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News Article | May 18, 2017
Site: phys.org

By 2040, there will be 9 billion people in the world. "That's like adding another China onto today's global population," said Professor Sophien Kamoun of the Sainsbury Laboratory in Norwich, UK. Prof. Kamoun is one of a growing number of food scientists trying to figure out how to feed the world. As an expert in plant pathogens such as Phytophthora infestans – the fungus-like microbe responsible for potato blight – he wants to make crops more resistant to disease. Potato blight sparked the Irish famine in the 19th century, causing a million people to starve to death and another million migrants to flee. European farmers now keep the fungus in check by using pesticides. However, in regions without access to chemical sprays, it continues to wipe out enough potatoes to feed hundreds of millions of people every year. "Potato blight is still a problem," said Prof. Kamoun. "In Europe, we use 12 chemical sprays per season to manage the pathogen that causes blight, but other parts of the world cannot afford this." Plants try to fight off the pathogens that cause disease but these are continuously changing to evade detection by the plant's immune system. In nature, every time a plant gets a little better at fighting off infection, pathogens adapt to evade their defences. Now biologists are getting involved in the fight. "It's essentially an arms race between plants and pathogens," said Prof. Kamoun. "We want to turn it into an arms race between biotechnologists and pathogens by generating new defences in the lab." Five years ago, Prof. Kamoun embarked on a project called NGRB, funded by the EU's European Research Council. The plan was to find a way to make potatoes more resistant to infection using advanced plant-breeding techniques. Then serendipity struck. In the early stages of the project, scientists in another lab discovered a ground-breaking gene-editing technique known as CRISPR-Cas which allows scientists to delete or add genes at will. As well as having potential medical applications in humans, this powerful tool is unlocking new approaches to perfecting plants. "If we think of the genome as text, CRISPR is a word processor that allows us to change just a letter or two," explained Prof. Kamoun. "The precision that this allows makes CRISPR the ultimate in genetic editing. It's really beautiful." One of the simplest ways to use CRISPR to improve plants is to remove a gene that makes them vulnerable to infection. This alone can make potatoes more resilient, helping to meet the world's growing demand for food. The resulting crop looks and tastes just the same as any other potato. Prof. Kamoun says that potatoes which are missing a gene or two should not be viewed in the same way as genetically modified foods which sometimes contain genes introduced from another species. "It's a very important technical difference but not all regulators have updated their rules to make this distinction." Potatoes are not the only food crops that can be improved by CRISPR-Cas. Prof. Kamoun is now working on a project that aims to protect wheat from wheat blast – a fungal disease decimating yields in Bangladesh and spreading in Asia. Looking ahead, CRISPR will be used to improve the quality and nutritional value of wheat, rice, potatoes and vegetables. It could even be used to remove genes that cause allergic reactions in people with tomato or wheat intolerance. "If we can remove allergens, consumers may soon see hypoallergenic tomatoes on supermarket shelves," Prof. Kamoun said. "It's a very exciting technology." While targeting disease in this way could be a game changer for global food security in the years ahead, experts believe other approaches to plant breeding will continue to have a role. Understanding meiosis – a type of cell division that can reshuffle genes to improve plants – can help farmers and the agribusiness sector select for hardier crops, according to Professor Chris Franklin of the University of Birmingham, UK. He leads the COMREC project, which trains young scientists to understand and manipulate meiosis in plants. The project applies the wealth of knowledge generated by leaders in the field to tackle the pressing problem of feeding a hungry world. "COMREC has begun to translate fundamental research into (applications in) key crop species such as cereals, brassicas and tomato," said Prof. Franklin. "Close links with plant-breeding companies have provided important insight into the specific challenges confronted by the breeders." There may be untapped potential in this approach to plant breeding: most of the genes naturally reshuffled during meiosis in cereal crops are at the far ends of chromosomes – genes in the middle of chromosomes are rarely reshuffled, limiting the scope for new crop variations. COMREC's academic and industry partners hope to understand why this is so that they can find a way to shuffle the genes in the middle of chromosomes too. And the food industry is keen to produce new 'elite varieties' that are better adapted to confront the challenges arising from climate change, says Prof. Franklin. "A number of genes have now been identified that can make this reshuffling relatively more frequent," he said. "CRISPR-Cas provides a way to modify the corresponding genes in crop species, helping to translate this basic research to target crops." Explore further: US approves 3 types of genetically engineered potatoes (Update) More information: Targeted mutagenesis in the model plant Nicotiana benthamiana using Cas9 RNA-guided endonuclease by Vladimir Nekrasov, Brian Staskawicz, Detlef Weigel, Jonathan D G Jones & Sophien Kamoun in Nature Biotechnology 31, 691–693 (2013). DOI: 10.1038/nbt.2655 Involvement of the Cohesin Cofactor PDS5 (SPO76) During Meiosis and DNA Repair in Arabidopsis thaliana by Mónica Pradillo, Alexander Knoll, Cecilia Oliver, Javier Varas, Eduardo Corredor, Holger Puchta and Juan L. Santos in Front. Plant Sci., 01 December 2015 . DOI: 10.3389/fpls.2015.01034


