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The study is the result of a long-standing collaboration between researchers at the University of Arizona and in China. Over 11 years, they tested more than 66,000 pink bollworm caterpillars from China's Yangtze River Valley, a vast region of southeastern China that is home to millions of smallholder farmers. According to the study's authors, this is the first reversal of substantial pest resistance to a Bt crop. "We have seen blips of resistance going up and down in a small area," said senior author Bruce Tabashnik, a Regents' Professor in the UA's College of Agriculture and Life Sciences. "But this isn't a blip. Resistance had increased significantly across an entire region, then it decreased below detection level after this novel strategy was implemented." Cotton, corn and soybean have been genetically engineered to produce pest-killing proteins from the widespread soil bacterium Bacillus thuringiensis, or Bt. These Bt proteins are considered environmentally friendly because they are not toxic to people and wildlife. They have been used in sprays by organic growers for more than 50 years, and in engineered Bt crops planted by millions of farmers worldwide on more than 1 billion acres since 1996. Unfortunately, without adequate countermeasures, pests can quickly evolve resistance. The primary strategy for delaying resistance is providing refuges of the pests' host plants that do not make Bt proteins. This allows survival of insects that are susceptible to Bt proteins and reduces the chances that two resistant insects will mate and produce resistant offspring. Before 2010, the U.S. Environmental Protection Agency required refuges in separate fields or large blocks within fields. Planting such non-Bt cotton refuges is credited with preventing evolution of resistance to Bt cotton by pink bollworm in Arizona for more than a decade. By contrast, despite a similar requirement for planting refuges in India, farmers there did not comply and pink bollworm rapidly evolved resistance. The ingenious strategy used in China entails interbreeding Bt cotton with non-Bt cotton, then crossing the resulting first-generation hybrid offspring and planting the second-generation hybrid seeds. This generates a random mixture within fields of 75 percent Bt cotton plants side-by-side with 25 percent non-Bt cotton plants. "Because cotton can self-pollinate, the first-generation hybrids must be created by tedious and costly hand pollination of each flower," said Tabashnik, who also is a member of the UA's BIO5 Institute. "However, hybrids of the second generation and all subsequent generations can be obtained readily via self-pollination. So, the hybrid mix and its benefits can be maintained in perpetuity." Tabashnik calls this strategy revolutionary because it was not designed to fight resistance and arose without mandates by government agencies. Rather, it emerged from the farming community of the Yangtze River Valley. While most previous attention has focused on the drawbacks of interbreeding between genetically engineered and conventional plants, the authors point out that the new results demonstrate gains from such hybridization. "For the growers in China, this practice provides short-term benefits," Tabashnik added. "It's not a short-term sacrifice imposed on them for potential long-term gains. The hybrid plants tend to have higher yield than the parent plants, and the second-generation hybrids cost less, so it's a market-driven choice for immediate advantages, and it promotes sustainability. Our results show 96 percent pest suppression and 69 percent fewer insecticide sprays." Although seed mixtures of corn have been planted in the U.S. since 2010, the effects of seed mixtures on pest adaptation were not tested before on a large scale, he explained. "Our study provides the first evidence that planting mixtures of Bt and non-Bt seeds within fields has a resistance-delaying or, in this case, resistance-reversing effect," Tabashnik said. Unlike the strategy in China, the corn seed mixtures planted in the U.S. do not involve interbreeding. Also, the corn seed mixtures have as little as 5 percent non-Bt corn, which may not be enough to battle resistance effectively. "This study gives a new option for managing resistance that is very convenient for small-scale farmers and could be broadly helpful in developing countries like China and India," explained coauthor Kongming Wu, who led the work conducted in China and is a professor in the Institute of Plant Protection in Beijing. "A great thing about this hybrid seed mix strategy is that we don't have to worry about growers' compliance or regulatory issues," Tabashnik said. "We know it works for millions of farmers in the Yangtze River Valley. Whether it works elsewhere remains to be determined." More information: Peng Wan el al., "Hybridizing transgenic Bt cotton with non-Bt cotton counters resistance in pink bollworm," PNAS (2017). www.pnas.org/cgi/doi/10.1073/pnas.1700396114


News Article | May 8, 2017
Site: www.eurekalert.org

Researchers have discovered an unexpected strategy that can delay, and even reverse, evolution of resistance by pests to genetically engineered crops Insect pests that are rapidly adapting to genetically engineered crops threaten agriculture worldwide. A new study published in the Proceedings of the National Academy of Sciences reveals the success of a surprising strategy for countering this problem: Hybridizing genetically engineered cotton with conventional cotton reduced resistance in the pink bollworm, a voracious global pest. The study is the result of a long-standing collaboration between researchers at the University of Arizona and in China. Over 11 years, they tested more than 66,000 pink bollworm caterpillars from China's Yangtze River Valley, a vast region of southeastern China that is home to millions of smallholder farmers. According to the study's authors, this is the first reversal of substantial pest resistance to a Bt crop. "We have seen blips of resistance going up and down in a small area," said senior author Bruce Tabashnik, a Regents' Professor in the UA's College of Agriculture and Life Sciences. "But this isn't a blip. Resistance had increased significantly across an entire region, then it decreased below detection level after this novel strategy was implemented." Cotton, corn and soybean have been genetically engineered to produce pest-killing proteins from the widespread soil bacterium Bacillus thuringiensis, or Bt. These Bt proteins are considered environmentally friendly because they are not toxic to people and wildlife. They have been used in sprays by organic growers for more than 50 years, and in engineered Bt crops planted by millions of farmers worldwide on more than 1 billion acres since 1996. Unfortunately, without adequate countermeasures, pests can quickly evolve resistance. The primary strategy for delaying resistance is providing refuges of the pests' host plants that do not make Bt proteins. This allows survival of insects that are susceptible to Bt proteins and reduces the chances that two resistant insects will mate and produce resistant offspring. Before 2010, the U.S. Environmental Protection Agency required refuges in separate fields or large blocks within fields. Planting such non-Bt cotton refuges is credited with preventing evolution of resistance to Bt cotton by pink bollworm in Arizona for more than a decade. By contrast, despite a similar requirement for planting refuges in India, farmers there did not comply and pink bollworm rapidly evolved resistance. The ingenious strategy used in China entails interbreeding Bt cotton with non-Bt cotton, then crossing the resulting first-generation hybrid offspring and planting the second-generation hybrid seeds. This generates a random mixture within fields of 75 percent Bt cotton plants side-by-side with 25 percent non-Bt cotton plants. "Because cotton can self-pollinate, the first-generation hybrids must be created by tedious and costly hand pollination of each flower," said Tabashnik, who also is a member of the UA's BIO5 Institute. "However, hybrids of the second generation and all subsequent generations can be obtained readily via self-pollination. So, the hybrid mix and its benefits can be maintained in perpetuity." Tabashnik calls this strategy revolutionary because it was not designed to fight resistance and arose without mandates by government agencies. Rather, it emerged from the farming community of the Yangtze River Valley. While most previous attention has focused on the drawbacks of interbreeding between genetically engineered and conventional plants, the authors point out that the new results demonstrate gains from such hybridization. "For the growers in China, this practice provides short-term benefits," Tabashnik added. "It's not a short-term sacrifice imposed on them for potential long-term gains. The hybrid plants tend to have higher yield than the parent plants, and the second-generation hybrids cost less, so it's a market-driven choice for immediate advantages, and it promotes sustainability. Our results show 96 percent pest suppression and 69 percent fewer insecticide sprays." Although seed mixtures of corn have been planted in the U.S. since 2010, the effects of seed mixtures on pest adaptation were not tested before on a large scale, he explained. "Our study provides the first evidence that planting mixtures of Bt and non-Bt seeds within fields has a resistance-delaying or, in this case, resistance-reversing effect," Tabashnik said. Unlike the strategy in China, the corn seed mixtures planted in the U.S. do not involve interbreeding. Also, the corn seed mixtures have as little as 5 percent non-Bt corn, which may not be enough to battle resistance effectively. "This study gives a new option for managing resistance that is very convenient for small-scale farmers and could be broadly helpful in developing countries like China and India," explained coauthor Kongming Wu, who led the work conducted in China and is a professor in the Institute of Plant Protection in Beijing. "A great thing about this hybrid seed mix strategy is that we don't have to worry about growers' compliance or regulatory issues," Tabashnik said. "We know it works for millions of farmers in the Yangtze River Valley. Whether it works elsewhere remains to be determined." Registered journalists can access an embargoed copy of the research article through https:/ , or by contacting the PNAS News Office by phone: 202-334-1310, email: PNASnews@nas.edu, or fax: 202-334-2739.


