and technology going to address the problems facing our food supply? 


To find answers, agricultural scientists turn to data—big data.  Genomics, the field of science responsible for cataloging billions of DNA base pairs that encode thousands of genes in an organism, is fundamentally changing our understanding of plants and animals.  USDA has already helped to fund and collect genomes for 25 crop plant species, important livestock and fish species, and numerous bacteria, fungi, and insect species related to agricultural production. Other USDA-supported research projects expanding these efforts are currently underway, including genome sequencing of 1,000 breeds of bulls and 5,000 insect species in the i5K initiative. But classifying and understanding DNA is only part of the story.


Even if neighboring farmers were to raise identical varieties of tomato, small variations in the environment can reduce crop performance and/or increase pests and disease. So, scientists and farmers are increasingly using technology like satellites, drones, sensors, and laser-guided tractors to collect thousands of data points about the environmental conditions in a field, such as temperature, humidity, soil composition, or slope of the land. Using these “precision agriculture” techniques, farmers could reduce their environmental footprint by matching land management practices to the unique environments on their farm.


In the long term, USDA researchers are hoping to combine precision agriculture and genomics in a remarkable way—to develop crops with combinations of genes that lead to the best performance in specific environments. To support this goal, USDA continues to lead the way in collecting and maintaining open access to these types of agriculture data.  As a result, your local farmer’s market or grocery store may one day have even more varieties of produce to choose from on Thanksgiving, with each optimized for the farm or field on which it was grown.


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They work for seeds: Pigeons diagnose breast cancer on X-rays as well as radiologists

They work for seeds: Pigeons diagnose breast cancer on X-rays as well as radiologists | Amazing Science | Scoop.it

“Pigeons do just as well as humans in categorizing digitized slides and mammograms of benign and malignant human breast tissue,” said Richard Levenson, professor of pathology and laboratory medicine at UC Davis Health System and lead author of a new open-access study in PLoS One by researchers at the University of California, Davis and The University of Iowa.


“The pigeons were able to generalize what they had learned, so that when we showed them a completely new set of normal and cancerous digitized slides, they correctly identified them,” Levenson  said. “The pigeons also learned to correctly identify cancer-relevant microcalcifications on mammograms, but they had a tougher time classifying suspicious masses on mammograms — a task that is extremely difficult, even for skilled human observers.”


Although a pigeon’s brain is no bigger than the tip of an index finger, the neural pathways involved operate in ways very similar to those at work in the human brain. “Research over the past 50 years has shown that pigeons can distinguish identities and emotional expressions on human faces, letters of the alphabet, misshapen pharmaceutical capsules, and even paintings by Monet vs. Picasso,” said Edward Wasserman, professor of psychological and brain sciences at The University of Iowa and co-author of the study. “Their visual memory is equally impressive, with a proven recall of more than 1,800 images.”


For the study, each pigeon learned to discriminate cancerous from non-cancerous images and slides using traditional “operant conditioning,” a technique in which a bird was rewarded only when a correct selection was made; incorrect selections were not rewarded and prompted correction trials. Training with stained pathology slides included a large set of benign and cancerous samples from routine cases at UC Davis Medical Center.


“The birds were remarkably adept at discriminating between benign and malignant breast cancer slides at all magnifications, a task that can perplex inexperienced human observers, who typically require considerable training to attain mastery,” Levenson said. He said the pigeons achieved nearly 85 percent correct within 15 days.


“When we showed a cohort of four birds a set of uncompressed images, an approach known as “flock-sourcing,” the group’s accuracy level reached an amazing 99 percent correct, higher than that achieved by any of the four individual birds.” Wasserman has conducted studies on pigeons for more than 40 years.


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Taste comes from the brain, not the tongue, scientists discover

Taste comes from the brain, not the tongue, scientists discover | Amazing Science | Scoop.it

Researchers in the US have turned taste on and off in mice simply by activating and silencing certain brain cells. This demonstrates for the first time that taste is hardwired in the brain, and not dictated by our tastebuds, flipping our previous understanding of how taste works on its head.

It was previously thought that the taste receptors on our tongue perceived the five basic tastes – sweet, salty, sour, bitter, and umami – and then passed these messages onto our brain, where it registered what we'd just tasted. But the new study shows that although our tongues do detect the presence of certain chemicals, it's our brains that perceive flavor.


“Taste, the way you and I think of it, is ultimately in the brain,” said lead researcher Charles S. Zuker from Columbia University Medical Centre. “Dedicated taste receptors in the tongue detect sweet or bitter and so on, but it’s the brain that affords meaning to these chemicals.”