Farmers are constantly spraying pesticides on their crops to combat an array of viral, bacterial, and fungal invaders. Scientists have been trying to get around these chemicals for years by genetically engineering hardy plants resilient to the array of diseases caused by microbial beasties. Most attempts so far confer protection against a single disease, but now researchers have developed a rice plant that fights multiple pathogens at once—without loss to the crop yield—by hooking up a tunable amplifier to the plant’s immune system. “For as long as I have been in this field, people have been scratching their heads about how to activate a defense system where and when it is needed,” says Jonathan Jones, who studies plant defense mechanisms at the Sainsbury Laboratory in Norwich, U.K. “It is among the most promising lines of research in this field that I have seen.” Plants don’t have a bloodstream to circulate immune cells. Instead, they use receptors on the outsides of their cells to identify molecules that signal a microbial invasion, and respond by releasing a slew of antimicrobial compounds. Theoretically, identifying genes that kick off this immune response and dialing up their activity should yield superstrong plants. Plant biologist Xinnian Dong at Duke University in Durham, North Carolina, has been studying one of these genes for 20 years—a “master regulator,” she says, of plant defense. The gene, called NPR1 in the commonly studied thale cress plant (Arabidopsis thaliana)—a small and weedy plant topped with white flowers—has been a popular target for scientists trying to boost immune systems of rice, wheat, apples, tomatoes, and more. But turning up NPR1 works too well and “makes the plants miserable, so it is not very useful for agriculture,” Dong says. To understand why, consider the human immune system. Just as sick people aren’t very productive at work when their fever is high, plants grow poorly when their own immune systems are overloaded. Likewise, keeping the NPR1 gene turned on all the time stunts plant growth so severely there is no harvest for the farmers. To make NPR1 useful, researchers needed a better control switch—one that would crank up the immune response only when the plant was under attack, but otherwise would turn it down to let the plants grow. Two papers published in this week from Dong’s team at Duke, in collaboration with researchers at Huazhong Agricultural University in Wuhan, China, describe the discovery and application of such a mechanism. While investigating an immune system-activating protein called TBF1 in Arabidopsis, Dong discovered an intricate system that speedily instigates an immune response. It works by taking ready-to-go messenger RNA molecules that encode TBF1, and quickly translating these molecules into TBF1 proteins, which then kick-start an array of immune defenses. Dong quickly recognized that a segment of DNA, which she calls the “TBF1 cassette,” was acting as a control switch for this plant immune response, so she copied that TBF1 cassette from the Arabidopsis genome and pasted it alongside and in front of the NPR1 gene in rice plants. The result is a strain of rice that can rapidly and reversibly ramp up its immune system in bursts that are strong enough to fend off offending pathogens but short enough to avoid the stunted growth seen in previously engineered crops. The researchers demonstrated that their rice was superior compared with regular rice by inoculating their leaves with the bacterial pathogens that cause rice blight (Xanthomonas oryzae pv. oryzae) and leaf streak (X. oryzae pv. oryzicola), as well as the fungus responsible for blast disease (Magnaporthe oryzae). Whereas the infections spread over the leaves of the wild rice plants, the engineered plants readily confined the invaders to a small area. “These plants perform very well in the field, and there is no obvious fitness penalty, especially in the grain number and weight,” Dong says. The research could be a boon for farmers in developing countries someday, says Jeff Dangl, an expert on plant immunity at the University of North Carolina in Chapel Hill, who was not involved in the study. For instance, rice blast disease, which the plants effectively combatted, causes an estimated 30% loss of the annual rice crop worldwide. “In the developing world, when farmers that can’t afford fungicide get the disease in their fields, they can lose their whole crop,” Dangl says. Julia Bailey-Serres, a plant biologist at the University of California, Riverside, is excited about the study too. “They haven’t done large trials yet to show how robust it will be, but our back of the envelope calculation shows that this really could have a big impact,” she says. “It could easily be applicable to multiple species of crops,” she says, adding that “it is impressive that it worked across two kingdoms” of fungal and bacterial pathogens. But all are careful to note that it is still early days for immune-boosted crops. For one, the particular kind of uplift conferred by NPR1 is unlikely to provide protection against plant-munching insects. A second caveat is that the study only tested the rice’s response to microbes that parasitize living host cells; their defense against a different class of pathogens that kill cells for food is still untested. “I would keep the champagne on ice until there are a few more pathogen systems tested in the field,” Jones says. Still, Jones says he’s hopeful the work—and more like it—could eventually lead to the end of pesticides. “I like to imagine in 50 years’ time my grandchildren will say, ‘Granddad, did people really use chemicals to control disease when they could have used genetics?’ And I’ll say, ‘Yeah, they did.’ That’s where we want to get to.”


