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.”

The CNIO team, in collaboration with Eduard Ayuso and Fátima Bosch of the Centre of Animal Biotechnology and Gene Therapy at the Universitat Autònoma de Barcelona (UAB), treated adult (one‐year‐old) and aged (two‐year‐old) mice, with the gene therapy delivering a “rejuvenating” effect in both cases, according to the authors.

Mice treated at the age of one lived longer by 24% on average, and those treated at the age of two, by 13%. The therapy, furthermore, produced an appreciable improvement in the animals’ health, delaying the onset of age‐related diseases – like osteoporosis and insulin resistance – and achieving improved readings on aging indicators like neuromuscular coordination.

The gene therapy consisted of treating the animals with a DNA-­modified virus, the viral genes having been replaced by those of the telomerase enzyme, with a key role in aging. Telomerase repairs the extreme ends or tips of chromosomes, known as telomeres, and in doing so slows the cell’s and therefore the body’s biological clock. When the animal is infected, the virus acts as a vehicle depositing the telomerase gene in the cells.

This study “shows that it is possible to develop a telomerase-­based anti-­aging gene therapy without increasing the incidence of cancer,” the authors affirm. “Aged organisms accumulate damage in their DNA due to telomere shortening, [this study] finds that a gene therapy based on telomerase production can repair or delay this kind of damage,” they add.

‘Resetting’ the biological clock

Telomeres are the caps that protect the end of chromosomes, but they cannot do so indefinitely: each time the cell divides the telomeres get shorter, until they are so short that they lose all functionality. The cell, as a result, stops dividing and ages or dies. Telomerase gets around this by preventing telomeres from shortening or even rebuilding them. What it does, in essence, is stop or reset the cell’s biological clock.

But in most cells the telomerase gene is only active before birth; the cells of an adult organism, with few exceptions, have no telomerase. The exceptions in question are adult stem cells and cancer cells, which divide limitlessly and are therefore immortal — in fact several studies have shown that telomerase expression is the key to the immortality of tumour cells.

It is precisely this risk of promoting tumour development that has set back the investigation of telomerase­‐based anti­‐aging therapies.

In 2007, Blasco’s group demonstrated that it was feasible to prolong the lives of transgenic mice, whose genome had been permanently altered at the embryonic stage, by causing their cells to express telomerase and, also, extra copies of cancer­‐resistant genes. These animals live 40% longer than normal and do not develop cancer.

The mice subjected to the gene therapy now under test are likewise free of cancer. Researchers believe this is because the therapy begins when the animals are adult so do not have time to accumulate sufficient number of aberrant divisions for tumors to appear.

Also important is the kind of virus employed to carry the telomerase gene to the cells. The authors selected demonstrably safe viruses that have been successfully used in gene therapy treatment of hemophilia and eye disease. Specifically, they are non-­‐replicating viruses derived from others that are non-­‐pathogenic in humans.

This study is viewed primarily as “a proof-­‐of-­‐principle that telomerase gene therapy is a feasible and generally safe approach to improve healthspan and treat disorders associated with short telomeres,” state Virginia Boccardi (Second University of Naples) and Utz Herbig (New Jersey Medical School-­‐University Hospital Cancer Centre) in a commentary published in the same journal.

Although this therapy may not find application as an anti‐aging treatment in humans, in the short term at least, it could open up a new treatment option for ailments linked with the presence in tissue of abnormally short telomeres, as in some cases of human pulmonary fibrosis.

As Blasco says, “aging is not currently regarded as a disease, but researchers tend increasingly to view it as the common origin of conditions like insulin resistance or cardiovascular disease, whose incidence rises with age. In treating cell aging, we could prevent these diseases.”

With regard to the therapy under testing, Bosch explains: “Because the vector we use expresses the target gene (telomerase) over a long period, we were able to apply a single treatment. This might be the only practical solution for an anti‐aging therapy, since other strategies would require the drug to be administered over the patient’s lifetime, multiplying the risk of adverse effects.”

The scientists tested their approach by creating a generator that produces enough current to operate a small liquid-crystal display. It works by tapping a finger on a postage stamp-sized electrode coated with specially engineered viruses. The viruses convert the force of the tap into an electric charge.

Their generator is the first to produce electricity by harnessing the piezoelectric properties of a biological material. Piezoelectricity is the accumulation of a charge in a solid in response to mechanical stress.

The milestone could lead to tiny devices that harvest electrical energy from the vibrations of everyday tasks such as shutting a door or climbing stairs.

It also points to a simpler way to make microelectronic devices. That’s because the viruses arrange themselves into an orderly film that enables the generator to work. Self-assembly is a much sought after goal in the finicky world of nanotechnology.

“More research is needed, but our work is a promising first step toward the development of personal power generators, actuators for use in nano-devices, and other devices based on viral electronics,” says Seung-Wuk Lee, a faculty scientist in Berkeley Lab’s Physical Biosciences Division and a UC Berkeley associate professor of bioengineering.

Notes from the Field: Multistate Outbreak of Postprocedural Fungal Endophthalmitis Associated with a Single Compounding Pharmacy — United States, March–April 2012