MicroRNA mediates gene-diet interaction related to obesity

Eating more n-3 polyunsaturated fatty acids, commonly known as omega-3 fatty acids, may help carriers of a genetic variant on the perilipin 4 (PLIN4) gene locus lose weight more efficiently.

Led by Jose M. Ordovas, PhD, director of the Nutrition and Genomics Laboratory at the USDA HNRCA, researchers genotyped seven single nucleotide polymorphisms (SNPs), also known as gene variants, from men and women of mostly white European ancestry enrolled in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) study and the Framingham Offspring Study. Carriers of the gene variant tended to weigh more and exhibit higher body mass index (BMI), which would increase their risk of becoming obese. Yet carriers with higher omega-3 fatty acid intakes tended to weigh less than carriers who consumed little or no omega-3 fatty acids.

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Scientists identify new longevity genes

Scientists at the University of Washington and other institutions have identified 25 genes regulating lifespan in two organisms separated by about 1.5 billion years in evolutionary change. At least 15 of those genes have very similar versions in humans, suggesting that scientists may be able to target those genes to help slow down the aging process and treat age-related conditions.

Genes that protect against atherosclerosis identified

One way of combating atherosclerosis is to reduce levels of “bad cholesterol” in the blood. Scientists at the Swedish medical university Karolinska Institutet have now identified the genes that bring about this beneficial effect.

Researchers find trigger gene for muscle development

University of Oregon scientists say they have identified a gene that is the key switch that allows embryonic cells to form into muscles in zebrafish.

‘Telepathic’ Genes Recognize Similarities In Each Other

Genes have the ability to recognise similarities in each other from a distance, without any proteins or other biological molecules aiding the process, according to new research. This discovery could explain how similar genes find each other and group together in order to perform key processes involved in the evolution of species.

Nanotechnology innovation may revolutionize gene detection in a single cell

Scientists at Arizona State University’s Biodesign Institute have developed the world’s first gene detection platform made up entirely from self-assembled DNA nanostructures. The results, appearing in the January 11 issue of the journal Science, could have broad implications for gene chip technology and may also revolutionize the way in which gene expression is analyzed in a single cell.

 

Genomic screen nets hundreds of human proteins exploited by HIV

In some ways, HIV resembles a minimalist painter, using a few basic components to achieve dramatic effects. The virus contains just nine genes encoding 15 proteins, which wreak havoc on the human immune system. But this bare bones approach could have a fatal flaw. Lacking robust machinery, HIV hijacks human proteins to propagate, and these might represent powerful therapeutic targets.

Using a technique called RNA interference to screen thousands of genes, Harvard Medical School researchers have now identified 273 human proteins required for HIV propagation. The vast majority had not been connected to the virus by previous studies. The work appears online in Science Express on Jan. 10.

Researchers discover a gene that might control fat accumulation

Researchers at UT Southwestern Medical Center have found that a single gene might control whether or not individuals tend to pile on fat, a discovery that may point to new ways to fight obesity and diabetes.

“From worms to mammals, this gene controls fat formation,” said Dr. Jonathan Graff, associate professor of developmental biology and internal medicine at UT Southwestern and senior author of a study appearing in the Sept. 5 issue of Cell Metabolism. “It could explain why so many people struggle to lose weight and suggests an entirely new direction for developing medical treatments that address the current epidemic of diabetes and obesity.

“People who want to fit in their jeans might someday be able to overcome their genes.”

Gene regulation, not just genes, is what sets humans apart from primates

The striking differences between humans and chimps aren’t so much in the genes we have, which are 99 percent the same, but in the way those genes are used, according to new research from a Duke University team.

It’s rather like the same set of notes being played in very different ways.

In two major traits that set humans apart from chimps and other primates – those involving brains and diet – gene regulation, the complex cross-talk that governs when genes are turned on and off, appears to be significantly different.

Risk genes for multiple sclerosis uncovered

A large-scale genomic study has uncovered new genetic variations associated with multiple sclerosis (MS), findings that suggest a possible link between MS and other autoimmune diseases. The study, led by an international consortium of clinical scientists and genomics experts, is the first comprehensive study investigating the genetic basis of MS. Findings appear in the July 29 online edition of the New England Journal of Medicine.

