This minimally invasive technique, called Polarization Gating Spectroscopy, will now be tested in a much larger international clinical trial led by the Mayo Clinic researchers. The preliminary study suggests it may be possible, one day, to use a less invasive endoscope to screen patients for early development of pancreatic cancer.

The pancreas is notoriously hard to reach and see due to its very deep location in the abdomen, surrounded by intestines. The study investigators theorized that there may be changes in the nearby “normal appearing” tissue of the small intestine which is much more accessible.

“No one ever thought you could detect pancreatic cancer in an area that is somewhat remote from the pancreas, but this study suggests it may be possible,” says Dr. Michael Wallace, chairman of the Division of Gastroenterology at Mayo Clinic in Florida. “Although results are still preliminary, the concept of detection field effects of nearby cancers holds great promise for possible early detection of pancreatic cancer.”

In this study, the Mayo Clinic physicians tested a light probe developed by their long-time collaborators at Northwestern University.

The light, attached to a small fiber-optic probe known as an endoscope, measures the amount of oxygenated blood as well as the size of blood vessels in tissue near the duct where the pancreas joins the small intestine. Because a growing tumor requires a heightened supply of blood, normal tissue in the vicinity of the cancer reveals evidence of enlarged blood vessels and changes in the amount of oxygen within the blood.

Such “field effects” from cancer can be measured in other areas of the GI tract, says Dr. Wallace. “With this technology, others studies have shown that cancerous polyps can be detected more than 11 inches from the polyp itself. Early studies are evaluating if esophageal cancers can also be detected remotely,” he says.

The probe acts “a bit like a metal detector that beeps faster and louder as you get close to cancer,” he says. The researchers are measuring within six to 10 inches of the pancreas in the small intestine immediately next to the pancreas.

Dr. Wallace and his team tested the probe on 10 patients who were later determined to have pancreatic cancer, and on nine participants who did not have pancreatic cancer.

They found that testing both measures — blood vessel diameter and blood oxygenation — detected all 10 pancreatic cancers. But the probe was less precise (63 percent accurate) in determining which of the healthy volunteers did not have pancreatic cancer.

“There is room for improvement in this instrument, and our group is working on that,” he says. “If the studies confirm the early results, it would make the pancreas accessible to a much simpler upper endoscope and that would be a real advance in the treatment of pancreatic cancer.”

Patients now often undergo an endoscopic examination of the upper intestine to search for the cause of heartburn or stomach pain, Dr. Wallace says. An endoscopic probe could be easily outfitted to explore for evidence of pancreatic cancer in patients at heightened risk, he says.

Mihir Patel, M.D., a gastroenterologist who worked with Dr. Wallace on the study, says that despite of intense research, we haven’t been successful in significantly improving the overall survival associated with pancreatic cancer in the past several decades. That’s because we haven’t been able to detect the cancer early enough. Developing a technique to screen the patients and detect pancreatic cancer at an early stage would be a potential breakthrough. In preliminary data, this technology has shown to hold similar potential.

Lyden possesses an extensive background in biostatistical analysis in pharmaceutical, biotechnical and medical device clinical research. Prior to founding BioStat International, Inc., Lyden served as the Manager of Clinical and Statistical Affairs at Bausch and Lomb Pharmaceutical Division.

“It can be challenging to get young people interested in biostatistics.” said Lyden. “Biostatistics can be a very rewarding career and it is the goal of this panel to impart students contemplating a future in biostatistics with career possibilities, industry challenges and rewards that exist in our field.”

The discussion panel occurred on the first day of the SIBS six-week learning program. Undergraduate students from across the nation interested in pursuing a graduate program in Biostatistics enroll in the program to learn more about graduate studies and gain insight from biostatistics experts. Participants have access to the university’s computing systems and libraries and will also receive hands-on training from top biostaticians, clinicians and epidemiologists.