News Article | April 17, 2017
Site: www.eurekalert.org

Nematodes are a huge threat to agriculture since they parasitize important crops such as wheat, soybean, and banana; but plants can defend themselves. Researchers at Bonn University, together with collaborators from the Sainsbury Laboratory in Norwich, identified a protein that allows plants to recognize a chemical signal from the worm and initiate immune responses against the invaders. This discovery will help to develop crop plants that feature enhanced protection against this type of parasites. The work is published in the current issue of PLOS Pathogens. Plant-parasitic nematodes are microscopic worms that parasitize their host plants to withdraw water and nutrients. The feeding process seriously damages the host plant. Nematode infection distorts root and shoot structure, compromises the plant´s ability to absorb nutrients from soil, and eventually reduces crop yield. Yearly losses exceed ten percent in important crops such as wheat, soybean, and banana. In addition to causing direct damage, nematode infection also provides an opportunity for other pathogens to invade and attack the host plants. Until now, near to nothing was known about the general innate immune response of plants against nematodes. A team of researchers at the University of Bonn, in cooperation with scientists from the Sainsbury Laboratory in Norwich, has now identified a gene in thale cress (Arabidopsis thaliana), called NILR1, that helps plants sense nematodes. "The NILR1 is the genetic code for a receptor protein that is localized to the surface of plant cells and is able to bind and recognize other molecules," says Prof. Florian Grundler, chair at the Department of Molecular Phytomedicine at the University of Bonn. "NILR1 most probably recognizes a molecule from nematodes, upon which, it becomes activated and immune responses of plants are unleashed." Although a few receptors, so-called resistance genes, providing protection against specific types of plant-parasitic nematodes have already been identified, NILR1 recognizes rather a broader spectrum of nematodes. "The nice thing about NILR1 is that it seems to be conserved among various crop plants and that it provides protection against many nematode species," says group leader Dr. Shahid Siddique. "The discovery of NILR1 also raises questions about the nematode derived molecule, whose recognition is thought to be integral to this process." Now that an important receptor is discovered, the scientists are working to find the molecule which binds to NILR1 to switch on the immune responses. The two first authors, PhD students at the department share tasks in the project. Whereas Mary Wang´ombe focuses on the receptor protein and its function, Badou Mendy concentrates on isolating the signal molecule released by the nematodes. The findings of the University Bonn Scientists open new perspectives in making crops more resistant against nematodes. They could already show that important crop plants such as tomato and sugar beet also possess a functional homologue of NILR1 - an excellent basis for further specific breeding. Once the nematode signal is characterized, a new generation of natural compounds will be available that is able to induce defense responses in plants thus paving the way for safe and sustainable nematode control. Publication: Mendy, B., Wang'ombe, M.W., Radakovic, Z., Holbein, J., Ilyas, M., Chopra, D., Holton, N., Zipfel, C., Grundler, F.M.W., and Siddique, S.: Arabidopsis leucine-rich repeat receptor-like kinase NILR1 is required for induction of innate immunity to parasitic nematodes, PLOS Pathogens, Internet: https:/


News Article | February 23, 2017
Site: www.bbc.co.uk

Science is facing a "reproducibility crisis" where more than two-thirds of researchers have tried and failed to reproduce another scientist's experiments, research suggests. This is frustrating clinicians and drug developers who want solid foundations of pre-clinical research to build upon. From his lab at the University of Virginia's Centre for Open Science, immunologist Dr Tim Errington runs The Reproducibility Project, which attempted to repeat the findings reported in five landmark cancer studies. "The idea here is to take a bunch of experiments and to try and do the exact same thing to see if we can get the same results." You could be forgiven for thinking that should be easy. Experiments are supposed to be replicable. The authors should have done it themselves before publication, and all you have to do is read the methods section in the paper and follow the instructions. Sadly nothing, it seems, could be further from the truth. After meticulous research involving painstaking attention to detail over several years (the project was launched in 2011), the team was able to confirm only two of the original studies' findings. Two more proved inconclusive and in the fifth, the team completely failed to replicate the result. "It's worrying because replication is supposed to be a hallmark of scientific integrity," says Dr Errington. Concern over the reliability of the results published in scientific literature has been growing for some time. According to a survey published in the journal Nature last summer, more than 70% of researchers have tried and failed to reproduce another scientist's experiments. Marcus Munafo is one of them. Now professor of biological psychology at Bristol University, he almost gave up on a career in science when, as a PhD student, he failed to reproduce a textbook study on anxiety. "I had a crisis of confidence. I thought maybe it's me, maybe I didn't run my study well, maybe I'm not cut out to be a scientist." The problem, it turned out, was not with Marcus Munafo's science, but with the way the scientific literature had been "tidied up" to present a much clearer, more robust outcome. "What we see in the published literature is a highly curated version of what's actually happened," he says. "The trouble is that gives you a rose-tinted view of the evidence because the results that get published tend to be the most interesting, the most exciting, novel, eye-catching, unexpected results. "What I think of as high-risk, high-return results." The reproducibility difficulties are not about fraud, according to Dame Ottoline Leyser, director of the Sainsbury Laboratory at the University of Cambridge. That would be relatively easy to stamp out. Instead, she says: "It's about a culture that promotes impact over substance, flashy findings over the dull, confirmatory work that most of science is about." She says it's about the funding bodies that want to secure the biggest bang for their bucks, the peer review journals that vie to publish the most exciting breakthroughs, the institutes and universities that measure success in grants won and papers published and the ambition of the researchers themselves. "Everyone has to take a share of the blame," she argues. "The way the system is set up encourages less than optimal outcomes." For its part, the journal Nature is taking steps to address the problem. It's introduced a reproducibility checklist for submitting authors, designed to improve reliability and rigour. "Replication is something scientists should be thinking about before they write the paper," says Ritu Dhand, the editorial director at Nature. "It is a big problem, but it's something the journals can't tackle on their own. It's going to take a multi-pronged approach involving funders, the institutes, the journals and the researchers." But we need to be bolder, according to the Edinburgh neuroscientist Prof Malcolm Macleod. "The issue of replication goes to the heart of the scientific process." Writing in the latest edition of Nature, he outlines a new approach to animal studies that calls for independent, statistically rigorous confirmation of a paper's central hypothesis before publication. "Without efforts to reproduce the findings of others, we don't know if the facts out there actually represent what's happening in biology or not." Without knowing whether the published scientific literature is built on solid foundations or sand, he argues, we're wasting both time and money. "It could be that we would be much further forward in terms of developing new cures and treatments. It's a regrettable situation, but I'm afraid that's the situation we find ourselves in." You can listen to Tom Feilden's report and the further discussion on BBC Radio 4's Today programme.