Previous work by Zuker's lab discovered that our tongue has dedicated receptors for each taste, and that each class of receptors sends a specific signal to the brain. More recently, the team built on this by showing that in addition to dedicated receptors, there are unique sets of brain cells – each in different locations – that receive these signals. The red area below is the bitter neurons, and the aqua shows where the sweet brain cells are.


In this study, they decided to play with these brain cells and see if they could activate or deactivate them in order to trick mice into thinking they were tasting something sweet or bitter, without them actually tasting either.


"In this study, we wanted to know if specific regions in the brain really represent sweet and bitter. If they do, silencing these regions would prevent the animal from tasting sweet or bitter, no matter how much we gave them," said Zuker. "And if we activate these fields, they should taste bitter or sweet, even though they’re only getting plain water."


What they observed was exactly as they'd expected – when the sweet neurons were silenced using an injectable drug, the mice couldn't taste anything sweet, but they could still detect bitter flavors. And when the researchers activated the sweet neurons using laser light, the mice tasted sweet flavors, even though they were only drinking plain water. The same thing happened when they stimulated or silenced the bitter brain cells. The team was able to tell what the mice were tasting by their obvious reactions – they licked their lips when they tasted real or simulated sweet flavors, and gagged and looked disgusted when they tasted bitter.


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Human ARF Gene Prevents Zebrafish Regeneration

Human ARF Gene Prevents Zebrafish Regeneration | Amazing Science | Scoop.it

Regenerative medicine could one day allow physicians to correct congenital deformities, regrow damaged fingers, or even mend a broken heart. But to do it, they will have to reckon with the body’s own anti-cancer security system. Now UCSF researchers have found a human gene that may be a key mediator of this trade-off, blocking both tumors and healthy regeneration.


As a child, UCSF’s Jason Pomerantz, MD, was amazed by the fact that salamanders can regenerate limbs. Now, as a plastic surgeon and stem cell researcher, he believes that insights from creatures like zebrafish and salamanders, which routinely regrow damaged tails, limbs, jaws and even hearts, may one day endow humans with heightened regenerative abilities.


“In the last 10 to 15 years, as regenerative organisms like zebrafish have become genetically tractable to study in the lab, I became convinced that these animals might be able to teach us what is possible for human regeneration,” Pomerantz said. “Why can these vertebrates regenerate highly complex structures, while we can’t?”


In a study published Nov. 17, 2015, in the journal eLife, Pomerantz and his team showed new evidence suggesting that mammals may have given up the ability to regenerate limbs partly in exchange for advanced cancer-fighting genes.


The question of whether the regenerative powers of zebrafish and salamanders represent ancient abilities that mammals have lost, perhaps in exchange for advanced tumor-suppression systems remains an open question for biologists. Most tumor suppressor genes, being extremely useful for preventing cancer and for forming tissues during development, are broadly distributed and conserved across many different species. Recent studies, however, suggest that one, the Arf gene, arose more recently in the avian and mammalian lineage, and has no equivalent in the genomes of highly regenerative animals.


To explore whether this gene might play a role in preventing tissue regeneration in humans, the researchers added human ARF to the zebrafish genome and assessed how it affected the fishes’ normal ability to regrow damaged fins after injury. They found that human ARF had no effect on the fishes’ normal development or response to superficial injury, but when the researchers trimmed off the tip of a fish’s tail fin, the gene became strongly activated and almost completely prevented fin regrowth by activating a conserved tumor-blocking pathway.


“It’s like the gene is mistaking the regenerating fin cells for aspiring cancer cells,” said Pomerantz, who is an associate professor of plastic and reconstructive surgery at UCSF and surgical director of the Craniofacial Center at UCSF’s Medical Center and School of Dentistry. “And so it springs into action to block it.”

It’s remarkable that ARF can so readily integrate itself into the fish’s existing tumor-blocking pathways, Pomerantz said.


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Genome sequencing shows that myxozoan parasite is actually a 'micro' jellyfish

Genome sequencing shows that myxozoan parasite is actually a 'micro' jellyfish | Amazing Science | Scoop.it
It's a shocking discovery that may redefine how scientists interpret what it means to be an animal.


This week in the Proceedings of the National Academy of Sciences (PNAS), researchers at the University of Kansas reveal how a jellyfish—those commonplace sea pests with stinging tentacles—has evolved over time into a "really weird" microscopic organism, made of only a few cells, that lives inside other animals.


Genome sequencing confirms that myxozoans, a diverse group of microscopic parasites that infect invertebrate and vertebrate hosts, are actually are "highly reduced" cnidarians—the phylum that includes jellyfish, corals and sea anemones.


"This is a remarkable case of extreme degeneration of an animal body plan," said Paulyn Cartwright, associate professor of ecology and evolutionary biology at KU and principal investigator on the research project. "First, we confirmed they're cnidarians. Now we need to investigate how they got to be that way."