Following the discussion panel, the students were invited to a reception with the SIBS staff to kick off the six-week program. Upon completion of the program, students may transfer 3 college credits to their home institution.

Assistant Professor Dimitrios Vavylonis and graduate student Tyler Drake joined a University of Miami research team led by Associate Professor Fulvia Verde to learn that protein Cdc42 begins the ballet of proteins that change cell polarity, by oscillating throughout the cellular membrane of new cells. By changing polarity, Cdc42 regulates shape, structure and function in yeast cells. This oscillatory mechanism may be a general strategy among all self-organizing biological systems, not just simple yeast.

Researchers used fluorescent markers to tag each of the many proteins involved, observing the protein oscillate, switching sides about every five minutes. The fluctuations provide an adaptable mechanism for cells to control their size and structure in the fast-changing environment within.

The findings demonstrate just part of the complex process of cell growth and differentiation, but mark how advanced the science of biophysics has become. Only recently has the clear imaging and monitoring of protein activity become possible at the minute sizes and shortened time scales of individual cell maturation.

Now, researchers at Weill Cornell Medical College have made a discovery that once again forces us to revise the textbooks. This time, however, the findings pertain to RNA, which like DNA carries information about our genes and how they are expressed. The researchers have identified a novel base modification in RNA which they say will revolutionize our understanding of gene expression.

Their report, published in the journal Cell as Comprehensive Analysis of mRNA Methylation Reveals Enrichment in 3′ UTRs and near Stop Codons shows that messenger RNA (mRNA), long thought to be a simple blueprint for protein production, is often chemically modified by addition of a methyl group to one of its bases, adenine. Although mRNA was thought to contain only four nucleobases, their discovery shows that a fifth base, N6-methyladenosine (m6A), pervades the transcriptome. The researchers found that up to 20 percent of human mRNA is routinely methylated. Over 5,000 different mRNA molecules contain m6A, which means that this modification is likely to have widespread effects on how genes are expressed.

“This finding rewrites fundamental concepts of the composition of mRNA because, for 50 years, no one thought mRNA contained internal modifications that control function,” says the study’s senior investigator, Dr. Samie R. Jaffrey, an associate professor of pharmacology at Weill Cornell Medical College.

“We know that DNA and proteins are routinely modified by chemical switches that have profound effects on their function in both health and disease. But biologists believed mRNA was simply an intermediate between DNA and protein,” he says. “Now we know mRNA is much more complex, and defects in RNA methylation can lead to disease.”

Indeed, as part of the study, the researchers demonstrated that the obesity risk gene, FTO (fat mass and obesity-associated), encodes an enzyme capable of reversing this modification, converting m6A residues in mRNA back to regular adenosine. Humans with FTO mutations have an overactive FTO enzyme, which results in low levels of m6A and causes abnormalities in food intake and metabolism that lead to obesity.

The researchers uncovered links between m6A and other diseases as well.

“We found that m6A is present in many mRNAs encoded by genes linked to human diseases, including cancer as well as several brain disorders, such as autism, Alzheimer’s disease, and schizophrenia,” says the study’s lead investigator, Dr. Kate Meyer, a postdoctoral researcher in Dr. Jaffrey’s laboratory.

“Methylation in RNA is a reversible modification that appears to be a central step in a wide variety of biological pathways and physiological processes,” she says.

The first time that m6A was detected in mRNA was in 1975, but at the time scientists were unsure whether this finding was a result of contamination by other RNA molecules, Dr. Jaffrey says. Over 90 percent of RNA is either transfer RNA (tRNA) or ribosomal RNA (rRNA), cellular workhorses that are routinely modified.

But Dr. Jaffrey says he has always been interested in the idea that mRNA may be modified — “DNA, proteins, other forms of RNA are modified, so why not mRNA?” he says — so he and investigators in his laboratory developed a technique to help them uncover methylation in mRNA taken from both mouse and human samples.