An international team of scientists led by the University of Cambridge has discovered the 'thermometer' molecule that enables plants to develop according to seasonal temperature changes. Researchers have revealed that molecules called phytochromes - used by plants to detect light during the day - actually change their function in darkness to become cellular temperature gauges that measure the heat of the night. The new findings, published today in the journal Science, show that phytochromes control genetic switches in response to temperature as well as light to dictate plant development. At night, these molecules change states, and the pace at which they change is "directly proportional to temperature" say scientists, who compare phytochromes to mercury in a thermometer. The warmer it is, the faster the molecular change - stimulating plant growth. Farmers and gardeners have known for hundreds of years how responsive plants are to temperature: warm winters cause many trees and flowers to bud early, something humans have long used to predict weather and harvest times for the coming year. The latest research pinpoints for the first time the molecular mechanism in plants that reacts to temperature - often triggering the buds of spring we long to see at the end of winter. With weather and temperatures set to become ever more unpredictable due to climate change, researchers say the discovery that this light-sensing molecule moonlights as the internal thermometer in plant cells could help us breed tougher crops. "It is estimated that agricultural yields will need to double by 2050, but climate change is a major threat to such targets. Key crops such as wheat and rice are sensitive to high temperatures. Thermal stress reduces crop yields by around 10% for every one degree increase in temperature," says lead researcher Dr Philip Wigge from Cambridge's Sainsbury Laboratory. "Discovering the molecules that allow plants to sense temperature has the potential to accelerate the breeding of crops resilient to thermal stress and climate change." In their active state, phytochrome molecules bind themselves to DNA to restrict plant growth. During the day, sunlight activates the molecules, slowing down growth. If a plant finds itself in shade, phytochromes are quickly inactivated - enabling it to grow faster to find sunlight again. This is how plants compete to escape each other's shade. "Light driven changes to phytochrome activity occur very fast, in less than a second," says Wigge. At night, however, it's a different story. Instead of a rapid deactivation following sundown, the molecules gradually change from their active to inactive state. This is called "dark reversion". "Just as mercury rises in a thermometer, the rate at which phytochromes revert to their inactive state during the night is a direct measure of temperature," says Wigge. "The lower the temperature, the slower phytochromes revert to inactivity, so the molecules spend more time in their active, growth-suppressing state. This is why plants are slower to grow in winter. "Warm temperatures accelerate dark reversion, so that phytochromes rapidly reach an inactive state and detach themselves from DNA - allowing genes to be expressed and plant growth to resume." Wigge believes phytochrome thermo-sensing evolved at a later stage, and co-opted the biological network already used for light-based growth during the downtime of night. Some plants mainly use day-length as an indicator of the season. Other species, such as daffodils, have considerable temperature sensitivity, and can flower months in advance during a warm winter. In fact, the discovery of the dual role of phytochromes provides the science behind a well-known rhyme long used to predict the coming season: Oak before Ash we'll have a splash, Ash before Oak we're in for a soak. Wigge explains: "Oak trees rely much more on temperature, likely using phytochromes as thermometers to dictate development, whereas Ash trees rely on measuring day length to determine their seasonal timing. "A warmer spring, and consequently a higher likeliness of a hot summer, will result in Oak leafing before Ash. A cold spring will see the opposite. As the British know only too well, a colder summer is likely to be a rain-soaked one." The new findings are the culmination of twelve years of research involving scientists from Germany, Argentina and the US, as well as the Cambridge team. The work was done in a model system, a mustard plant called Arabidopsis, but Wigge says the phytochrome genes necessary for temperature sensing are found in crop plants as well. "Recent advances in plant genetics now mean that scientists are able to rapidly identify the genes controlling these processes in crop plants, and even alter their activity using precise molecular 'scalpels'," adds Wigge. "Cambridge is uniquely well-positioned to do this kind of research as we have outstanding collaborators nearby who work on more applied aspects of plant biology, and can help us transfer this new knowledge into the field."