CHANDLER, Ariz.--(BUSINESS WIRE)--On May 12, 2017, Governor Doug Ducey signed Arizona’s $9.8 billion 2018-2019 Budget which provides bonding authority for $1 billion for investments in University Research Infrastructure. This investment continues a collaboration between the State of Arizona, Industry Leaders, Philanthropists, and Arizona’s Universities that is driving Arizona towards its goal of becoming a top-tier bioscience state. The Biotechnology Innovation Organization in partnership with TEConomy Partners publishes the biennial report on the economic impact of the bioscience industry that provides a national overview and ranks the 50 states and Puerto Rico across five quintiles or tiers. The 2016 Report, The Value of Bioscience Innovation in Growing Jobs and Improving Quality of Life 2016, was released in June of 2016 at the BIO International Convention in San Francisco. The report includes a wide range of metrics and economic indicators on a national and state basis. As reported in 2016, the top 10 states based on the number of bioscience firms (Tier I) were California, Florida, Illinois, Massachusetts, New Jersey, New York, North Carolina, Pennsylvania, Ohio, and Texas. Could Arizona achieve the growth necessary to reach the top-tiers? Arizona’s leaders began the journey to achieve this goal twenty years ago. In 1997, the Arizona Bioindustry Cluster was founded by Bob Case and Michael E. Berens, Ph.D. laying the foundation for what would become the Arizona Bioindustry Association or AZBio in 2003. Work by the Arizona Legislature and a coalition of community leaders supported voter passage of Proposition 301 in the year 2000. Prop. 301 established a six-tenths of one cent sales tax to support education that included funding for an estimated $1 billion (generated and disbursed over 20 years) for research at Arizona universities. The resulting Technology Research Initiative Fund (TRIF) is administered by the Arizona Board of Regents and has distributed $892 million for the period spanning from 2001-2016 and is well on its way to reach the billion dollar goal by June 30, 2021. The following year, the Flinn Foundation committed to 10 years of major funding for Arizona biosciences and brought together over 100 leaders to begin to craft what would become the Arizona Bioscience Roadmap. Under the stewardship of the Flinn Foundation, the strategic plan for the biosciences in Arizona would include key initiatives along with a commitment to measurement and reporting of the results. The first decade of the new century marked the completion of The Human Genome Project and a new era for life science research and development globally. From 2000 to 2010, Arizona’s Bioscience community activity included the International Genomics Consortium establishing its home in Phoenix and the subsequent creation of the Translational Genomics Research Institute (TGen) which was funded by a $90 million fundraising effort and spun out of IGC. In addition to the funding from Prop. 301, the Arizona legislature approved $440 million for construction of new university research facilities supporting the growth of the Biodesign Institute at Arizona State University, the BIO5 Institute at the University of Arizona, new research facilities at Northern Arizona University and more. An additional $100 million was approved by the voters for bioscience and health care training and facilities at Maricopa Community Colleges. The Virginia G. Piper Charitable Trust committed $50 million to personalized medicine in Arizona and local philanthropists have supported the community with additional resources for research and patient care across the state. Over the last two decades, Arizona’s bioscience industry has focused and grown. Arizona has risen in the rankings to take its place in the second tier of the Bioscience rankings based on number of firms. The Biodesign Institute at Arizona State University has grown from one building to two with a third building under construction. Arizona is now home to the Critical Path Institute, the National Biomarker Development Alliance, the Arizona Alzheimer’s Alliance, the Banner Alzheimer’s Institute, Cancer Treatment Centers of America, and Banner MD Anderson. Barrow Neurological Institute, founded in 1962 as a regional specialty center, has grown into one of the premiere destinations in the world for neurology and neurosurgery. Phoenix Children’s Hospital is now one of the largest children’s hospitals in the country and is ranked in 10 out of 10 specialties. Mayo Clinic has expanded its research and patient care capacity, added proton beam capabilities and will welcome the first class to its Arizona-based Mayo Medical School in 2017. The University of Arizona extended its reach from Tucson to Phoenix which now includes the The University of Arizona College of Medicine-Phoenix and the The University of Arizona Cancer Center at Dignity Health St. Joseph's Hospital and Medical Center on the Phoenix Biomedical Campus. The number of life science companies in Arizona is now over 1,400 and multi-billion dollar exits include the sale of Ventana Medical Systems, Inc. to Roche for $3.4 Billion and Abraxis Biosciences for $2.9 billion to Celgene. Today, companies that were born in Arizona are now publicly traded including Insys, HTG Molecular, and SensTech while others have been acquired by AMAG Pharmaceuticals, Caris Diagnostics, Thermo Fischer, IMS Health, Merz, Stryker and more. These companies have continued to grow in Arizona joining global leaders including BARD, Medtronic, and W.L. Gore. The combined benefits of Arizona’s world-class healthcare institutions and diverse population demographics are driving the number of active clinical trials in the state which have more than doubled over the period from 2012 – 2017 based on data at ClinicalTrials.gov. Long-time residents and new industry partners are benefiting from Arizona’s business-friendly public policy and regulatory environment, affordable operating cost structures, stable and reliable energy suppliers, well-managed water resources, talent, and an affordable cost of living in communities that provide their employees the opportunity for an excellent quality of life. Free from the business disruptions that can be caused by earthquakes, hurricanes, tornadoes, and floods, Arizona has become a go-to site for both high-tech manufacturing and corporate data centers. The Arizona Innovation Challenge, which made its first awards in 2011 and is powered by the Arizona Commerce Authority, awards the most money in the country for a technology commercialization challenge – $3 million ($1.5 million twice yearly) to the world’s most promising technology ventures. Awards range from $100,000 to $250,000 per company. Over this 20-year span, Arizona has gained a reputation as the state with the “collaborative gene” and attracts thought leaders looking to discover, develop, and deliver life-changing and life-saving innovations to patients. Globally recognized thought leaders have left the hallowed halls of Harvard, the National Institutes of Health and other world-class institutions to innovate and collaborate in Arizona. One real-world example of this collaboration is Arizona State University’s International School of Biomedical Diagnostics. A global center for research, teaching and service in the emerging field of biomedical diagnostics, the school pulls expertise from faculty across ASU, in collaboration with Dublin City University (DCU), Ventana Medical Systems, and other industry partners. ASU faculty come from: the Biodesign Institute, College of Health Solutions, Ira A. Fulton Schools of Engineering, School of Life Sciences in the College of Liberal Arts and Sciences, the W. P. Carey School of Business, and the Consortium for Science, Policy & Outcomes. The initiative also leverages the expertise of the National Biomarker Development Alliance that is led by ASU. Under the leadership of President Michael Crow, Arizona State University has been named the Most Innovative University in the United states for two years running and out-ranking Stanford and MIT. Throughout the Arizona Bioscience Roadmap’s first decade, Battelle tracked performance data that was released annually by the Flinn Foundation. The performance metrics released in 2014 serve as the benchmark for the second decade of the Roadmap, with new data reported on a biennial basis. The most current data is available in “2015 Progress of the Biosciences in Arizona,” a report produced by TEConomy Partners (a spinoff of Battelle) that was released in March 2016. The Flinn Foundation will continue to track the progress of the bioscience sector each year by highlighting the state’s major developments. In April of 2017, the Flinn Foundation released its most recent update, the 2016 Progress of the Biosciences in Arizona. Could Arizona achieve the growth necessary to reach the top-tiers? Absolutely. Now, twenty years into the process, Arizona’s Bioindustry has a new funding catalyst. With the Governor’s vision and the Legislature’s support, an additional $1 billion dollars will be invested in university research infrastructure beginning in July of 2018. Arizona’s leaders are already discussing what the next iteration of Prop. 301 will look like as it approaches its renewal on or before 2020. The Arizona Legislature has passed HB2191 which authorizes an additional $10 million in Angel Investor Tax Credits spread over the next four years and SB1416 which continues Arizona’s Quality Jobs Tax Credit, Arizona's Research and Development Tax Credits and other business incentives. Both bills have been sent to the Governor for his signature. Arizona’s leaders are continuing the journey to take the state into the top tiers of the bioscience rankings. The Flinn Foundation has extended its commitment to steward the Arizona Bioscience Roadmap through the year 2025 with the support of the 100-person Arizona Bioscience Roadmap Steering Committee and the Arizona Bioindustry Association (AZBio) Board of Directors is committed to the vision of making Arizona a top-tier bioscience state and works collaboratively to make that vision a reality. A key component in Arizona’s life science ecosystem, the Arizona Bioindustry Association (AZBio) is the only statewide organization exclusively focused on Arizona’s bioscience industry. AZBio membership includes patient advocacy organizations, life science innovators, educators, healthcare partners, municipalities and leading business organizations. AZBio is the statewide affiliate of the Biotechnology Innovation Organization (BIO) and works in partnership with AdvaMed, MDMA, and PhRMA to advance innovation and to ensure that the value delivered from life-changing and life-saving innovation benefits people in Arizona and around the world. For more information visit www.AZBio.org and www.AZBio.TV To learn more about Arizona’s Bioindustry:


News Article | May 5, 2017
Site: www.businesswire.com

CHANDLER, Ariz.--(BUSINESS WIRE)--At 11:01 p.m. on Thursday, May 4, 2017, the Arizona Senate passed HB 2547: university infrastructure capital financing; appropriations, paving the way for up to $1 billion in bonds to expand and maintain university research infrastructure at Arizona’s public universities. HB2547 is part of a set of budget bills that make up Arizona’s $9.8 billion budget for the fiscal year the begins on July 1, 2017. The bill’s primary sponsor was Representative Paul Boyer (LD-20). Representative Boyer is the Chairman of the House Education Committee, and is a member of the House Health and County and Municipal Affairs Committees. A vehicle supporting the $1 billion investment in Arizona’s University Research Infrastructure was originally proposed in Arizona Governor Doug Ducey’s Executive Budget on January 13, 2017. The Governor’s Plan proposed allowing Arizona’s three state universities to apply the Transaction Privilege Tax (TPT) revenue that they create to support up to $1 billion in bonding for research and development, and deferred maintenance construction projects. While support for investing in Arizona’s future by expanding our university research infrastructure was strong in the community and with members of the legislature, concerns over the use of TPT revenue and the impact that it could have on other stakeholders was a legislative concern. Achieving the goal of an $1 billion investment would require creativity, collaboration and compromise. Reaching the Destination with a Different Vehicle Following months of committee hearings, discussions, stakeholder meetings and communication with constituents, a new funding plan was developed that combines a percentage of the new licensure and royalty agreements that are the result of research at Arizona’s public universities, with state funding support and a university match to allow for up to $1 billion in bonding capacity for Arizona’s public universities. This plan became HB2547, which first passed in the Arizona House of Representatives (33-26), followed by the Arizona Senate (23-7), paves the way for a $1 billion investment in Arizona’s public universities and is on the way to the Governor’s desk. To view the full summary of HB 2547, visit http://www.azleg.gov/legtext/53leg/1R/summary/H.HB2547_05-04-17_HOUSEENGROSSED.DOCX.htm. In 2003, the Arizona Legislature authorized an annual appropriation of $35 million to construct roughly $500 million worth of university research facilities that was championed by then-Speaker Pro Tempore Bob Robson. These projects included the Biodesign Institute at Arizona State University, The University of Arizona’s Keating Bioresearch Building, which houses the UA BIO5 Institute, and Arizona Biomedical Collaborative 1 on the Phoenix Biomedical Campus. At Northern Arizona University, the Applied Research and Development facility has enabled the university to expand its research in the areas of national defense and infectious disease. Since the state’s investment in 2003, research activity conducted at Arizona’s public universities has increased 77 percent and now totals nearly $1.1 billion each year. University invention disclosures have increased 154 percent. Degrees awarded in high-demand fields, including key STEM (Science, Technology, Engineering and Math) fields, have increased 40 percent in the past six years alone. In fiscal 2015, Arizona’s three public universities were responsible for an estimated 102,000 jobs and $11 billion in total economic impact. “Our investments in university research infrastructure have been and will be a major economic driver,” shared Joan Koerber-Walker, president & CEO of the Arizona Bioindustry Association (AZBio). “Yet, measuring this impact in a purely economic sense overlooks the greater value that life science research represents. The greatest value comes from the life-saving and life-changing innovations that will make life better for people in Arizona and around the world. Arizona university researchers and their industry partners are discovering, developing, and delivering products and services that will help people stay healthy, aid them when they are ill and improve their quality of life. By doubling down on our earlier research infrastructure investments, Arizona’s leaders are paving the way to a brighter future for the people of Arizona. We are truly grateful to Governor Doug Ducey and the Arizona Legislature for their vision and their commitment to invest in Arizona’s future.” “Arizona has passed a budget that prioritizes education, boosts teacher pay and invests in our universities — all without raising taxes on hardworking Arizonans,” said Governor Ducey. “For the first time in a decade, we are making significant and lasting investments to grow our state — in state parks, in public schools and universities, in our roads and highways, and in programs to combat drug addiction, provide second chances to inmates and place foster children in permanent homes. This would not be possible without the hard work to balance our budget over recent years. And it should come as no surprise that we are investing where it can really make a difference. I thank the legislature for their hard work and look forward to building on these gains to continue expanding opportunity for all Arizonans.” About the Arizona Bioindustry Association, Inc. (AZBio) A key component in Arizona’s life science ecosystem, the Arizona Bioindustry Association (AZBio) is the only statewide organization exclusively focused on Arizona’s bioscience industry. AZBio membership includes patient advocacy organizations, life science innovators, educators, healthcare partners and leading business organizations. AZBio is the statewide affiliate of the Biotechnology Innovation Organization (BIO) and works in partnership with AdvaMed, MDMA, and PhRMA to advance innovation and to ensure that the value delivered from life-changing and life-saving innovation benefits people in Arizona and around the world.


News Article | April 26, 2017
Site: www.eurekalert.org

