Genetics & Molecular Biology

Using proteosome inhibitors to trick cells into producing a chaperone protein called Hsp70 may be one way of enhancing the natural ability of cells to restore their own mutant proteins. Researchers at the Fox Chase Cancer Center say the discovery may help treat certain debilitating – or even fatal – genetic diseases.

Scientists have just identified several molecules capable of reversing the brain abnormalities of Parkinson’s disease (PD), while also uncovering new clues for its origin in a study just published in the journal Disease Models and Mechanisms (1). PD is characterised by abnormal deposits of a brain protein called alpha-synuclein throughout the damaged brain regions, but exactly what they do there is not clear.

Why should we bother building mathematical models of biological systems? Scientists from other fields might wonder why one would as such a question - physicists, climate scientists, economists, engineers, and chemists all use mathematical models to understand the world.

Some biologists do too - individual proteins are studied with quantum mechanical models by biophysicists, enzyme reactions are modeled by biochemists, physiologists have mathematical models of the circulatory system, and population geneticists model the evolution of gene frequencies in populations.
Why are some people willing to take risks by gambling on "longshot" payoffs while, on the other hand, taking the opposite tack by buying insurance to reduce their risks? An international team of economists and molecular geneticists says the answer can be found in our genetic makeup.

In an article recently published online in PLoS ONE, researchers combined the tools of experimental economics and molecular genetics to examine the role of a well-characterized
gene, monoamine oxidase A (MAOA), in predicting whether subjects are more likely to buy the lottery or insurance (or both) under well-controlled laboratory conditions.
A molecule called Alda-1 can repair Aldehyde dehydrogenase 2 (ALDH2), an often defective alcohol metabolism enzyme that affects an estimated 1 billion people worldwide, according to research published Jan. 10 in the advance online edition of Nature Structural and Molecular Biology. The findings suggest the possibility of a treatment to reduce the health problems associated with the enzyme defect.

After alcohol is consumed, it is metabolized into acetaldehyde, a toxic chemical that causes DNA damage.  Aldehyde dehydrogenase 2 (ALDH2) is the main enzyme responsible for breaking down acetaldehyde into acetate, a nontoxic metabolite in the body.  It also removes other toxic aldehydes that can accumulate in the body.
The latest issue of Cell has some goodies on synthetic and systems biology: "Engineering Static and Dynamic Control of Synthetic Pathways, by William Holtz and Jay Keasling:
Maximizing the production of a desired small molecule is one of the primary goals in metabolic engineering. Recent advances in the nascent field of synthetic biology have increased the predictability of small-molecule production in engineered cells growing under constant conditions. The next frontier is to create synthetic pathways that adapt to changing environments.
Researchers have demonstrated for the first time that calcium channels on the tongue are the targets of compounds that can enhance taste. In addition to molecules that directly trigger specific taste buds (salty, sweet etc.), there are other substances which have no flavor of their own but can enhance the flavors they are paired with (known as kokumi taste in Japanese cuisine). The results appear in the January 8 issue of the Journal of Biological Chemistry.

Exploiting this enhancement could have practical uses in food modulation; for example, creating healthy foods that contain minimal sugar or salt but still elicit strong taste. At the moment, though, the mode of action for these substances is poorly understood.

Here is a molecular biology discovery that we can chalk up to our increasing love of lean bacon:

"ZBED6, a Novel Transcription Factor Derived from a Domesticated DNA Transposon Regulates IGF2 Expression and Muscle Growth", in PLoS Biology.

If you're a bacon lover, you may not realize how much your culinary satisfaction is intertwined with genetics. The drive to breed leaner pigs has led to the search for genetic variants that affect muscle mass and fat deposition in pigs. Some years back, in order to find such genetic variants, a Swedish research group crossed European Wild Boars and Large White domestic pigs.
According to a new study published in this month's Genomics journal, so called 'junk' DNA may  help doctors diagnose breast and bowel cancer. Researchers from the University of Nottingham discovered that a group of genetic rogue elements--called chimeric transcripts--produced by 'junk' DNA sequences are more common in breast cancer cells. Five were only present in breast cancer cells while two were found in both normal and breast cancer cells.

These chimeric transcripts are produced by DNA sequences called LINE-1 (L1). Despite being labelled as 'junk DNA' it is clear that some of these sequences have important roles in the genome, such as influencing when genes are switched on.
Researchers from the Mayo Clinic and the University of Iowa say that the key to bringing obesity under control is to make our muscle a little less efficient and they may have found a way to do it. In a new study in the January issue of Cell Metabolism, the team discusses the possibility that treatments designed to disrupt so-called sarcolemmal ATP-sensitive K+ (KATP) channels specifically in muscles might allow us to control our weight by increasing the number of calories our muscles will burn with regular activity or exercise.