They used two different antibodies that recognize and bind to m6A in mRNA in order to selectively isolate the mRNAs that contain m6A. By subjecting these mRNAs to next-generation sequencing, they were able to identify the sequence of each individual mRNA they had isolated. Co-authors Dr. Christopher Mason and Dr. Olivier Elemento, assistant professors from the Department of Physiology and Biophysics and Computational Genomics in Computational Biomedicine at Weill Cornell Medical College, then developed computational algorithms to reveal the identity of each of these methylated mRNAs.

The Weill Cornell researchers don’t know how the thousands of m6As they detected in humans work to control the function of mRNAs, but they do note that the m6As are located near “stop codons” in mRNA sequences. These areas signal the end of translation of the mRNA, suggesting that m6A might influence ribosomal function. “But we really don’t know yet,” says Dr. Mason, a co-lead investigator on the study. “It may allow other proteins to bind to mRNA, or subject these mRNAs to a whole new regulatory pathway. Our bioinformatics analyses are providing several hints about the possible impact of methylation on RNA function.”

Indeed, in their study, the investigators have already found that m6A sites frequently occur in regions of mRNA that are highly conserved across several species of vertebrates. “This shows that m6A sites are not just important for humans, but rather are maintained under selection across hundreds of millions of years of evolution, and thus are likely of critical importance for all animals,” Dr. Mason says.

“This is the first demonstration of an epitranscriptomic modification — alterations in RNA function that are not due to changes in the underlying sequence,” he adds.

“These findings are very, very exciting, and amazing, really, when you consider that mRNA has been around for so long and that nobody realized, in all this time, that they were being regulated in this way,” Dr. Jaffrey says. “It was right under our noses.”

In addition to investigating how m6A regulates mRNAs within cells, the researchers are now focused on identifying the enzymes and pathways that control mRNA methylation.

Their study already demonstrates that FTO is capable of reversing adenosine methylation and suggests that it acts on a large proportion of cellular mRNA. “FTO mutations are estimated to occur in one billion people worldwide and are a leading cause of obesity and type 2 diabetes. Our studies link m6A levels in mRNA to these major health problems and identify for the first time the mRNAs which are potentially targeted by FTO,” Dr. Meyer says.

The investigators are currently working to understand how defective regulation of m6A in patients with FTO mutations causes obesity and metabolic disorders, and they are also developing tests to rapidly identify compounds that inhibit FTO activity. These compounds are expected to inhibit the overactive FTO found in humans, potentially leading to novel therapeutics for diabetes and obesity.

Now, a team of scientists from the University of Chicago, the Ludwig Institute for Cancer Research, the University of California, San Diego and Emory University has developed and tested a technique to accomplish this task. The results are published in Cell as Base-Resolution Analysis of 5-Hydroxymethylcytosine in the Mammalian Genome

The team used the technique to map 5-methylcytosine (5-mC) and 5-hydroxymethylcytosine (5-hmC) in DNA from human and mouse embryonic stem cells, revealing new information about their patterns of distribution. These studies have revealed that these DNA modifications play major roles in fundamental life processes such as cell differentiation, cancer and brain function.

“They regulate gene expression and have a broad impact on stem cell development, various human diseases such as cancer, and potentially on neurodegenerative disease. They may even shape the development of the human brain,” said Chuan He, professor in chemistry at UChicago.

Scientists have been examining the patterns of 5-mC for decades, as part of the field of epigenetics: the study of the information that lies “on top” of the DNA sequence. However, researchers only recognized that 5-hmC was present at significant levels in our DNA a few years ago. 5-mC is generally found on genes that are turned off, and helps silence genes that aren’t supposed to be turned on. In contrast, 5-hmC appears to be enriched on active genes, especially in brain cells. Also, defects in the Tet enzymes that convert 5-mC into 5-hmC can drive leukemia formation, hinting that changes in 5-hmC are important in cancer.