New genes are more likely to emerge full-fledged from a genome's 'junk' DNA, according to UA scientists. New genes are more likely to appear on the stage of evolution in full-fledged form rather than gradually take shape through successive stages of "proto genes" that become more and more refined over generations. This is the surprising upshot from research led by Benjamin Wilson and Joanna Masel at the University of Arizona, published as an Advance Online Publication by the scientific journal Nature Ecology & Evolution on April 24. Evolutionary biologists have long pored over the question of where new genes come from, which poses something of a chicken-and-egg problem. Conventional wisdom has it that new genes -- DNA sequences that code for a protein molecule -- evolve from existing genes through duplication and divergence. This happens when DNA copying mechanisms accidentally leave behind an extra copy of a particular gene. Naturally occurring mutations subsequently introduce changes that alter the DNA sequence such that the new gene assumes a function previously not found in the organism's lineage. Previous studies by other researchers suggested that new genes also emerge from non-coding DNA sequences, via primitive "proto-genes" that become refined over generations, resulting in an "adult," fully functional gene. Masel and her team found the opposite to be more likely, based on the fact that non-coding DNA sequences are likely to give rise to highly ordered proteins. Proteins, which consist of amino acids chained together into so-called polypeptides, tend to fold into three-dimensional structures that range from simple to mindbogglingly complicated. And while "ordered" may sound like a good thing, Masel is quick to point out that a healthy dose of disorder is key to success when it comes to evolution coming up with new genes that serve as blueprints for new proteins. For the study, the researchers compiled data on full-genome DNA sequences downloaded from yeast and mouse databases. "We take all the known mouse genes and yeast genes and query them against everything that's ever been sequenced and see what they're related to," explains Masel, a professor in the Department of Ecology and Evolution and a member of the UA's BIO5 Institute, "and based on that, we assign each gene an age that tells us when it was born." In the next step, the team used statistical analyses to create a model revealing the average degree of order that would be present in each gene's product. "We found that the youngest genes are the least ordered of all, which is what you would expect to get if you birthed a gene," Masel says. The key to a protein that can contribute a useful function for its organism while not harming it is a healthy mix between regions that are soluble because they consist of hydrophilic, or "water-loving," amino acids and stretches that are insoluble because of their hydrophobic, or "water-repelling," amino acids. If a protein consists of too many water-loving amino acids, it will remain largely unfolded, floating around inside the cell as an unorganized chain incapable of performing biological tasks. If too much of its length is water-repelling, the amino acids will clump together, rendering the protein unusable, and even dangerous, because when such misfolded proteins bump into each other, they tend to stick to each other and accumulate. "Now think about the most highly ordered proteins we know -- amyloids," Masel says, referring to the infamous piles of proteins found in the brain of Alzheimer's patients. "Because of this, the first order of business for any prospective gene is: 'Do no harm. Do not misfold.'" This has profound implications for the evolution of new genes from non-coding DNA sequences. Because such sequences are likely to give rise to highly ordered proteins, they are likely to be deleterious to the organism. In this scenario, any prospective new gene must start out as some kind of "super gene," in contrast to a "proto gene." Rather than making its debut in the gene pool as an unrefined gene that still bears many similarities to the non-coding DNA sequences it came from, the protein it encodes must start with a higher-than average degree of disorder to prove itself before evolution would allow it becoming a permanent member of the gene pool. "Instead of gradually working up to having more hydrophilic regions, young genes work their way down from being more hydrophilic and disordered, to more hydrophobic regions," Masel says. "In other words, when it comes to structural disorder, a polypeptide has the highest chance of being born if it is 'extra gene-like,' rather than 'sort of gene-like.'" The probability that a gene could arise from a random, non-coding sequence -- also known as "junk DNA," on the other hand, used to be considered negligible, based on the premise that in the vast majority of cases, a random sequence does more harm than good. This may not be so, argues a second paper in the same issue by Rafik Neme, one of the co-authors of the study discussed here. Neme, currently a postdoctoral researcher at Columbia University Medical Center in New York, found the first experimental evidence that non-coding, "silent" stretches of DNA are anything but that. "Until now, nobody knew whether a randomly sequence could immediately have any effect that would result in a function, or whether function was slowly acquired over time," Neme says. "It's similar to the idea of having a monkey typewriting at random, and expecting it to produce meaningful work." Neme's experiments show that many sequences exhibit relevant activities immediately, some good and some bad. This, in turn, suggests a discrete transition between non-genes and genes and would favor certain kind of sequences and functions over others. Based on their findings, Neme and Masel point out, the pool from which genes are born might be more conducive to birthing new genes than one might expect. "In our scenario, a gene precursor would be a transcript that happened to be translated into a protein sometimes but has no function," she says. "These things come up in evolution all the time, and mutation will quickly destroy it unless that polypeptide provides the organism with some advantage. There either is an advantage that natural selection can act on, or there isn't, so we don't think the would-be genes stick around for very long." This in turn suggests that gene birth is a sudden transition, rather than a gradual process involving many intermediate steps. In addition to Wilson, Neme and Masel, the paper was co-authored by Scott Foy, currently at St. Jude Children's Research Hospital in Memphis, Tennessee. Funding was provided by the John Templeton Foundation, the National Institutes of Health and the European Research Council.