Mutating the entire genome

Genes account for only 2.5 percent of DNA in the human genetic blueprint, yet diseases can result not only from mutant genes, but from mutations of other DNA that controls genes. University of Utah researchers report in the journal Nature Genetics that they have developed a faster, less expensive technique for mutating those large, non-gene stretches of DNA.

 

 

 

New ‘asthma gene’ could lead to new therapies

A gene that is strongly associated with a risk of developing childhood onset asthma was identified by an international team of scientists, whose findings are published today in the journal Nature.

In a genetic study of more than 2,000 children, scientists from the University of Michigan and colleagues from London, France and Germany found genetic markers that dramatically increase a child’s risk for asthma. These markers are located on chromosome 17, and children with this marker had higher levels of a new gene called ORMDL3 in their blood, which occurs in higher amounts in children with asthma. The presence of the disease-associated version of ORMDL3 increases the risk of asthma by 60-70 percent, the study suggests.

Scientists find key to stem cell immortality

One of the medical marvels of stem cells is that they continue to divide and renew themselves when other cells would quit. But what is it that gives stem cells this kind of immortality. Researchers now report in the June 16, 2005 issue of the journal Nature that microRNAs — tiny snippets of genetic material that have now been linked to growth regulation in normal cells as well as cancer growth in abnormal cells — appear to shut off the “stop signals” or brakes that would normally tell cells to stop dividing.

Serious diseases genes revealed

A major advance in understanding the genetics behind several of the world’s most common diseases has been reported.The landmark Wellcome Trust study analysed DNA from the blood of 17,000 people to find genetic differences. They found new genetic variants for depression, Crohn’s disease, coronary heart disease, hypertension, rheumatoid arthritis and type 1 and 2 diabetes.

The remarkable findings, published in Nature, have been hailed as a new chapter in medical science.

Read rest of the article at BBC Newssite

Mechanism of microRNAs deciphered

Over 30% of our genes are under the control of small molecules called microRNAs. They prevent specific genes from being turned into protein and regulate many crucial processes like cell division and development, but how they do so has remained unclear. Now researchers from the European Molecular Biology Laboratory (EMBL) have developed a new method that uncovered the mode of action of microRNAs in a test tube. The study, which is published in the current online issue of Nature, reveals that microRNAs block the initiation of translation, the earliest step in the process that turns genetic information stored on messenger RNAs into proteins.

Vitamin extends life in yeast

Imagine taking a vitamin for longevity! Not yet, but a Dartmouth discovery that a cousin of niacin prolongs lifespan in yeast brings the tantalizing possibility a step closer.

The research, reported in the May 4 issue of Cell, shows how a new vitamin extends lifespan in yeast cells, much like calorie restriction does in animals. It could pave the way for developing supplements to benefit humans.

New Genetic Risk Factors For Type 2 Diabetes Identified

In the most comprehensive look at genetic risk factors for type 2 diabetes to date, a U.S.-Finnish team, working in close collaboration with two other groups, has identified at least four new genetic variants associated with increased risk of diabetes and confirmed existence of another six. The findings of the three groups, published in the journal Science, boost to at least 10 the number of genetic variants confidently associated with increased susceptibility to type 2 diabetes — a disease that affects more than 200 million people worldwide.

Scientists create mice with enhanced color vision

Researchers at the Johns Hopkins School of Medicine and their colleagues have found that mice simply expressing a human light receptor in addition to their own can acquire new color vision, a sign that the brain can adapt far more rapidly to new sensory information than anticipated.

This work, appearing March 23 in Science, also suggests that when the first ancestral primate inherited a new type of photoreceptor more than 40 million years ago, it probably experienced immediate color enhancement, which may have allowed this trait to spread quickly.

Gene profiling predicts resistance to breast cancer drug Herceptin

Using gene chips to profile tumors before treatment, researchers at Harvard and Yale Universities found markers that identified breast cancer subtypes resistant to Herceptin, the primary treatment for HER2-positive breast cancer. They say this advance could help further refine therapy for the 25 to 30 percent of breast cancer patients with this class of tumor.

