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Segonzac C.,Sainsbury Laboratory | Feike D.,John Innes Center | Gimenez-Ibanez S.,CSIC - National Center for Biotechnology | Hann D.R.,University of Basel | And 2 more authors.
Plant Physiology | Year: 2011

Our current understanding of pathogen-associated molecular pattern (PAMP)-triggered immunity signaling pathways in plants is limited due to the redundancy of several components or the lethality of mutants in Arabidopsis (Arabidopsis thaliana). To overcome this, we used a virus-induced gene silencing-based approach in combination with pharmacological studies to decipher links between early PAMP-triggered immunity events and their roles in immunity following PAMP perception in Nicotiana benthamiana. Two different calcium influx inhibitors suppressed the reactive oxygen species (ROS) burst: activation of the mitogen-activated protein kinases (MAPKs) and PAMP-induced gene expression. The calcium burst was unaffected in plants specifically silenced for components involved in ROS generation or for MAPKs activated by PAMP treatment. Importantly, the ROS burst still occurred in plants silenced for the two major defense-associated MAPK genes NbSIPK (for salicylic acid-induced protein kinase) and NbWIPK (for wound-induced protein kinase) or for both genes simultaneously, demonstrating that these MAPKs are dispensable for ROS production. We further show that NbSIPK silencing is sufficient to prevent PAMP-induced gene expression but that both MAPKs are required for bacterial immunity against two virulent strains of Pseudomonas syringae and their respective nonpathogenic mutants. These results suggest that the PAMP-triggered calcium burst is upstream of separate signaling branches, one leading to MAPK activation and then gene expression and the other to ROS production. In addition, this study highlights the essential roles of NbSIPK and NbWIPK in antibacterial immunity. Unexpectedly, negative regulatory mechanisms controlling the intensity of the PAMP-triggered calcium and ROS bursts were also revealed by this work. © 2011 American Society of Plant Biologists.


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.


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.”


Farid A.,University of Natural Resources and Life Sciences, Vienna | Gro Malinovsky F.,Sainsbury Laboratory | Veit C.,University of Natural Resources and Life Sciences, Vienna | Schoberer J.,University of Natural Resources and Life Sciences, Vienna | And 2 more authors.
Plant Physiology | Year: 2013

Asparagine-linked glycosylation of proteins is an essential cotranslational and posttranslational protein modification in plants. The central step in this process is the transfer of a preassembled oligosaccharide to nascent proteins in the endoplasmic reticulum by the oligosaccharyltransferase (OST) complex. Despite the importance of the catalyzed reaction, the composition and the function of individual OST subunits are still ill defined in plants. Here, we report the function of the highly conserved OST subunit OST3/6. We have identified a mutant in the OST3/6 gene that causes overall underglycosylation of proteins and affects the biogenesis of the receptor kinase EF-TU RECEPTOR involved in innate immunity and the endo-b-1,4-glucanase KORRIGAN1 required for cellulose biosynthesis. Notably, the ost3/6 mutation does not affect mutant variants of the receptor kinase BRASSINOSTEROID-INSENSITIVE1. OST3/6 deficiency results in activation of the unfolded protein response and causes hypersensitivity to salt/osmotic stress and to the glycosylation inhibitor tunicamycin. Consistent with its role in protein glycosylation, OST3/6 resides in the endoplasmic reticulum and interacts with other subunits of the OST complex. Together, our findings reveal the importance of Arabidopsis (Arabidopsis thaliana) OST3/6 for the efficient glycosylation of specific glycoproteins involved in different physiological processes and shed light on the composition and function of the plant OST complex. © 2013 American Society of Plant Biologists. All Rights Reserved.


Beck M.,Sainsbury Laboratory | Zhou J.,Sainsbury Laboratory | Faulkner C.,Sainsbury Laboratory | Mac D.,Sainsbury Laboratory | Robatzek S.,Sainsbury Laboratory
Plant Cell | Year: 2012

The activity of surface receptors is location specific, dependent upon the dynamic membrane trafficking network and receptor-mediated endocytosis (RME). Therefore, the spatio-temporal dynamics of RME are critical to receptor function. The plasma membrane receptor FLAGELLIN SENSING2 (FLS2) confers immunity against bacterial infection through perception of flagellin (flg22). Following elicitation, FLS2 is internalized into vesicles. To resolve FLS2 trafficking, we exploited quantitative confocal imaging for colocalization studies and chemical interference. FLS2 localizes to bona fide endosomes via two distinct endocytic trafficking routes depending on its activation status. FLS2 receptors constitutively recycle in a Brefeldin A (BFA)- sensitive manner, while flg22-activated receptors traffic via ARA7/Rab F2b- and ARA6/Rab F1-positive endosomes insensitive to BFA. FLS2 endocytosis required a functional Rab5 GTPase pathway as revealed by dominant-negative ARA7/Rab F2b. Flg22-induced FLS2 endosomal numbers were increased by Concanamycin A treatment but reduced by Wortmannin, indicating that activated FLS2 receptors are targeted to late endosomes. RME inhibitors Tyrphostin A23 and Endosidin 1 altered but did not block induced FLS2 endocytosis. Additional inhibitor studies imply the involvement of the actin-myosin system in FLS2 internalization and trafficking. Altogether, we report a dynamic pattern of subcellular trafficking for FLS2 and reveal a defined framework for ligand-dependent endocytosis of this receptor. © 2012 American Society of Plant Biologists. All rights reserved.


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.


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."

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