Evolutionary biologists have long pored over the question of where new genes come from, which poses something of a chicken-and-egg problem. Conventional wisdom has it that new genes—DNA sequences that code for a protein molecule—evolve from existing genes through duplication and divergence. This happens when DNA copying mechanisms accidentally leave behind an extra copy of a particular gene. Naturally occurring mutations subsequently introduce changes that alter the DNA sequence such that the new gene assumes a function previously not found in the organism's lineage. Previous studies by other researchers suggested that new genes also emerge from non-coding DNA sequences, via primitive "proto-genes" that become refined over generations, resulting in an "adult," fully functional gene. Masel and her team found the opposite to be more likely, based on the fact that non-coding DNA sequences are likely to give rise to highly ordered proteins. Proteins, which consist of amino acids chained together into so-called polypeptides, tend to fold into three-dimensional structures that range from simple to mindbogglingly complicated. And while "ordered" may sound like a good thing, Masel is quick to point out that a healthy dose of disorder is key to success when it comes to evolution coming up with new genes that serve as blueprints for new proteins. For the study, the researchers compiled data on full-genome DNA sequences downloaded from yeast and mouse databases. "We take all the known mouse genes and yeast genes and query them against everything that's ever been sequenced and see what they're related to," explains Masel, a professor in the Department of Ecology and Evolution and a member of the UA's BIO5 Institute, "and based on that, we assign each gene an age that tells us when it was born." In the next step, the team used statistical analyses to create a model revealing the average degree of order that would be present in each gene's product. "We found that the youngest genes are the least ordered of all, which is what you would expect to get if you birthed a gene," Masel says. The key to a protein that can contribute a useful function for its organism while not harming it is a healthy mix between regions that are soluble because they consist of hydrophilic, or "water-loving," amino acids and stretches that are insoluble because of their hydrophobic, or "water-repelling," amino acids. If a protein consists of too many water-loving amino acids, it will remain largely unfolded, floating around inside the cell as an unorganized chain incapable of performing biological tasks. If too much of its length is water-repelling, the amino acids will clump together, rendering the protein unusable, and even dangerous, because when such misfolded proteins bump into each other, they tend to stick to each other and accumulate. "Now think about the most highly ordered proteins we know—amyloids," Masel says, referring to the infamous piles of proteins found in the brain of Alzheimer's patients. "Because of this, the first order of business for any prospective gene is: 'Do no harm. Do not misfold.'" This has profound implications for the evolution of new genes from non-coding DNA sequences. Because such sequences are likely to give rise to highly ordered proteins, they are likely to be deleterious to the organism. In this scenario, any prospective new gene must start out as some kind of "super gene," in contrast to a "proto gene." Rather than making its debut in the gene pool as an unrefined gene that still bears many similarities to the non-coding DNA sequences it came from, the protein it encodes must start with a higher-than average degree of disorder to prove itself before evolution would allow it becoming a permanent member of the gene pool. "Instead of gradually working up to having more hydrophilic regions, young genes work their way down from being more hydrophilic and disordered, to more hydrophobic regions," Masel says. "In other words, when it comes to structural disorder, a polypeptide has the highest chance of being born if it is 'extra gene-like,' rather than 'sort of gene-like.'" The probability that a gene could arise from a random, non-coding sequence—also known as "junk DNA," on the other hand, used to be considered negligible, based on the premise that in the vast majority of cases, a random sequence does more harm than good. This may not be so, argues a second paper in the same issue by Rafik Neme, one of the co-authors of the study discussed here. Neme, currently a postdoctoral researcher at Columbia University Medical Center in New York, found the first experimental evidence that non-coding, "silent" stretches of DNA are anything but that. "Until now, nobody knew whether a randomly sequence could immediately have any effect that would result in a function, or whether function was slowly acquired over time," Neme says. "It's similar to the idea of having a monkey typewriting at random, and expecting it to produce meaningful work." Neme's experiments show that many sequences exhibit relevant activities immediately, some good and some bad. This, in turn, suggests a discrete transition between non-genes and genes and would favor certain kind of sequences and functions over others. Based on their findings, Neme and Masel point out, the pool from which genes are born might be more conducive to birthing new genes than one might expect. "In our scenario, a gene precursor would be a transcript that happened to be translated into a protein sometimes but has no function," she says. "These things come up in evolution all the time, and mutation will quickly destroy it unless that polypeptide provides the organism with some advantage. There either is an advantage that natural selection can act on, or there isn't, so we don't think the would-be genes stick around for very long." This in turn suggests that gene birth is a sudden transition, rather than a gradual process involving many intermediate steps. Explore further: What happens to gene transcription during DNA damage? More information: Benjamin A. Wilson et al. Young genes are highly disordered as predicted by the preadaptation hypothesis of de novo gene birth, Nature Ecology & Evolution (2017). DOI: 10.1038/s41559-017-0146