In the February 15 issue of Clinical Cancer Research, the researchers found that HER2-positive tumors that did not respond to Herceptin expressed certain basal markers, growth factors and growth factor receptors. One of these, insulin-growth factor receptor 1(IGF-1R), was associated with a Herceptin response rate that was half that of tumors that did not express IGF-1R.

Mapping the Cancer Genome

Pinpointing the genes involved in cancer will help chart a new course across the complex landscape of human malignancies.

“If we wish to learn more about cancer, we must now concentrate on the cellular genome.” Nobel laureate Renato Dulbecco penned those words more than 20 years ago in one of the earliest public calls for what would become the Human Genome Project. “We are at a turning point,” Dulbecco, a pioneering cancer researcher, declared in 1986 in the journal Science. Discoveries in preceding years had made clear that much of the deranged behavior of cancer cells stemmed from damage to their genes and alterations in their functioning. “We have two options,” he wrote. “Either try to discover the genes important in malignancy by a piecemeal approach, or & sequence the whole genome.”

Scientists find new genetic clue to cause of Alzheimer’s disease

Variations in a gene known as SORL1 may be a factor in the development of late onset Alzheimer’s disease, an international team of researchers has discovered. The genetic clue, which could lead to a better understanding of one cause of Alzheimer’s, is reported in Nature Genetics online, Jan. 14, 2007, and was supported in part by the National Institutes of Health (NIH).

The researchers suggest that faulty versions of the SORL1 gene contribute to formation of amyloid plaques, a hallmark sign of Alzheimer’s in the brains of people with the disease. They identified 29 variants that mark relatively short segments of DNA where disease-causing changes could lie. The study did not, however, identify specific genetic changes that result in Alzheimer’s.

Researchers map gene that regulates adult stem cell growth

The researchers genetically mapped a stem cell gene and its protein product, Laxetin, and building on that effort, carried the investigation all the way through to the identification of the gene itself. This is the first time such a complete study on a stem cell gene has been carried out. This particular gene is important because it helps regulate the number of adult stem cells in the body, particularly in bone marrow. Now that it has been identified, researchers hope the gene, along with its protein product Latexin, can be used clinically, such as for ramping up the stem cell count in cancer patients undergoing chemotherapy and bone marrow transplantation.

The researchers agreed that this very process is not only interesting, but important because of its usefulness in a wide variety of future genetics studies.

‘Marathon mice’ elucidate little-known muscle type

Researchers report in the January issue of the journal Cell Metabolism, published by Cell Press, the discovery of a genetic “switch” that drives the formation of a poorly understood type of muscle. Moreover, they found, animals whose muscles were full of the so-called IIX fibers were able to run farther and at higher work loads than normal mice could.

The findings could ultimately lead to novel drugs designed to change the composition of muscle, the researchers said. Such treatments might have the potential to boost physical strength and endurance in patients with a variety of muscle wasting conditions.

Scientists Crack the Genome of the Parasite Causing Trichomoniasis

Scientists have finally deciphered the genome of the parasite causing trichomoniasis, a feat that is already providing new approaches to improve the diagnosis and treatment of this sexually transmitted disease. According to the World Health Organization trichomoniasis affects an estimated 170 million people a year and is an under-diagnosed global health problem.

Led by Jane Carlton, Ph.D., an Associate Professor in the Department of Medical Parasitology at New York University School of Medicine, the team of scientists took four years to crack the surprisingly large genome of the single-celled parasite Trichomonas vaginalis. They published the draft sequence of the parasite’s genome in the Jan. 12, 2007, issue of the journal Science.

How does a zebrafish grow a new tail?

If a zebrafish loses a chunk of its tail fin, it’ll grow back within a week. Like lizards, newts, and frogs, a zebrafish can replace surprisingly complex body parts. A tail fin, for example, has many different types of cells and is a very intricate structure. It is the fish version of an arm or leg.

The question of how cold-blooded animals re-grow missing tails and other appendages has fascinated veterinary and medical scientists. They also wonder if people, and other warm-blooded animals that evolved from these simpler creatures, might still have untapped regenerative powers hidden in their genes.

Longevity gene keeps mind sharp

A gene variation that helps people live to a ripe old age also appears to preserve memory and thinking power, US work suggests. The “longevity” gene alters the size of fatty cholesterol particles in the blood, making them bigger than normal.