The Cell paper describes a method called TAB-Seq that directly measures 5-hmC, and presents the first map of the entire genome of 5-hmC at single-base resolution. He and three of his students conceived and developed the technique at UChicago. A patent is pending on their invention; UChicago is working with Chicago-based Wisegene to further develop the technology.

“This is a major breakthrough in that TAB-Seq allows precise mapping of all 5-hydroxymethylcytosine sites in a mammalian genome using well-established, next-generation DNA sequencing methods,” said Joseph Ecker, a professor at the Salk Institute for Biological Studies, who was not involved in the Cell study. “The study showed very clearly that deriving useful knowledge about this poorly understood epigenetic regulator requires determination of the exact locations of 5hmC with base-level accuracy. I expect that their new method will immediately become widely adopted.”

The other two laboratories of the team, Bing Ren’s Ludwig Institute for Cancer Research/UCSD group applied TAB-Seq to human embryonic stem cells, while Peng Jin’s group at Emory University applied the method to mouse embryonic stem cells.

Previous studies had shown that 5-hmC was found on genes that are turned on. Now, the additional resolution and subsequent research on mouse and human embryonic stem cells reveals that it is found most often on the stretches of DNA that control a gene’s activity, called enhancers, in comparison with the parts of genes that are actually read out into RNA.

“We learned using this new technique that this modification is most abundant in the areas of the genome known as enhancers, which regulate the expression of genes. This potential regulatory role of hmC may explain its importance in embryonic stem cells, and why its disruption may result in the development of leukemia,” said Gary Hon, a postdoctoral fellow in the laboratory of Bing Ren, who carried out the genome-wide analysis of 5hmC in the human embryonic stem cells at the Ludwig Institute for Cancer Research at UCSD.

Another difference with 5-mC is that 5-hmC is usually on only one side of the DNA. In contrast, 5-mC is most often found symmetrically. Overall, 5-hmC is around 14 times less abundant than 5-mC. Even at sites where 5-hmC is the most abundant, it is still present at about one fifth the frequency as 5-mC, the team found using the new technique.

Previous research has found that 5-hmC is 10 times more abundant in brain than in stem cells, so it may have an especially important role there. Jin’s laboratory is using the new technique to finely map 5-hmC in the developing brain.

“To really see the kinds of functions 5-hmC can have, we need to look at how it appears and disappears over time, during processes like brain development. This technique will allow us, and other investigators, to dive in and get that information at high resolution,” said Jin, an associate professor of human genetics at Emory.

With the award, the Miller School’s Developmental Center for AIDS Research (D-CFAR) is transitioning to a full CFAR after proving its ability to operate at the highest scientific level and will receive a significant increase in NIH funding – nearly $7 million over five years – to enhance existing research and nurture new research in HIV/AIDS.

“The grant recognizes that the work we are doing at the Miller School and across the University is contributing significantly to understanding how the virus creates havoc on the immune system and the sanctuaries where it chooses to hide – which is essential for developing a cure that has eluded us for so long,’’ said Savita Pahwa, M.D., director of the Miami CFAR, and professor of microbiology and immunology, pediatrics and medicine. “The designation also means, as a University, we are being counted on to make even greater strides toward the control and eradication of HIV/AIDS, and that’s what we’re prepared to do.”

Pascal J. Goldschmidt, M.D., Senior Vice President for Medical Affairs and Dean of the Miller School, said Miller School researchers have earned the designation by putting UM on the map as the premier AIDS research center in the world. “They have been at the forefront of the battle against HIV/AIDS for decades and have developed or contributed to some of the most significant scientific, clinical and behavioral approaches to fighting the disease,” Goldschmidt said. “With a CFAR, we are being given a great opportunity to push the envelope even further toward a cure.”