News Article | February 22, 2017
Site: www.eurekalert.org

Quick! Name the top-performing athletes in the animal kingdom. Cheetah? Try again. Blue whale? Nope. Here's a clue: If you take a walk in the desert on a moonlit night, you might see them, darting from flower to flower and hovering in midair: moths of the hawkmoth family (Sphingidae). Nectar-feeding moths, pollinating bats and hummingbirds are masters in sustaining the most intense exercise of all animals. To extract nectar from a flower, they must hover in front of the flower before darting off to the next one. But how can these organisms perform such feats on a diet that's mostly sugar? New research by University of Arizona biologists not only offers an explanation, but also suggests that these animals stay healthy not despite, but because of, their sugary diet. Oxygen, while necessary for life to exist, is a double-edged sword. The more we engage in intense aerobic exercise, such as hovering, the more oxygen reveals its ugly side in the form of reactive oxygen species -- small reactive molecules that wreak havoc on cells. Researchers in the lab of Goggy Davidowitz in the Department of Entomology in the UA's College of Agriculture and Life Sciences discovered that hawkmoths (also known as Manduca moths) have evolved a strategy that helps them minimize the muscle damage inflicted by the oxidative stress generated during sustained flight. The results are published in the journal Science. "If you wanted to consume the equivalent amount of sugar that a moth takes up in one meal, you'd have to drink 80 cans of soda," says Eran Levin, who led the research as a postdoctoral fellow in Davidowitz's group. "It's amazing that an animal can process such an amount of sugar in such a short time." Nectar-feeding moths and hummingbirds don't take up any antioxidants with their diet, which begs the question of how they deal with the oxidative damage their muscles are suffering during the moths' nightly foraging flights. Two sophisticated pieces of equipment set up to work in tandem made it possible to study in great detail the metabolism of Manduca moths during sustained flight. The team found that the insects actually use the sugar in their diet to make their own antioxidants. They accomplish this by shunting the carbohydrates they consume to a metabolic pathway that evolved early on in the evolution of life: the pentose phosphate pathway. Humans, too, have this pathway, but it cannot, on its own, produce all the antioxidants needed, which is why athletes drink antioxidant-laced sports drinks and parents tell their children to eat their veggies. Fitting this pattern, migrating birds often are observed eating berries and fruit -- both rich in antioxidants -- during stopovers. "Manduca is a well-suited model system to study this metabolic pathway, which is the same for bacteria and sequoia trees," Levin explains. "If we understand how the moth is doing it, you can find out how we do it. And we can learn about what goes wrong with our sugar consumption." During the flight experiments, the researchers noticed something strange: The measurements tracking how much oxygen the moths consumed and how much carbon dioxide they produced didn't add up. "If you burn all the sugar you're eating, you expect the same ratio of carbon dioxide exhaled to oxygen consumed," Levin says. "This is normal when you feed on carbohydrates, but we obtained results that shouldn't have been possible according to the scientific literature." Reluctant to trust the data their moths were generating, Davidowitz contacted the manufacturer of the flight measurement apparatus. The CEO of the company came out, and after much troubleshooting, tinkering and adjusting, the readings still did not change. One day, a colleague suggested flying a bumblebee in place of a moth, because bumblebees are known to burn only carbohydrates during flight. Sure enough, the machine spat out the expected values. "That told us our data were correct," Levin says. "They indicated that 40 percent of the carbon in our moth flight experiments had to come from something other than carbohydrates, so we looked for an explanation, and the only such pathway that would produce those results is the pentose phosphate pathway." While flying, it turned out the moths were not only burning carbohydrates, but fat as well. As soon as they rested, within seconds, they shunted their metabolism to the pentose phosphate pathway. In addition to solving the issue of the higher-than-what-theory-allows measurements, the results provided the answer to the mystery of how a nectar-feeding organism avoids killing itself from oxidative stress. "On our flight apparatus, moths fly about three miles a night on average," Davidowitz says. "We don't know how much they are actually flying in the wild." When moths burn lipids during intense exercise, they produce more reactive oxygen species that pose further danger to their flight muscles. "We think the tissue repair occurs when they rest, but we haven't measured that," Davidowitz says. If You Rest, You Rust Moths that were frequent and intense flyers were found to have less oxidative cell damage than those that did not, which seemed counterintuitive, Levin says. "There is this common notion out there where we tend to think that all animals that feed on sugar are very active and fast-living creatures," he says. "But our experiments suggest that this is actually not the case. In fact, there is much more energy to be gained by burning fats, so we suggest these high-performing animals consume a sugar-heavy diet to protect their muscles from damage." Levin says he thinks the principles observed in Manduca moths apply to all animals, as similar respiratory values have been measured in marsupials, mammals and birds. "But because they seemed to contradict theory, those measurements usually didn't make it into the paper, or they were ascribed to lipid synthesis," Levin says. Adds Davidowitz: "We think the ability to shunt glucose through an ancient metabolic pathway has allowed animals that only feed on nectar to embark on long migrations, such as monarch butterflies, hummingbirds and bats." The co-authors on the paper are Giancarlo López-Martinez at New Mexico State University in Las Cruces, New Mexico, and Bentley Fane, in the UA School of Plant Sciences and the UA's BIO5 Institute.