Not only has the parasitic micro jellyfish evolved a stripped-down body plan of just a few cells, but via data generated at the KU Medical Center's Genome Sequencing Facility researchers also found the myxozoan genome was drastically simplified.


"These were 20 to 40 times smaller than average jellyfish genomes," Cartwright said. "It's one of the smallest animal genomes ever reported. It only has about 20 million base pairs, whereas the average Cnidarian has over 300 million. These are tiny little genomes by comparison."


Despite its radical reduction of the modern jellyfish's body structure and genome over millions of years, Myxozoa has retained the essential characteristic of the jellyfish—its stinger, or "nematocyst"—along with the genes needed to make it. "Because they're so weird, it's difficult to imagine they were jellyfish," she said. "They don't have a mouth or a gut. They have just a few cells. But then they have this complex structure that looks just like stinging cell of cnidarian. Jellyfish tentacles are loaded with them—little firing weapons."


The findings are the stuff of scientific fascination but also could have a commercial effect. Myxozoa commonly plague commercial fish stock such as trout and salmon. "They're a very diverse group of parasites, and some have been well-studied because they infect fish and can wreak havoc in aquaculture of economic importance," Cartwright said. "They cause whirling disease in salmon. The fish start swimming in circles—it's a neurological problem caused by a myxozoan."


Cartwright said the confirmation that myxozoans are cnidarians would necessitate the re-classification of Myxozoa into the phylum Cnidaria. Moreover, these micro jellyfish could expand understanding of what makes up an animal. "Their biology was well-known, but not their evolutionary origins," she said. "They're microscopic, only a few cells measuring 10 to 20 microns. Some people originally thought they were single-celled organisms. But when their DNA was sequenced, researchers started to surmise they were animals—just really weird ones."

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Long-sought biological compass may finally have been discovered

Long-sought biological compass may finally have been discovered | Amazing Science | Scoop.it
Protein complex offers explanation for how animals sense Earth's magnetic pull.


Beluga whales are among the species that are thought to use Earth’s weak magnetic field for navigation. In the cells of fruit flies, Chinese scientists say that they have found a biological compass needle: a rod-shaped complex of proteins that can align with Earth’s weak magnetic field.


The biocompass — whose constituent proteins exist in related forms in other species, including humans — could explain a long-standing puzzle: how animals such as birds and insects sense magnetism. It might also become an invaluable tool for using magnetic fields to control cells, report researchers led by biophysicist Xie Can at Peking University in Beijing, in a paper published on 16 November in Nature Materials (S. Qin et al. Nature Mater.http://dx.doi.org/10.1038/nmat4484; 2015).


“It’s an extraordinary paper,” says Peter Hore, a biochemist at the University of Oxford, UK. But Xie’s team has not shown that the complex actually behaves as a biocompass inside living cells, nor explained exactly how it senses magnetism. “It’s either a very important paper or totally wrong. I strongly suspect the latter,” says David Keays, a neuroscientist who studies magnetoreception at the Institute of Molecular Pathology in Vienna.


Many organisms — ranging from whales to butterflies, and termites to pigeons — use Earth’s magnetic field to navigate or orient themselves in space. But the molecular mechanism behind this ability, termed magneto-reception, is unclear. Some researchers have pointed to magnetically sensitive proteins called ‘cryptochromes’, or ‘Cry’. Fruit flies lacking the proteins lose their sensitivity to magnetic fields, for example. But the Cry proteins alone cannot act as a compass, says Xie, because they cannot sense the polarity (north–south orientation) of magnetic fields.


Xie says that he has found a protein in fruit flies that both binds to iron and interacts with Cry. Known as CG8198, it binds iron and sulfur atoms and is involved in fruit-fly circadian rhythms. Together with Cry, it forms a nanoscale ‘needle’: a rod-like core of CG8198 polymers with an outer layer of Cry proteins that twists around the core (see 'Protein biocompass').


Using an electron microscope, Xie’s team saw assemblies of these rods orienting themselves in a weak magnetic field in the same way as compass needles. Xie gave CG8198 the new name of MagR, for magnetic receptor.


The discovery offers scientists the prospect of using magnetic fields to control cells. Over the past decade, scientists have commandeered the light-sensing capacity of some proteins to manipulate neurons, usually by inserting a fibre-optic cable directly into the brain — a tool called optogenetics. But magnetosensing proteins have the advantage that they could be manipulated by magnetic fields outside the brain.


Zhang Sheng-jia, a neuroscientist at Tsinghua University in Beijing, claims to have already demonstrated this ‘magnetogenetic’ capability. In September, he provided a surprise preview of Xie’s work when he published a paper reporting use of the biocompass to manipulate neurons in worms (X. Long et al. Sci. Bull. http://doi.org/883; 2015).

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