This stops them causing the fatty build up in blood vessels that is linked with brain impairment, and deadly strokes and heart attacks, Neurology reports.

Low folate diets found to increase risk of colorectal cancer

A new study by scientists at the MUHC has revealed that a diet low in folate may increase the risk of developing colorectal cancer. Published in the scientific journal Cancer Research today, the study not only illustrates a way to prevent the disease but also provides further insight into the mechanisms of the disease, which could lead to novel therapies. Using animal models, the MUHC study is the first to demonstrate directly that diets low in folate cause colorectal cancer, and follows on the heels of earlier research by the same team that revealed how high folate diets can protect against heart disease.

Researchers find smallest cellular genome

The smallest collection of genes ever found for a cellular organism comes from tiny symbiotic bacteria that live inside special cells inside a small insect.

The bacteria Carsonella ruddii has the fewest genes of any cell. The bacteria’s newly sequenced genome, the complete set of DNA for the organism, is only one-third the size of the previously reported “smallest” cellular genome.

Antibiotic inhibits cancer gene activity

A little-known antibiotic shows early promise as an anti-cancer agent, inhibiting a gene found at higher-than-normal levels in most human tumors, according to researchers at the University of Illinois at Chicago College of Medicine.

Genome code cracked for breast and colon cancers

Scientists have completed the first draft of the genetic code for breast and colon cancers. Their report, published online in the September 7 issue of Science Express, identifies close to 200 mutated genes, now linked to these cancers, most of which were not previously recognized as associated with tumor initiation, growth, spread or control.

Researchers Identify Gene that May Block Blood Supply to Tumors

An Australian research team has identified a gene that could be used to stop tumours growing by blocking their blood supply.

A study led by Professor Peter Koopman, from the Institute for Molecular Bioscience at The University of Queensland, showed that tumours in mice with a mutant form of the gene SOX18 actually stopped growing and became benign, unlike the lethal tumours that grew in normal mice.

Family Of Life-extending Genes Discovered

Mice, rats, worms, flies, and yeast all live longer on a low-calorie diet, which also seems to protect mammals against cancer and other aging-related diseases. A gene called SIR2 is thought to control this process. Now, researchers at Harvard Medical School and UC Davis have discovered four cousins of the SIR2 gene that also extend lifespan, suggesting that the whole family of SIR2 genes is involved in controlling lifespan. The research indicates potential targets for developing drugs to lengthen life and prevent or treat aging-related diseases. The findings are reported July 28 in the advance online edition of Science. This discovery comes on the heels of the Harvard group’s discovery of a molecule in red wine that extends the lifespan of every organism so far tested.

Scientists find rate of aging is at least in part genetically determined

We can dye gray hair, lift sagging skin or boost lost hearing, but no visit to the day spa would be able to hide a newly discovered genetic marker for the toll that time takes on our cells. “We’ve found something that is at the core of aging,” said Stuart Kim, PhD, professor of developmental biology and of genetics at the Stanford University School of Medicine.

In a study to be published in the July 21 issue of Public Library of Science-Genetics, Kim and colleagues report finding a group of genes that are consistently less active in older animals across a variety of species. The activity of these genes proved to be a consistent indicator of how far a cell had progressed toward its eventual demise.

The aging-clock connection

In the July 15th issue of G&D, Dr. Marina Antoch and colleagues (The Lerner Research Institute) establish a link between the innate biological clock – known as the circadian clock – and aging.

Speeding discovery of the ‘human cancer genome’

Two gene discoveries announced in separate reports in the June 30, 2006 issue of Cell highlight one way to speed through the human genome in search of those genes most important for spawning cancer. Both groups say that a critical element in the enterprise to efficiently characterize the “human cancer genome” –a comprehensive collection of the genetic alterations responsible for major cancers–is the strategic comparison of human tumors with those of mice.

As a demonstration of the value of such strategic comparisons between species, the researchers report promising finds: one of the research teams identified two genes that can–in some circumstances–conspire to produce liver cancer, while the second uncovered a gene important to the spread of melanoma, the most serious form of skin cancer. Such functionally important genes, and the larger genetic pathways of which they are a part, are also those with the most promise as potential targets for cancer drugs, according to the researchers.

