Research led by the German Institute of Human Nutrition (DIfE) has identified a new gene associated with diabetes, together with a mechanism that makes obese mice less susceptible to diabetes. A genomic fragment that occurs naturally in some mouse strains diminishes the activity of the risk gene Zfp69. The researchers also found that the corresponding human gene (ZNF642) is especially active in overweight individuals with diabetes. The results of the study, which also involved scientists from the University of Leipzig and the German Cancer Research Center in Heidelberg, are published July 3 in the open-access journal PLoS Genetics.

It has been known for a long time that T cells can attack the body's own structures and, if they infiltrate the CNS, cause diseases such as multiple sclerosis (MS). The T cells damage the myelin sheath, the material that surrounds and protects the fibers of nerve cells. This damage slows down or blocks messages between the brain and the body, leading to various symptoms of MS such as impaired movements.

People smell them, thump them and eyeball their shape. But ultimately, it's sweetness and a sense of healthy eating that lands a melon in a shopper's cart.

Researchers at The University of Texas M. D. Anderson Cancer Center have identified a protein that marks the tumor suppressor p53 for destruction, providing a potential new avenue for restoring p53 in cancer cells.

The goal of DNA barcoding is to find a simple, cheap, and rapid DNA assay that can be converted to a readily accessible technical skill that bypasses the need to rely on highly trained taxonomic specialists for identifications of the world's biota. This is driven by a desire to open taxonomic identifications to all user groups and by the short supply of taxonomists that do not even exist in many groups. Although DNA barcoding is being rapidly accepted in the scientific literature and popular press, some scientists warn that we are being too hasty in wholeheartedly embracing this technique. Dr. David Spooner, a researcher with the USDA and an expert in the potato and tomato family (Solanaceae), offers just such a cautionary note against accepting this technique without closer examination in his recent article, "DNA Barcoding will Frequently Fail in Complicated Groups: An example in Wild Potatoes" in the June 2009 issue of the American Journal of Botany.

Although every cell in the body carries the genes necessary to function as an antibody-producing B cell, only a small proportion of stem cells mature into those important immune-system cells. James Hagman, PhD, Professor of Immunology at National Jewish Health and his colleagues have identified two "molecular motors" that work in opposing directions to control the development of B cells. They published their findings June 19 in the online version of The Proceedings of the National Academy of Sciences USA.

In a landmark technical achievement, investigators in the Vanderbilt Center for Structural Biology have used nuclear magnetic resonance (NMR) methods to determine the structure of the largest membrane-spanning protein to date.

Experiment after experiment confirms that a diet on the brink of starvation expands lifespan in mice and many other species. But the molecular mechanism that links nutrition and survival is still poorly understood. Now, researchers at the Salk Institute for Biological Studies have identified a pivotal role for two enzymes that work together to determine the health benefits of diet restriction.

Mitochondria are the powerhouses of cells. Underneath their smooth surface they harbor an elaborately folded inner membrane. It holds a multitude of bottleneck like invaginations, which expand into elongated cavities (cristae). The narrow shape of the entrance or pore to the cristae ('crista junction') allows separation of the intracristal space and storage of molecules. Cytochrome c, for example, an important signaling protein in programmed cell death (apoptosis), is stored in this compartment. When apoptosis is triggered, the pores enlarge and cytochrome c is released into the cytosol. Thus, understanding of how the pore diameter and the shape of the inner membrane are regulated on a molecular basis is of great relevance to a better understanding of mitochondrial function in general. Recently, in cooperation with other research teams, the group of Prof. Andreas Reichert, who has been appointed as professor for Mitochondrial Biology to the Goethe University within the Cluster of Excellence Macromolecular Complexes in 2007, has identified two proteins linked in an antagonistic manner that are relevant for governing inner membrane structure.

The pursuit of happiness characterizes the human condition. But for those suffering from stress, money trouble or chronic illness, a positive outlook on life can be difficult to find. Now, a Tel Aviv University researcher says we should look to our genes.

Researchers at the University of Illinois report that a toxic molecule known to damage cells and cause disease may also play a pivotal role in bird migration. The molecule, superoxide, is proposed as a key player in the mysterious process that allows birds to "see" Earth's magnetic field.

A protein called neuroligin that is implicated in some forms of autism is critical to the construction of a working synapse, locking neurons together like "molecular Velcro," a study lead by a team of UC Davis researchers has found.

A new study published by University of Leicester researchers has found "convincing evidence" that cannabis smoke damages DNA in ways that could potentially increase the risk of cancer development in humans.

For many years scientists have known that the numerous biological functions of an organism are not regulated solely by the DNA sequence of its genes: Superordinate regulatory mechanisms exist that contribute to determining the fate of genes. Although they are not anchored in the DNA, they can even be passed on to subsequent generations to a certain extent. Intensive research in recent years has shown that these mechanisms – bundled under the term epigenetics, are very multifaceted and complex.

In 2004, researchers at the University of North Carolina at Chapel Hill Lineberger Comprehensive Cancer Center announced a crucial discovery in the understanding of cellular aging. They found that as cells and tissues age, the expression of a key protein, called p16INK4a, dramatically increases in most mammalian organs. Because p16INK4a is a tumor suppressor protein, cancer researchers are interested in its role in cellular aging and cancer prevention.