Florida remains home to one of the nation’s largest and most diverse populations of HIV-infected people. The Miller School’s commitment and contributions to HIV/AIDS research and treatment date back to 1981, soon after a mysterious immune disorder was diagnosed in homosexual men. UM doctors were the first to recognize that the disorder also was affecting heterosexuals, including Haitians who were erroneously thought to be infected through IV drug use or homosexual sex. UM researchers were among the first to describe pediatric HIV infection and the transmission of HIV from pregnant mothers to their babies. They also investigated and pioneered the use of AZT, led studies that showed a combination of antiretroviral drugs improved health and survival, and provided major insights into the relationship between drug use and HIV infection.

Like the D-CFAR, the Miami CFAR is specifically designed to provide scientific leadership and infrastructure that, in partnership with the community, advances innovative multidisciplinary HIV/AIDS research in basic, clinical, epidemiological, behavioral/social sciences and translational research to prevent, treat and cure HIV/AIDS.

Among its scientific areas of research are drug use and HIV prevention, HIV in women, therapeutics and prevention, vaccines and immunology, and AIDS malignancies. A critical part of the CFAR mission is to facilitate recruitment of expert faculty in different areas of AIDS research, enable UM researchers to move to the next level, and give young investigators opportunities and mentorship to enter the arena of HIV research and become competitive in obtaining federal funds.

“We are talking about how to broaden the umbrella of AIDS research and the growth and evolution of young scientists,” Pahwa said. “It’s an opportunity to build onto what we’ve already built and make it better.’’

The University’s application to transition its D-CFAR to a full-fledged CFAR was rated “exceptional” by the NIH, garnering high ratings for the institution’s support of HIV/AIDS initiatives, the diversity of the population it serves, the five established core areas—administrative, developmental, clinical sciences, laboratory sciences, and behavioral/social sciences and community outreach—and the University’s support for the AIDS Malignancies Scientific Working Group.

The NIH also was impressed that the “strong” faculty members who led the D-CFAR’s cores will continue leading their sections. Pahwa will continue as leader of the administrative core, with valuable input from co-directors Margaret Fischl, M.D., professor of medicine and director of the AIDS Clinical Research Unit, and Mario Stevenson, Ph.D., an internationally known HIV/AIDS researcher who was named chief of the Division of Infectious Diseases in the Department of Medicine in 2010.

Pahwa also will continue to lead the laboratory sciences core, while Gwendolyn Scott, M.D., professor of pediatrics and director of the Division of Pediatric Infectious Disease and Immunology, who pioneered the use of AZT to prevent perinatal infection, will continue to lead the developmental core.

Fischl, an original investigator of AZT and lead author of the study that led to its FDA approval, will continue to lead the clinical core, and Guillermo “Willy” Prado, Ph.D., associate professor of epidemiology and public health, will lead the behavioral/social sciences and community outreach core.

“The success we have achieved is a reflection of the hard work and standards of excellence in the leadership – from directors, co-directors and investigators assigned to the cores, and administrative staff, as this program requires teamwork and initiative,’’ Pahwa said, noting that several new members will join the team in the new funding cycle.

As was the case with the D-CFAR, the Miami CFAR will be funded for five years and reviewed after that time.

Part of the difficulty in creating a vaccine against malaria is that it requires a system that can produce complex, three-dimensional proteins that resemble those made by the parasite, thus eliciting antibodies that disrupt malaria transmission. Most vaccines created by engineered bacteria are relatively simple proteins that stimulate the body’s immune system to produce antibodies against bacterial invaders. More complex proteins can be produced, but this requires an expensive process using mammalian cell cultures, and the proteins those cells produce are coated with sugars due to a chemical process called glycosylation.

“Malaria is caused by a parasite that makes complex proteins, but for whatever reason this parasite doesn’t put sugars on those proteins,” said Stephen Mayfield, a professor of biology at UC San Diego who headed the research effort. “If you have a protein covered with sugars and you inject it into somebody as a vaccine, the tendency is to make antibodies against the sugars, not the amino acid backbone of the protein from the invading organism you want to inhibit. Researchers have made vaccines without these sugars in bacteria and then tried to refold them into the correct three-dimensional configuration, but that’s an expensive proposition and it doesn’t work very well.”