Research Identifies Protein In Mice That Regulates Bone Formation

Osteoporosis, a disease characterized by a decrease in bone mass and density and which makes people more susceptible to bone fractures and deformities, afflicts some 10 million Americans over the age of 50. Researchers at the Harvard School of Public Health (HSPH) have discovered that eliminating a protein, Schnurri-3 (Shn3), in mice led to profound increases in bone mass throughout their skeletal system. The results may have implications for the treatment of osteoporosis. The study was published in the May 26 edition of Science.

A Key Regulator Of Fat Synthesis Keeps Mice Lean Despite A High-fat Diet

Scientists at the Salk Institute for Biological Studies have identified a novel pathway that regulates the body's ability to store or burn fat, a discovery that suggests new ways to reduce obesity, diabetes and other fat-related human diseases.

Genetically engineered mice, in which the pathway was constantly revved up, were protected from the ravages of a high-fat diet, the Salk team led by Marc Montminy, Ph.D., a professor in the Clayton Foundation Laboratories for Peptide Biology reports in this week's issue of Science.

Reprogramming Biology

Visionary futurist Ray Kurzweil, whose remarkable ideas on technological progress have been an inspiration for Biosingularity blogs, have a wonderful concise article on biological advances in recent issue of Scientific American. 

As a scientist working on biological systems I fully agree and whole heartedly support Kurzweil's observations that: " Biology is now in the early stages of an historic transition to an information science, while also gaining the tools to reprogram the ancient information systems of life ….. We are now beginning to understand biology as a set of information processes, and we're developing realistic models and simulations of how the processes involved in disease and aging progress. Moreover, we are developing the tools to reprogram them."

In the article Kurzweil predicts that tinkering with our genetic programs will extend human lifespan beyond the current limits. He also reiterates that biological systems are also subject to the "law of accelerating returns", which had tremendous impact on information technologies. Indeed, the cost of sequencing and synthesizing gene base pairs have decreased more than 10,000 fold over the last 15 years, and this exponential progress is currently accelerating as predicted by Kurzweil in his recent book. 

Read rest of the article at Scientific American web site.
 

Scientists tie several cancers to common ‘oncogene engine’

Researchers at Dana-Farber Cancer Institute report that a common "oncogene engine" – a small family of malfunctioning cell growth switches – drives several seemingly unrelated, lethal forms of cancer, including malignant melanoma. The finding suggests that it may be possible to attack these different cancers with the same therapy.

HIV-1’s high virulence might be an accident of evolution

The virulence characteristic of HIV-1–the virus predominantly responsible for human AIDS–might amount to an accident of evolution, new evidence reveals. A gene function lost during the course of viral evolution predisposed HIV-1 to spur the fatal immune system failures that are the hallmarks of AIDS, researchers report in the June 16, 2006 Cell.

Cells use mix-and-match approach to tailor regulation of genes

Scientists eager to help develop a new generation of pharmaceuticals are studying cellular proteins called transcription factors, which bind to upstream sequences of genes to turn the expression of those genes on or off. Some pharmaceutical companies are also hoping to develop drugs that selectively block the binding of transcription factors as a way to short-circuit the harmful effects of diseases.

Bioengineering researchers at UCSD and two research institutes in Germany report in the June 16 issue of PLoS Computational Biology that transcription factors act not only in isolation, but also in pairs, trios, and combinations of up to 13 to regulate distinct sets of genes.

Free Radical Cell Death Switch Identified

"A common molecular denominator in aging and many age-related diseases is oxidative stress," says the study's lead author Azad Bonni, MD, PhD, HMS associate professor of pathology. The skin of a bitten apple will brown because of its exposure to air, and in some ways that is a good metaphor for the damage that oxidative stress is causing to neurons and other types of cells over time.

How the oxidative-stress signals trigger these profound effects in cells has remained unclear. But Bonni and his research team, have now defined how a molecular chain-of-events links oxidative-stress signals to cell death in brain neurons.

Scientists publishes first human microbiome analysis

For the first time, scientists have defined the collective genome of the human gut, or colon. Up to 100 trillion microbes, representing more than 1,000 species, make up a motley "microbiome" that allows humans to digest much of what we eat, including some vitamins, sugars, and fiber, an accomplishment that has far-reaching implications for clinical diagnosis and treatment of many human diseases.