News Article | October 28, 2016
Site: www.gizmag.com

Scientists have long known that molecules known as phytochromes help plants detect light during the day and adjust growth accordingly. Now, thanks to a 12-year study involving researchers from four countries, they have discovered that the very same molecules do double duty at night, switching from light-sensors to temperature detectors. The researchers say the discovery could lead to tougher crops. Phytochromes are something like internal brakes for plants. When phytochromes are activated by sunlight, they bind to a plant's DNA to slow its growth. That might sound counterintuitive, but when a plant is getting all the sunlight it needs, it doesn't necessarily need to grow faster. But when it's in shade and the phytochromes decouple from the DNA, growth speeds up so that the plant can reach new sources of light. Till now researchers thought that was the only function of phytochromes and that when the sun set, the molecules simply got deactivated. The new study says that instead, phytochromes gradually deactivate in direct proportion to the temperature in a process called "dark reversion." If it's cold out, the molecules return to their inactive state more slowly, meaning that the brakes stay on longer and the plant growth is slowed. When it's warmer out, the dark reversion is sped up. The foot (or is that root?) comes off the brake and growth speeds up. The research was conducted using a mustard plant called Arabidopsis, which is frequently used in scientific studies (and the first plant to have its genome sequenced), but the researchers say that crops have phytochromes as well, and understanding the complete picture of how they work could help us battle difficult growing conditions brought about by climate change. "It is estimated that agricultural yields will need to double by 2050, but climate change is a major threat to such targets," said lead researcher Dr. Philip Wigge from Cambridge University's Sainsbury Laboratory. "Key crops such as wheat and rice are sensitive to high temperatures. Thermal stress reduces crop yields by around 10 percent for every one degree increase in temperature." "Discovering the molecules that allow plants to sense temperature has the potential to accelerate the breeding of crops resilient to thermal stress and climate change." The work of Wigge and his team has been published in the journal Science.


Researchers have revealed that molecules called phytochromes - used by plants to detect light during the day - actually change their function in darkness to become cellular temperature gauges that measure the heat of the night. The new findings, published today in the journal Science, show that phytochromes control genetic switches in response to temperature as well as light to dictate plant development. At night, these molecules change states, and the pace at which they change is "directly proportional to temperature" say scientists, who compare phytochromes to mercury in a thermometer. The warmer it is, the faster the molecular change - stimulating plant growth. Farmers and gardeners have known for hundreds of years how responsive plants are to temperature: warm winters cause many trees and flowers to bud early, something humans have long used to predict weather and harvest times for the coming year. The latest research pinpoints for the first time the molecular mechanism in plants that reacts to temperature - often triggering the buds of spring we long to see at the end of winter. With weather and temperatures set to become ever more unpredictable due to climate change, researchers say the discovery that this light-sensing molecule moonlights as the internal thermometer in plant cells could help us breed tougher crops. "It is estimated that agricultural yields will need to double by 2050, but climate change is a major threat to such targets. Key crops such as wheat and rice are sensitive to high temperatures. Thermal stress reduces crop yields by around 10% for every one degree increase in temperature," says lead researcher Dr Philip Wigge from Cambridge's Sainsbury Laboratory. "Discovering the molecules that allow plants to sense temperature has the potential to accelerate the breeding of crops resilient to thermal stress and climate change." In their active state, phytochrome molecules bind themselves to DNA to restrict plant growth. During the day, sunlight activates the molecules, slowing down growth. If a plant finds itself in shade, phytochromes are quickly inactivated - enabling it to grow faster to find sunlight again. This is how plants compete to escape each other's shade. "Light driven changes to phytochrome activity occur very fast, in less than a second," says Wigge. At night, however, it's a different story. Instead of a rapid deactivation following sundown, the molecules gradually change from their active to inactive state. This is called "dark reversion". "Just as mercury rises in a thermometer, the rate at which phytochromes revert to their inactive state during the night is a direct measure of temperature," says Wigge. "The lower the temperature, the slower phytochromes revert to inactivity, so the molecules spend more time in their active, growth-suppressing state. This is why plants are slower to grow in winter. "Warm temperatures accelerate dark reversion, so that phytochromes rapidly reach an inactive state and detach themselves from DNA - allowing genes to be expressed and plant growth to resume." Wigge believes phytochrome thermo-sensing evolved at a later stage, and co-opted the biological network already used for light-based growth during the downtime of night. Some plants mainly use day-length as an indicator of the season. Other species, such as daffodils, have considerable temperature sensitivity, and can flower months in advance during a warm winter. In fact, the discovery of the dual role of phytochromes provides the science behind a well-known rhyme long used to predict the coming season: Oak before Ash we'll have a splash, Ash before Oak we're in for a soak. Wigge explains: "Oak trees rely much more on temperature, likely using phytochromes as thermometers to dictate development, whereas Ash trees rely on measuring day length to determine their seasonal timing. "A warmer spring, and consequently a higher likeliness of a hot summer, will result in Oak leafing before Ash. A cold spring will see the opposite. As the British know only too well, a colder summer is likely to be a rain-soaked one." The new findings are the culmination of twelve years of research involving scientists from Germany, Argentina and the US, as well as the Cambridge team. The work was done in a model system, a mustard plant called Arabidopsis, but Wigge says the phytochrome genes necessary for temperature sensing are found in crop plants as well. "Recent advances in plant genetics now mean that scientists are able to rapidly identify the genes controlling these processes in crop plants, and even alter their activity using precise molecular 'scalpels'," adds Wigge. "Cambridge is uniquely well-positioned to do this kind of research as we have outstanding collaborators nearby who work on more applied aspects of plant biology, and can help us transfer this new knowledge into the field." More information: "Phytochromes function as thermosensors in Arabidopsis," Science, science.sciencemag.org/cgi/doi/10.1126/science.aaf6005