News Article | February 23, 2017
Site: www.futurity.org

If you take a walk in the desert on a moonlit night, you might see the animal kingdom’s top-performing athletes darting from flower to flower and hovering in midair: moths of the hawkmoth family. Nectar-feeding moths, pollinating bats, and hummingbirds are masters in sustaining the most intense exercise of all animals. To extract nectar from a flower, they must hover in front of the flower before darting off to the next one. But how can these organisms perform such feats on a diet that’s mostly sugar? New research not only offers an explanation, but also suggests that these animals stay healthy not despite, but because of, their sugary diet. Oxygen, while necessary for life to exist, is a double-edged sword. The more we engage in intense aerobic exercise, such as hovering, the more oxygen reveals its ugly side in the form of reactive oxygen species—small reactive molecules that wreak havoc on cells. Researchers in the lab of Goggy Davidowitz in the entomology department in the University of Arizona’s College of Agriculture and Life Sciences discovered that hawkmoths (also known as Manduca moths) have evolved a strategy that helps them minimize the muscle damage inflicted by the oxidative stress generated during sustained flight. The results appear in the journal Science. “If you wanted to consume the equivalent amount of sugar that a moth takes up in one meal, you’d have to drink 80 cans of soda,” says Eran Levin, who led the research as a postdoctoral fellow in Davidowitz’s group. “It’s amazing that an animal can process such an amount of sugar in such a short time.” Nectar-feeding moths and hummingbirds don’t take up any antioxidants with their diet, which begs the question of how they deal with the oxidative damage their muscles are suffering during the moths’ nightly foraging flights. Two sophisticated pieces of equipment set up to work in tandem made it possible to study in great detail the metabolism of Manduca moths during sustained flight. The team found that the insects actually use the sugar in their diet to make their own antioxidants. They accomplish this by shunting the carbohydrates they consume to a metabolic pathway that evolved early on in the evolution of life: the pentose phosphate pathway. Humans, too, have this pathway, but it cannot, on its own, produce all the antioxidants needed, which is why athletes drink antioxidant-laced sports drinks and parents tell their children to eat their veggies. Fitting this pattern, migrating birds often are observed eating berries and fruit—both rich in antioxidants—during stopovers. “Manduca is a well-suited model system to study this metabolic pathway, which is the same for bacteria and sequoia trees,” Levin explains. “If we understand how the moth is doing it, you can find out how we do it. And we can learn about what goes wrong with our sugar consumption.” During the flight experiments, the researchers noticed something strange: The measurements tracking how much oxygen the moths consumed and how much carbon dioxide they produced didn’t add up. “If you burn all the sugar you’re eating, you expect the same ratio of carbon dioxide exhaled to oxygen consumed,” Levin says. “This is normal when you feed on carbohydrates, but we obtained results that shouldn’t have been possible according to the scientific literature.” Reluctant to trust the data their moths were generating, Davidowitz contacted the manufacturer of the flight measurement apparatus. The CEO of the company came out, and after much troubleshooting, tinkering, and adjusting, the readings stayed the same. One day, a colleague suggested flying a bumblebee in place of a moth, because bumblebees are known to burn only carbohydrates during flight. Sure enough, the machine spat out the expected values. “That told us our data were correct,” Levin says. “They indicated that 40 percent of the carbon in our moth flight experiments had to come from something other than carbohydrates, so we looked for an explanation, and the only such pathway that would produce those results is the pentose phosphate pathway.” While flying, it turned out the moths were not only burning carbohydrates, but fat as well. As soon as they rested, within seconds, they shunted their metabolism to the pentose phosphate pathway. In addition to solving the issue of the higher-than-what-theory-allows measurements, the results provided the answer to the mystery of how a nectar-feeding organism avoids killing itself from oxidative stress. “On our flight apparatus, moths fly about three miles a night on average,” Davidowitz says. “We don’t know how much they are actually flying in the wild.” When moths burn lipids during intense exercise, they produce more reactive oxygen species that pose further danger to their flight muscles. “We think the tissue repair occurs when they rest, but we haven’t measured that,” Davidowitz says. Moths that were frequent and intense flyers were found to have less oxidative cell damage than those that did not, which seemed counterintuitive, Levin says. “There is this common notion out there where we tend to think that all animals that feed on sugar are very active and fast-living creatures,” he says. “But our experiments suggest that this is actually not the case. In fact, there is much more energy to be gained by burning fats, so we suggest these high-performing animals consume a sugar-heavy diet to protect their muscles from damage.” Levin says he thinks the principles observed in Manduca moths apply to all animals, as similar respiratory values have been measured in marsupials, mammals, and birds. “But because they seemed to contradict theory, those measurements usually didn’t make it into the paper, or they were ascribed to lipid synthesis,” Levin says. Adds Davidowitz: “We think the ability to shunt glucose through an ancient metabolic pathway has allowed animals that only feed on nectar to embark on long migrations, such as monarch butterflies, hummingbirds, and bats.” Coauthors of the paper from New Mexico State University in Las Cruces, New Mexico, and the University of Arizona’s School of Plant Sciences BIO5 Institute. Funding came from the National Science Foundation.


News Article | October 24, 2016
Site: www.scientificcomputing.com

In his State of the Union address of January 12, 2016, President Barack Obama challenged America to tackle one of the world’s top killers: “For the loved ones we’ve all lost, for the families that we can still save, let’s make America the country that cures cancer once and for all.” In the weeks following the address, Obama announced the White House Cancer Moonshot project, which urges the nation’s scientists, industries, and families to come together to take on cancer. And in the months following the address, they have. University of Arizona (UA) research assistant professor Adam Buntzman and his colleagues are pushing the boundaries of cancer research using CyVerse data sharing and high-performance computing technology. “A staggering number of diseases are linked to the adaptive immune system,” noted Buntzman, an immunologist in the lab of Monica Kraft in the UA College of Medicine – Tucson. “Cancers such as lymphoma, myeloma, leukemia, and solid tumors, viral, bacterial, fungal, and parasitic infections, autoimmune diseases, asthma, inflammation, transplant tolerance or rejection… the list goes on.” Buntzman, who is based in the UA’s BIO5 Institute, and his colleagues recently developed a tool that uses CyVerse supercomputing resources to create the first nearly comprehensive map of the human immunome, all the possible immune receptors our bodies can make. Then, with the immunome at their fingertips, the researchers went on to develop an informatics tool to find patterns denoting which immune receptors may be responsible for protecting us from infectious disease, and which ones may cause autoimmune disorders, tissue rejection, or some types of cancer. “Once we find these receptors, scientists can design unique therapies to enhance the protective response, or add just the right receptors to a patient who may be missing them, or deplete the cells that harbor receptors that cause autoimmune disease.” Buntzman said. “This is the basis of the burgeoning field of immunotherapy.” “The same tools we use to study basic science questions in adaptive immunology can be used clinically,” he continued. Now, Buntzman and his colleagues at the UA Genetics Core(UAGC) and UA Cancer Center are developing methods to test for lymphoma, myeloma, and leukemia tumors. “Buntzman’s technique for immune-profiling with high-throughput informatics will help us to develop better clinical diagnostic tests, and will supplement our current clinical testing so that we can provide the UA clinical community with cutting-edge diagnostics to benefit the patients of the Banner-University Medical Center,” noted Michael Hammer, UA geneticist and UAGC Director. “This is an example of real-world precision diagnostics being developed here on the UA campus.” “The cancer cells of leukemia, myeloma, and lymphoma are unique in that the tumor cells themselves are immune cells,” Buntzman explained. “These three diseases occur when an immune cell gets a mutation and starts to outgrow the healthy immune cells. But the tumor cells harbor a unique biomarker that our tools can follow diagnostically through the course of treatment and, hopefully, into remission.” With the immunome at their fingertips courtesy of Buntzman’s informatics tool, “it’s very easy for us to see an overgrowth of immune receptors. We can sequence immune receptors to count the number of each receptor a person has in their bloodstream or at the site of the tumor. If there is one sequence that occurs out of proportion to the others, that’s a marker for an existing tumor.” A healthy person would have mostly unique immune cell receptors, he said. “Once we know the sequence of a cancerous immune cells, we know the tumor’s bio-signature. We can follow it for the time that the person is being treated and find the faintest trickle of it still remaining in their system. No other technique is as sensitive as this.” Buntzman envisions perfected tests to find cancer and cancerous remissions earlier, giving greater chance of successful treatment. According to one study, immunomic tests could be up to 100 times more sensitive than classical tests. Buntzman believes that immunomic tests, which require only a small genetic sample, could be vital for tracking cancer treatment and remission. A highly sensitive test is more likely to detect if a small amount of cancerous cells remain after treatment: “It’s a better test of the effectiveness of that treatment, and a better indicator of the next steps to take.” Immunomic tests also could be crucial for detecting cancer early by scanning people before they become ill. “When people go to a clinic, it’s usually because they’re already sick," Buntzman said. "If doctors could detect cancerous cells before they grow drastically out of proportion to healthy cells, patients would have much higher odds of successful cancer treatment and survival.”