In a study published in the June 2 issue of Science, scientists at The Institute for Genomic Research (TIGR) and their colleagues describe and analyze the colon microbiome, which includes more than 60,000 genes–twice as many as found in the human genome. Some of these microbial genes code for enzymes that humans need to digest food, suggesting that bacteria in the colon co-evolved with their human host, to mutual benefit.

Researchers Create New ‘Matchmaking Service’ Computer System To Study Gene Interactions

Biologists in recent years have identified every individual gene in the genomes of several organisms. While this has been quite an accomplishment in itself, the further goal of figuring out how these genes interact is truly daunting.

The difficulty lies in the fact that two genes can pair up in a gigantic number of ways. If an organism has a genome of 20,000 genes, for example, the total number of pairwise combinations is a staggering total of 200 million possible interactions.

Researchers can indeed perform experiments to see what happens when the two genes interact, but 200 million is an enormous number of experiments, says Weiwei Zhong, a postdoctoral scholar at the California Institute of Technology. “The question is whether we can prioritize which experiments we should do in order to save a lot of time.”

To get at this issue, Zhong and her supervising professor, Paul Sternberg, have derived a method of database-mining to make predictions about genetic interactions. In the current issue of the journal Science, they report on a procedure for computationally integrating several sources of data from several organisms to study the tiny worm C. elegans, or nematode, an animal commonly used in biological experiments.

Scientists discover how to extend lifespan without disrupting life-sustaining function

For the first time ever, researchers at the Salk Institute have pinpointed a protein specifically responsible for extending lifespan and youthfulness without disrupting an organism’s response to some forms of stress, development and fertility controlled by the insulin signaling pathway.

Genes involved in cell growth and cell division identified

A recent study shows that hundreds of genes contribute to cell growth and cell division. For the first time these genes, many of which are potential contributors to cancer, have been mapped in a single systematic study.

Making Mice Old Before Their Time

Knocking out a gene that helps repair nicks in DNA causes young mice to develop many of the degenerative characteristics of their wizened elders. Mice lacking the gene develop hunchback, thinning skin, decreasing bone density, and a declining immune system — all in the span of a month.

The researchers do not know whether the accelerated aging-like effects of losing the gene, called SIRT6, relate to its role in DNA repair. Nor do they know whether the degenerative effects are relevant to the natural aging process. However, they said, the discovery offers an intriguing new model for studying DNA repair, as well as its possible role in aging-related degeneration.

Discoveries may advance stem cell therapy for Parkinson’s, cancer patients

Two studies in the Jan. 27, 2006 issue of Cell have yielded evidence that could prove a boon for stem cell therapies aimed at patients with Parkinson’s disease and those with compromised immune systems due to intensive cancer therapy or autoimmune disease, according to researchers. The basic findings in mice revealed critical factors that determine the fate of one type of nerve cell progenitor and that set bone marrow stem cells into action.

Researchers at the Karolinska Institutet in Sweden discovered a “master determinant” that turns embryonic stem cells into bona fide dopamine neurons, brain cells that degenerate in those with Parkinson’s disease. The findings hold promise for the future of cell replacement therapy for the debilitating and incurable disease characterized by tremors, said study authors Thomas Perlmann and Johan Ericson. The results also underscore the general importance of a thorough understanding of development for producing authentic cells of a desired type from stem cells.

Decoding the cellular machinary

Researchers from Germany announce they have finished the first complete analysis of the “molecular machines” in one of biology’s most important model organisms: S. cerevisiae (baker’s yeast).

The study combined a method of extracting complete protein complexes from cells (tandem affinity purification, developed in 2001 by Bertrand Séraphin at EMBL), mass spectrometry and bioinformatics to investigate the entire protein household of yeast, turning up 257 machines that had never been observed. It also revealed new components of nearly every complex already known.

Scientists find unusual lung-cancer tumor-suppressor gene

Researchers have identified a new and unusual tumor suppressor gene that may be important in cancers of the lung and head and neck. The study shows that restoring the inactivated gene can slow the growth of tumor cells.

The gene, known as TCF21, is silenced in tumor cells through a chemical change known as DNA methylation, a process that is potentially reversible.