News Article | October 28, 2016
Site: www.sciencedaily.com

An international team of scientists led by the University of Cambridge has discovered the 'thermometer' molecule that enables plants to develop according to seasonal temperature changes. Researchers have revealed that molecules called phytochromes -- used by plants to detect light during the day -- actually change their function in darkness to become cellular temperature gauges that measure the heat of the night. The new findings, published today in the journal Science, show that phytochromes control genetic switches in response to temperature as well as light to dictate plant development. At night, these molecules change states, and the pace at which they change is "directly proportional to temperature" say scientists, who compare phytochromes to mercury in a thermometer. The warmer it is, the faster the molecular change -- stimulating plant growth. Farmers and gardeners have known for hundreds of years how responsive plants are to temperature: warm winters cause many trees and flowers to bud early, something humans have long used to predict weather and harvest times for the coming year. The latest research pinpoints for the first time the molecular mechanism in plants that reacts to temperature -- often triggering the buds of spring we long to see at the end of winter. With weather and temperatures set to become ever more unpredictable due to climate change, researchers say the discovery that this light-sensing molecule moonlights as the internal thermometer in plant cells could help us breed tougher crops. "It is estimated that agricultural yields will need to double by 2050, but climate change is a major threat to such targets. Key crops such as wheat and rice are sensitive to high temperatures. Thermal stress reduces crop yields by around 10% for every one degree increase in temperature," says lead researcher Dr Philip Wigge from Cambridge's Sainsbury Laboratory. "Discovering the molecules that allow plants to sense temperature has the potential to accelerate the breeding of crops resilient to thermal stress and climate change." In their active state, phytochrome molecules bind themselves to DNA to restrict plant growth. During the day, sunlight activates the molecules, slowing down growth. If a plant finds itself in shade, phytochromes are quickly inactivated -- enabling it to grow faster to find sunlight again. This is how plants compete to escape each other's shade. "Light driven changes to phytochrome activity occur very fast, in less than a second," says Wigge. At night, however, it's a different story. Instead of a rapid deactivation following sundown, the molecules gradually change from their active to inactive state. This is called "dark reversion." "Just as mercury rises in a thermometer, the rate at which phytochromes revert to their inactive state during the night is a direct measure of temperature," says Wigge. "The lower the temperature, the slower phytochromes revert to inactivity, so the molecules spend more time in their active, growth-suppressing state. This is why plants are slower to grow in winter. "Warm temperatures accelerate dark reversion, so that phytochromes rapidly reach an inactive state and detach themselves from DNA -- allowing genes to be expressed and plant growth to resume." Wigge believes phytochrome thermo-sensing evolved at a later stage, and co-opted the biological network already used for light-based growth during the downtime of night. Some plants mainly use day-length as an indicator of the season. Other species, such as daffodils, have considerable temperature sensitivity, and can flower months in advance during a warm winter. In fact, the discovery of the dual role of phytochromes provides the science behind a well-known rhyme long used to predict the coming season: Oak before Ash we'll have a splash, Ash before Oak we're in for a soak. Wigge explains: "Oak trees rely much more on temperature, likely using phytochromes as thermometers to dictate development, whereas Ash trees rely on measuring day length to determine their seasonal timing. "A warmer spring, and consequently a higher likeliness of a hot summer, will result in Oak leafing before Ash. A cold spring will see the opposite. As the British know only too well, a colder summer is likely to be a rain-soaked one." The new findings are the culmination of twelve years of research involving scientists from Germany, Argentina and the US, as well as the Cambridge team. The work was done in a model system, a mustard plant called Arabidopsis, but Wigge says the phytochrome genes necessary for temperature sensing are found in crop plants as well. "Recent advances in plant genetics now mean that scientists are able to rapidly identify the genes controlling these processes in crop plants, and even alter their activity using precise molecular 'scalpels'," adds Wigge. "Cambridge is uniquely well-positioned to do this kind of research as we have outstanding collaborators nearby who work on more applied aspects of plant biology, and can help us transfer this new knowledge into the field."