Instead, the biologists looked to produce their proteins with the help of an edible green alga, Chlamydomonas reinhardtii, used widely in research laboratories as a genetic model organism, much like the fruit fly Drosophila and the bacterium E. coli. Two years ago, a UC San Diego team of biologists headed by Mayfield, who is also the director of the San Diego Center for Algae Biotechnology, a research consortium seeking to develop transportation fuels from algae, published a landmark study demonstrating that many complex human therapeutic proteins, such as monoclonal antibodies and growth hormones, could be produced by Chlamydomonas.

That got James Gregory, a postdoctoral researcher in Mayfield’s laboratory, wondering if a complex protein to protect against the malarial parasite could also be produced by Chlamydomonas. Two billion people live in regions where malaria is present, making the delivery of a malarial vaccine a costly and logistically difficult proposition, especially when that vaccine is expensive to produce. So the UC San Diego biologists set out to determine if this alga, an organism that can produce complex proteins very cheaply, could produce malaria proteins that would inhibit infections from malaria.

“It’s too costly to vaccinate two billion people using current technologies,” explained Mayfield. “Realistically, the only way a malaria vaccine will ever be used is if it can be produced at a fraction of the cost of current vaccines.  Algae have this potential because you can grow algae any place on the planet in ponds or even in bathtubs.”

Collaborating with Joseph Vinetz, a professor of medicine at UC San Diego and a leading expert in tropical diseases who has been working on developing vaccines against malaria, the researchers showed that the proteins produced by the algae, when injected into laboratory mice, made antibodies that blocked malaria transmission from mosquitoes.

“It’s hard to say if these proteins are perfect, but the antibodies to our algae-produced protein recognize the native proteins in malaria and, inside the mosquito, block the development of the malaria parasite so that the mosquito can’t transmit the disease,” said Gregory.

“This paper tells us two things: The proteins that we made here are viable vaccine candidates and that we at least have the opportunity to produce enough of this vaccine that we can think about inoculating two billion people,” said Mayfield. “In no other system could you even begin to think about that.”

The scientists, who filed a patent application on their discovery, said the next steps are to see if these algae proteins work to protect humans from malaria and then to determine if they can modifiy the proteins to elicit the same antibody response when the algae are eaten rather than injected.

Other UC San Diego scientists involved in the discovery were Fengwu Li from Vinetz’s laboratory and biologists Lauren Tomosada, Chesa Cox and Aaron Topol from Mayfield’s group. The basic technology that led to the development was supported by the Skaggs family. The research was supported by grants from the National Institute of Allergy and Infectious Diseases and the San Diego Foundation.  The California Energy Commission supported work on recombinant protein production for biofuels use, and this technology helped enabled these studies.

The PLoS ONE article can be accessed at: http://dx.plos.org/10.1371/journal.pone.0037179

More than 300 people from across Florida attended. 100 more participated as vendors, biotech company reps, and volunteers. This year’s Gallery of Biotech companies included AxoGen, Applied Food Technologies, Nanotherapeutics, eTech, Pasteuria Bioscience, Tucker-Davis Technologies and RTI Biologics. There was tremendous give-and-take all day long on products, services and the state of the industry. There was a first-time exhibit of Art Inspired by Science.

“This really is a broad-based, multi-disciplinary team effort,” Kenny said. “We’ve assembled a team of first-class scientists at Scripps Florida with all the experience necessary to develop novel therapeutics for the treatment of tobacco abuse.”

Others involved in the study are Michael Cameron, Theodore Kamenecka, and Patricia McDonald of The Translational Research Institute on the Scripps Florida campus.