Stalled microtubules might be responsible for some cases of the neurological disorder Charcot-Marie-Tooth (CMT) disease, Tanabe and Takei report in the June 15, 2009 issue of the Journal of Cell Biology (www.jcb.org). A mutant protein makes the microtubules too stable to perform their jobs, the researchers find.

One of the mechanisms governing how our physical features and behavioural traits have evolved over centuries has been discovered by researchers at the University of Leeds.

From the valves in a human heart to the quills on a porcupine to the petals on a summer lily, the living world is as varied as it is vast. For this to be possible, the cells that make up these living things must be just as varied. Parent cells must be able to divide in ways that create daughter cells that are different from each other, a process called asymmetric division. Scientists know how this happens in animals, but the process in plants has been a mystery.

Jumping genes do most of their jumping, not during the development of sperm and egg cells, but during the development of the embryo itself. The research, published this month in Genes and Development, "challenges standard assumptions on the timing of when mobile DNA, so-called jumping genes, insert into the human genome," says senior author Haig H. Kazazian Jr., MD, Seymour Gray Professor of Molecular Medicine in Genetics at the University of Pennsylvania School of Medicine.

Two signals – an external one from retinoic acid and an internal one from the transcription factor Neurogenin2 – cooperate to activate chromatin (the basic material of chromosomes) and help determine that certain nerve progenitor cells become motor neurons, said researchers from Baylor College of Medicine (www.bcm.edu) in a report in the current issue of the journal Neuron.

In a new study, Dana-Farber Cancer Institute scientists disprove a century-old theory about why cancer cells often have too many or too few chromosomes, and show that the actual reason may hold the key to a novel approach to cancer therapy.

The genome of complex organisms is stashed away inside each cell's nucleus, a little like a sovereign shielded from the threatening world outside. The genome cannot govern from its protective chamber, however, without knowing what's going on in the realm beyond and having the ability to project power there. Guarding access to the nuclear chamber is the job of large, intimidating gatekeepers known as nuclear pore complexes (NPCs), which stud the nuclear membrane, filtering all of the biochemical information passing in or out. In new research, scientists have for the first time glimpsed in three dimensions an entire subcomplex of the NPC; it's the key building block of this little understood and evolutionarily ancient structure, an innovation fundamental to the development of nearly all multicellular life on earth.

In the quest for new approaches to treating and preventing disease, one appealing route involves turning genes on or off at will, directly intervening in ailments such as cancer and diabetes, which result when genes fail to turn on and off as they should.

By inserting a molecular shunt into the livers of mice, researchers have shown they can make the animals burn more fat. That so-called glycoxylate shunt consists of two metabolic enzymes normally found in bacteria and plants, but not in mammals, according to the report in the June issue of Cell Metabolism, a Cell Press publication.

It turns out that from the perspective of cell biology, Nietzsche may have been right after all: that which does not kill us does make us stronger. In a review article published in the June 2009 print issue of The FASEB Journal (http://www.fasebj.org), scientists from the Mayo Clinic explain how cell receptors (called "death receptors") used by the body to shut down old, diseased, or otherwise unwanted cells (called "apoptosis") may also be used to make cells heartier when facing a wide range of illnesses, from liver disease to cancer.

For the past century, changes in the Western diet have altered the consumption of omega-6 fatty acids (w6, found in meat and vegetable oils) compared with omega-3 fatty acids (w3, found in flax and fish oil). Many studies seem to indicate this shift has brought about an increased risk of inflammation (associated with autoimmunity and allergy), and now using a controlled diet study with human volunteers, researchers may have teased out a biological basis for these reported changes.

Most of our cells possess an internal clock, a group of genes displaying a cyclic expression pattern that reaches a peak once a day. A large number of circadian genes are expressed by organs such as the liver, whose activity needs to be precisely regulated over the course of the day. A team of researchers of the National Centre of Competence in Research Frontiers in Genetics, based at the University of Geneva, Switzerland, reveals that an important regulator of this molecular oscillator is a specific microRNA. The latter belongs to a class of small RNA molecules that regulate the production of proteins in our cells. Thus far, little was known about their function within the circadian clockwork. The study by Ueli Schibler's team, published in the 1st June edition of Genes & Development, fills in this important gap.

By using ultrafast laser pulses to slice off pieces of chromosomes and observe how the chromosomes behave, biomedical engineers at the University of Michigan have gained pivotal insights into mitosis, the process of cell division.

Researchers have identified the locking mechanism that allows some neurons to form synapses to pass along essential information. Mutations of genes that produce a critical cell-adhesion molecule involved in the work were previously linked to autism.

If we imagine our immune system to be a police force for our bodies, then previous work has suggested that the Lymph nodes would be the best candidate structures within the body to act as police stations – the regions in which the immune response is organised. However, Prof. Burkhard Becher, University of Zurich, suggests in a new paper – published in this week's issue of PLoS Biology – that lymph nodes are not essential in the mouse in marshalling T-cells (a main immune foot soldier) to respond to a breach of the skin barrier. This result is both surprising in itself, and suggests a novel function for the liver as an alternate site for T-cell activation.