News Article | April 27, 2016
Site: www.nature.com

Update: On 26 April, a team led by microbial population geneticist Daniel Croll, who is at the Swiss Federal Institute of Technology in Zurich, reported on github.com that the Bangladeshi wheat-blast strain is closely related to those collected in Brazilian wheat fields and on nearby weeds. His team’s analysis, which uses the data on the website Open Wheat Blast, reveals that the sample is not closely related to known rice-blast-causing strains of M. oryzae. Croll’s team concludes that wheat blast was probably introduced to Bangladesh from Brazil, and warns that other Asian countries that import Brazilian wheat, including Thailand, the Philippines and Vietnam, should be on the lookout for the disease. Fields are ablaze in Bangladesh, as farmers struggle to contain Asia’s first outbreak of a fungal disease that periodically devastates crops in South America. Plant pathologists warn that wheat blast could spread to other parts of south and southeast Asia, and are hurrying to trace its origins. “It’s important to know what the strain is,” says Sophien Kamoun, a biologist at the Sainsbury Laboratory in Norwich, UK, who has created a website, Open Wheat Blast (go.nature.com/bkczwf), to encourage researchers to share data. Efforts are also under way to find wheat genes that confer resistance to the disease. First detected in February and confirmed with genome sequencing by Kamoun’s lab this month, the wheat-blast outbreak has already caused the loss of more than 15,000 hectares of crops in Bangladesh. “It’s really an explosive, devastating disease,” says plant pathologist Barbara Valent of Kansas State University in Manhattan, Kansas. “It’s really critical that it be controlled in Bangladesh.” After rice, wheat is the second most cultivated grain in Bangladesh, which has a population of 156 million people. More broadly, inhabitants of south Asia grow 135 million tonnes of wheat each year. Wheat blast is caused by the fungus Magnaporthe oryzae. Since 1985, when scientists discovered it in Brazil’s Paraná state, the disease has raced across South America. The fungus is better known as a pathogen of rice. But unlike in rice, where M. oryzae attacks the leaves, the fungus strikes the heads of wheat, which are difficult for fungicides to reach. A 2009 outbreak in wheat cost Brazil one-third of that year’s crop. “There are regions in South America where they don’t grow wheat because of the disease,” Valent says. Wheat blast was spotted in Kentucky in 2011, but vigorous surveillance helped to stop it spreading in the United States. In South America, the disease tends to take hold in hot and humid spells. Such conditions are present in Bangladesh, and the disease could migrate across south and southeast Asia, say plant pathologists. In particular, it could spread over the Indo-Gangetic Plain through Bangladesh, northern India and eastern Pakistan, warn scientists at the Bangladesh Agricultural Research Institute (BARI) in Nashipur. Bangladeshi officials are burning government-owned wheat fields to contain the fungus, and telling farmers not to sow seeds from infected plots. The BARI hopes to identify wheat varieties that are more tolerant of the fungus and agricultural practices that can keep it at bay, such as crop rotation and seed treatment. It is unknown how wheat blast got to Bangladesh. One possibility is that a wheat-infecting strain was brought in from South America, says Nick Talbot, a plant pathologist at the University of Exeter, UK. Another is that an M. oryzae strain that infects south Asian grasses somehow jumped to wheat, perhaps triggered by an environmental shift: that is what happened in Kentucky, when a rye-grass strain infected wheat. To tackle the question, this month Kamoun’s lab sequenced a fungus sample from Bangladesh. The strain seems to be related to those that infect wheat in South America, says Kamoun, but data from other wheat-infecting strains and strains that plague other grasses are needed to pinpoint the outbreak’s origins conclusively. The Open Wheat Blast website might help. Kamoun has uploaded the Bangladeshi data, and Talbot has deposited M. oryzae sequences from wheat in Brazil. Talbot hopes that widely accessible genome data could help to combat the outbreak. Researchers could use them to screen seeds for infection or identify wild grasses that can transmit the fungus to wheat fields. Rapid data sharing is becoming more common in health emergencies, such as the outbreak of Zika virus in the Americas. Kamoun and Talbot say that their field should follow suit. “The plant-pathology community has a responsibility to allow data to be used to combat diseases that are happening now, and not worry too much about whether they may or may not get a Nature paper out of it,” says Talbot. Last month, Valent’s team reported the first gene variant known to confer wheat-blast resistance (C. D. Cruz et al. Crop Sci. http://doi.org/bfk7; 2016), and field trials of crops that bear the resistance gene variant have begun in South America. But plant pathologists say that finding one variant is not enough: wheat strains must be bred with multiple genes for resistance, to stop M. oryzae quickly overcoming their defences. The work could help in the Asian crisis, says Talbot. “What I would hope for out of this sorry situation,” he says, “is that there will be a bigger international effort to identify resistance genes.”