Tobacco smoking is a global scourge, killing more than 5 million people each year worldwide, according to the World Health Organization. It is estimated that if current trends continue, by 2020 smoking will become the largest single health problem worldwide. The World Bank estimates that in high-income countries, smoking-related healthcare accounts for between 6 and 15 percent of all healthcare costs, some $160 billion annually.

Nicotine addiction is notoriously hard to break. Even with the most effective smoking-cessation agents available, more than 80 percent of smokers who quit or attempt to quit will relapse.

To combat these dismal statistics, the study is focused on an entirely new mechanism to help smokers break the habit.

That mechanism is a receptor for a specific neuropeptide (short chain of amino acids found in nerve tissue) that, when blocked, significantly decreases the desire for nicotine in animal models.

The neuropeptide, known as hypocretin-1 or orexin A, initiates a key signaling cascade that maintains tobacco addiction in human smokers. In a 2008 study in the Proceedings of the National Academy of Sciences, Kenny and colleagues showed that blocking hypocretin-1 receptors not only decreased nicotine use in animal models, but also abolished the stimulatory effects of nicotine on brain reward circuitries. These results demonstrated that hypocretin-1 plays a major role in driving the desire for more nicotine.

These findings also highlighted the importance of hypocretin-1 receptors in a region of the brain called the insula, a walnut size part of the frontal lobe. While all mammals have insula regions that sense the body’s internal physiological state and direct responses to maintain homeostasis, this region has also been implicated in cravings. In one study, it was reported that smokers who sustained damage to the insula lost the desire to smoke, an insight that revealed the insula as key for sustaining the tobacco habit in smokers.

“This work has major implications for modulating the fatty-acid profiles in plants, which is terribly important, not only to sustainable food production and nutrition but now also to biorenewable chemicals and fuels,” said Joseph Noel, a professor and director of the Jack H. Skirball Center for Chemical Biology and Proteomics at the Salk Institute.

“Because very high-energy molecules such as fatty acids are created in the plant using the energy of the sun, these types of molecules may ultimately provide the most cost-effective and efficient sources for biorenewable products,” added Eve Syrkin Wurtele, a professor of genetics, development and cell biology at Iowa State.

The analysis of gene activity (by the Iowa group) and determination of protein structures (by the Salk group) independently identified in the model plant thale cress (Arabidopsis thaliana) three related proteins that appear to be involved in fatty-acid metabolism. The Iowa and Salk researchers then joined forces to test this hypothesis, demonstrating a role of these proteins in regulating the amounts and types of fatty acids accumulated in plants. The researchers also showed that the action of the proteins is very sensitive to temperature and that this feature may play an important role in how plants mitigate temperature stress using fatty acids.

Although the researchers now understand that the three proteins – dubbed fatty-acid-binding proteins one, two and three, or FAP1, FAP2 and FAP3 – are involved in fatty-acid accumulation in plant tissues such as leaves and seeds, Wurtele said researchers still don’t understand the physical mechanism these proteins employ at the molecular level. That knowledge will ultimately allow the two collaborating research groups to predictably engineer better functions in plants.

“The proteins appear to be crucial missing links in the metabolism of fatty acids in Arabidopsis, and likely serve a similar function in other plant species since we find the same genes spread throughout the plant kingdom,” said Ryan Philippe, a post-doctoral researcher in Noel’s lab.

“If the researchers can understand precisely what role the proteins play in seed oil production,” said first author Michelle Ngaki, “they might be able to modify the proteins’ activity in new plant strains that produce more oil or higher quality oil than current crops.”

Further, if the three proteins help plants regulate stress, plant scientists might be able to exploit that trait to develop plants that are more resistant to stress, Wurtele said. And that could allow farmers to grow crops for biorenewable fuels and chemicals on marginal land that’s not suited for food crops.

All of this, she said, could point to new directions in biological studies.

“We are entering the age of predictive biology,” Wurtele said. “That means harnessing computational approaches to deduce gene function, model biological processes and predict the consequences of altering a single gene to the complex biological network of an organism.”