News Article | October 4, 2016
Site: www.chromatographytechniques.com

University of Arizona research assistant professor and immunologist Adam Buntzman used CyVerse data-sharing and analysis capabilities to lead the first team to comprehensively map the human adaptive immune system. Knowing the full potential for our immune systems to protect us from harmful pathogens brings us one huge step closer to finding cures for illnesses such as cancer, infections, autoimmune diabetes and asthma, as well as developing improved diagnostic tests and immune therapies. "Understanding adaptive immunity is one of the grand challenges in science," said Yves Lussier, associate vice president for UA Health Sciences and executive director of the UA Center for Biomedical Informatics and Biostatics. "The unique genetics and massive diversity that occur exclusively in cells of the adaptive immune system has posed a dire need for computer tools created specifically to analyze adaptive immune receptors." Now Buntzman and his collaborators have combined the expertise of immunologists, mathematicians and computer scientists to develop these much-needed computational tools. "If we were on a treasure hunt, where the cure to many illnesses is the buried treasure, then we've just drawn the first map of Treasure Island," said Buntzman, an investigator in the lab of Monica Kraft, a physician-scientist specializing in research of dysfunctional autoimmune response in asthma and chair of the UA Department of Medicine. More Complex Than the Human Genome The adaptive immune system is perhaps the most mysterious — and certainly one of the most vital — systems of the human body, protecting us from everything from common cold germs to serious infections. Cells within the human adaptive immune system produce antibodies and T-cell receptors that identify and remove harmful foreign substances from the body. Unfortunately, the immune system can become a powerful enemy when it misidentifies a part of the body as pathogenic, leading to autoimmune diseases, or when it overreacts to foreign materials such as pollen, resulting in allergies such as asthma. The immune system is considered to be "adaptive" because it can respond to our unique environments. Once it has overcome a particular pathogen, the immune system will "remember" and quickly destroy that pathogen if it ever enters our bodies again, thus giving us immunity. Adaptive immune systems also vary from one person to the next, providing immunity depending upon what microbes an individual has been exposed to throughout their lifetime. "Humans have about 25,000 genes in our genome, but there are millions of harmful microbes, which begs the question: How does such a small number of genes code for all of the immune receptors needed to recognize the enormous array of microbes that can hurt us?" Buntzman said. It turns out that immune receptor genes do not code for immune receptors; rather, broken gene fragments combine in novel ways to produce new code. Every time a new antibody or T-cell receptor is created, the adaptive immune system "shuffles the deck" of gene fragments, blending together the broken pieces through a process called VDJ Recombination. "These gene fragments are then modified by enzymes, creating a dizzying array of variation," Buntzman said. The possible variation of immune receptors far exceeds the number of genes in our genome, at roughly 10 million times more than the number of stars in the Milky Way galaxy, he noted. That's also about 100-fold the number of ants on Earth. And therein lies the complication. "How do we study this much diversity? How do we find which receptors cause autoimmune disorders, and which receptors protect us from influenza?" Buntzman said. Genome sequencing instruments have addressed the problem yet remain incapable of handling the enormity of data. Until now. Just as genomics involves sequencing whole genomes, the field of immunomics involves mapping sequences of immune receptors — a mathematical challenge given that the human adaptive immune system swamps the diversity of most genomics studies. Buntzman calculated that using traditional computational methods to generate a complete genetic map of the immunome — all possible receptors the immune system might generate — would take roughly 106 years. "Waiting that long is clearly impractical," he said, "but this is where CyVerse comes in." Headquartered at the UA's BIO5 Institute, CyVerse is a National Science Foundation-funded project to provide computational infrastructure for big-data problems in the life sciences. Buntzman began working with CyVerse collaborator Ali Akoglu of the UA College of Engineering to develop computational tools to map the immunome using high-performance computing, or HPC, techniques. With access to HPC technology and support through CyVerse, Buntzman, Akoglu and Akoglu's graduate student Gregory Striemer developed a program to run the analysis in under 17 days on a computer chip housed inside a simple laptop. "My role was to restructure the algorithm to accelerate the results," Akoglu said. "This was the first study to generate and process terabytes of data exhaustively, going through all possible combinations of sequences, and in a relatively short amount of time. And CyVerse was the catalyzer that brought us together." Armed with the power of computation, Buntzman and his colleagues have developed a software tool capable of comprehensively mapping the adaptive immune system without limitation, and a computer program that is a community-accessible utility to database these complex immunome datasets, as described at the 2016 conference of the American Association of Immunologists and in an upcoming publication to be released in the journal BMC Bioinformatics. In addition, Buntzman's group has developed another computer program to run a novel algorithm called iWAS, or immunome-Wide Association Study, that can mine the immunome for patterns of immune receptors responsible for protecting us from specific diseases or causing autoimmune disorders. Understanding the role of individual immune receptors could pave the way to developing advanced therapies, potentially revolutionizing the field of adaptive immunity. "This work will aid in the study of cancer, autoimmunity, transplantation and vaccination, and assist in developing new precision medical diagnostics and patient-centered immunotherapies, as well as identify biomarkers for inflammatory diseases," Lussier said. "By working across disciplines as immunologists, mathematicians and computer scientists," he said, "we were able to tackle a problem that was untenable to any discipline alone. We've created an analytical infrastructure with CyVerse that allows for all the data to be stored and analyzed by researchers everywhere."

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