News Article | December 16, 2015
Site: www.nature.com

Plant geneticist Stefan Jansson is champing at the bit to start field trials on crops tweaked with powerful gene-editing technologies. He plans to begin by using edits to study how the cress plant Arabidopsis protects its photosynthetic machinery from damage in excessively bright light. But the future of his work depends on the European Commission’s answer to a legal conundrum. Should it regulate a gene-edited plant that has no foreign DNA as a genetically modified (GM) organism? Jansson, who works at Umeå University in Sweden, says that he will drop his experiments if the plants are classed as GM, because Europe’s onerous regulations would make his work too expensive and slow. He and many others are anxiously awaiting the commission’s decision, which will dictate how they approach experiments using the latest gene-editing techniques, including the popular CRISPR–Cas9 method. The commission has repeatedly stalled on delivering its verdict, which will apply to edited animals and microorganisms as well as plants. It now says that it will make its legal analysis public by the end of March. Swedish authorities, meanwhile, have told Jansson that unless the commission specifies otherwise, they will not require his cress to be subject to GM regulations. The legal limbo is having a big impact on research, says René Smulders of the plant-breeding division at Wageningen University and Research Centre in the Netherlands. He says that this year, he was rejected for a European Union grant — on changing the composition of a plant’s oils by editing a gene — because referees were concerned about the legal uncertainty. “Some scientists hesitate to start using the new methods in case they end up being regulated and their research projects hit a dead end,” he says. At issue is the interpretation of a 2001 European Commission directive on releasing GM organisms into the environment, which covers field trials and cultivation. It defines GM organisms as having alterations that cannot occur naturally, which were made by genetic engineering. What is unclear is how this relates to experiments, such as Jansson’s, in which researchers introduce foreign DNA to direct a precise edit in a plant’s own genetic material but then use selective breeding to remove the foreign gene. The final plant has a few tweaked nucleotides, but cannot be distinguished from a wild plant that might have acquired the same mutation naturally — so it cannot be traced in the environ­ment as EU regulations require. Many EU member states — including Sweden — have conducted their own analyses of the directive, and argue that it should not apply to edited plants that do not contain foreign DNA. But some non-governmental organizations (NGOs) hostile to genetic manipulation have produced analyses that conclude the directive should apply because genetic engineering is involved. Academic scientists and seed and crop companies fear that plants made with the latest gene-editing techniques may share the fate of conventional GM plants in Europe. Strict regulations, cumbersome bureaucracy and activism against GM organisms have meant that scientists in some countries, such as Germany, do not even attempt field trials. The regulations have increased the costs of bringing a GM crop to market, and many European nations do not allow such crops to be cultivated at all. That is frustrating for plant scientists who want their work to be useful to the world, says Jonathan Jones, a plant researcher at the Sainsbury Laboratory in Norwich, UK. “We hoped that the new plant-breeding techniques would offer ways of achieving the same outcome without the onerous regulations — and fear that might not turn out to be the case,” he says. Many countries outside Europe do not face the same uncertainty, because they regulate GM organisms according to the nature of the product, not how it was made. In the United States, gene-edited crops containing no foreign genetic material are assessed on a case-by-case basis. In 2004, the biotechnology company Cibus, based in San Diego, California, was told that the US Department of Agriculture would not need to regulate its herbicide-resistant oilseed rape, made with an earlier form of gene-editing. Its crop is now cultivated in the United States. (The White House did, however, begin a review of all US biotechnology regulation in July.) Since 2011, Cibus has asked six countries — Finland, Germany, Ireland, Spain, Sweden and the United Kingdom — whether they would consider its crop to come under the scope of the EU directive. Without guidelines from the commission, each conducted its own analysis and said that it would not. Cibus has now done field trials in the United Kingdom and Sweden, but it put its activities on hold after the commission sent a letter to all EU member states on 15 June, asking them to wait for its legal interpretation. Whatever the commission decides, it is likely that either a member state, an NGO or a company will sue — meaning that the European Court of Justice may make the final, binding decision on the matter. Many plant scientists do basic research, so their gene-edited plants never need to leave the greenhouse. But Jansson must plant his cress outside to test its photosynthetic abilities in natural conditions. With his country’s approval, he plans to plant the crop in the spring. “Lawyers talk and talk — I think it is important for Europe to have a test case,” he says.

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