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athletic frogs tended to have faster-changing genomes.

During exercise, the circulatory system provides blood and oxygen to the tissues that are needed most

When physical activity has stopped, the rush of blood and oxygen when circulation is restored to those tissues produces a burst of free radicals that can cause wear and tear on DNA, eventually causing genetic changes that -- if they affect the DNA of cells that make eggs or sperm -- can be passed to future generations.

most protein reconfigurations occur in nanoseconds

In research on proteins, it was assumed (given their chemical composition) proteins would uniformly fold as they cool down and unfold as they heat up. (Think of a balloon expanding and shrinking with the temperature of the air inside.) The experiments didn’t bear this out; the rate of folding or unfolding according to temperature change was unequal (asymmetric) and uneven (nonlinear).

In recent biochemistry a great deal of work is done with ‘tagging’ or ‘marking’ molecules with fluorescent and phosphorescent materials. It’s well known that fluorescence and phosphorescence are phenomena closely related to protein folding and they can only be understood in terms of quantum transition between molecules.

With a quantum transition, the protein could change configuration by ‘jumping’ – skipping all the transition steps – to the final configuration. They call this quantum folding and they developed a mathematical model that shows how the folding, which is virtually instantaneous, would react to change in temperature.

Their quantum transition model matched the folding curves for 15 different proteins and also provides an explanation for the different rates of folding and unfolding among these proteins.

Luo and Lu’s paper is short, a mere 16 pdf pages, and the model is unpretentious mathematically. (Luo has several other related papers on arXiv.) It comes from unknown researchers in an unknown corner of the academic world, and it’s published on the open-source arXiv system. The lack of pedigree means that it will take more time than usual for scientists around the world to learn of it, examine it, and possibly test it.

Epigenetics examines the inheritance of characteristics that are not set out in the DNA sequence.

important factors are the histones, a kind of packaging material for the DNA, in order to store DNA in an ordered and space-saving way. It is now clear that these proteins have additional roles to play. Depending on the chemical group they carry, if they are acetylated or methylated, they permanently activate or deactivate genes.

New methods now allow researchers to sometimes directly show which genes have been activated or deactivated by the histones

The genetic information of the DNA is passed on along with the relevant epigenetic information for the respective cell type.

A similar question remains for the inheritance of the epigenetic characteristics from parents to offspring. They now know that when the gametes are formed, certain epigenetic markers remain and are passed on to the offspring. The questions, which are currently being researched, are how much and which part of the epigenetic information is preserved and subsequently inherited.

Diet and epigenetics appear to be closely linked. The most well known example is that of the Agouti mice: they are yellow, fat and are prone to diabetes and cancer. If Agouti females are fed with a cocktail of vitamin B12, folic acid and cholin, directly prior to and during pregnancy, they give birth to mainly brown, slim and healthy offspring. They in turn mainly have offspring similar to themselves.

Environmental factors, which change the characteristics of an individual and are then passed on to its offspring, do not really fit into Darwin’s theory of evolution. According to his theory, evolution is the result of the population and not the single individual. “Passing on the gained characteristics fits more to Lamarck’s theory of evolution”, says Paro.

This year, however, Sauer won a round in court, convincing a judge to rule against Gov. Jay Nixon's signature bio-tech initiative, MOSIRA, which seeks to help tech start-ups in the state.

Genes consist of several modules, separated by non-coding DNA regions (introns).

Since the introns obstruct protein synthesis, they need to be removed from the mRNA, a procedure described as splicing.

t is thought that the introns even help the splicing enzymes by folding themselves into stable RNA structures, thus directing the enzymes to the right locations.

It was found that the transfer takes place without the involvement of RNA and that the DNA apparently jumps directly from the cell's chloroplasts into its nucleus.

the offspring of parents who experience famine are at heightened risk for developing schizophrenia, some research suggests — perhaps because of the chemical signatures on the genes that parents pass on.

in some people with autism, epigenetic markers had silenced the gene which makes the receptor for the hormone oxytocin. Oxytocin oils the brain’s social circuits, and is critical in cementing relationships; a brain short on receptors for it would most likely struggle in social situations.

In one large study of people with schizophrenia, researchers at Johns Hopkins are analyzing blood and other data to see whether the degree of epigenetic variation is related to the inherited risk of developing the disorder. In another, researchers at Tufts are studying the genes of animals dependent on opiates to see how epigenetic alterations caused by drug exposure affect the opiate sensitivity of the animals’ offspring.

It’s assumed the protein complex is analyzing, but the mechanism of analysis is unknown. It’s also unknown if the UvrAB complex (or similar complex) actually does the repair, or if it signals for some other protein complex(es) to make the repair.

now that doctors know that the SHANK 1 gene is involved and it can be tested for, they'll know to follow affected males very closely and offer treatments early on.

lved and it can be tested for, they'll know to follow affected males very c

The Bdnf gene generates one short transcript and one long transcript. He discovered that when the long-form Bdnf transcript is absent, the growth factor BDNF is only synthesized in the cell body of a neuron but not in its dendrites. The neuron then produces too many immature synapses, resulting in deficits in learning and memory in mice. Xu also found that the mice with the same Bdnf mutation grew to be severely obese

large-scale genome-wide association studies showed Bdnf gene variants are, in fact, linked to obesity.

both leptin and insulin stimulate synthesis of BDNF in neuronal dendrites in order to move their chemical message from one neuron to another through synapses. The intent is to keep the leptin and insulin chemical signals moving along the neuronal highway to the correct brain locations, where the hormones will turn on a program that suppresses appetite.

"If there is a problem with the Bdnf gene, neurons can't talk to each other, and the leptin and insulin signals are ineffective, and appetite is not modified

One possible strategy would be to produce additional long-form Bdnf transcript using adeno-associated virus-based gene therapy, Xu says. But although this kind of gene therapy has proven to be safe, it is difficult to deliver across the brain blood barrier,

The molecule turned on genes that make cartilage components called aggrecan and type II collagen. Tests of mice with cartilage damage similar to osteoarthritis showed that kartogenin injections lowered levels of a protein called cartilage oligomeric matrix protein. People with osteoarthritis have an excess of the protein, which is considered a marker of disease severity.

kartogenin inhibits a protein called filamin A in the mesenchymal stem cells

cording to the study by the University of Edinburgh.

Meanwhile, creatures who reproduce asexually are more likely to be lumbered with disease-causing genes

Combining the genes of two parents – rather than one in the case of fruit flies, stick insects and other animals – allows for damaging DNA to be removed within a few generations.

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This is because individuals who inherit healthy genes tend to flourish and pass on their DNA to the next generatio

The study defined a new role for a protein called polynucleotide phosphorylase (PNPASE) in regulating the import of RNA into mitochondria. Reducing the expression--or output--of PNPASE decreased RNA import, which impaired the processing of mitochondrial genome-encoded RNAs. Reduced RNA processing inhibited the translation of proteins required to maintain the mitochondrial electron transport chain that consumes oxygen during cell respiration to produce energy. With reduced PNPASE, unprocessed mitochondrial-encoded RNAs accumulated, protein translation was inhibited, and energy production was compromised, leading to stalled cell growth.

Geng Wang developed a strategy to target and import specific RNA molecules encoded in the nucleus into the mitochondria and, once there, to express proteins needed to repair mitochondrial gene mutations.

First, the researchers had to find a way to stabilize the reparative RNA so that it was moved out of the nucleus and then localized to the mitochondrial outer membrane. This was accomplished by modifying an export sequence to direct the RNA to the mitochondrion. Once the RNA was in the area of the transport machinery on the mitochondrial surface, then a second transport sequence was required to direct the RNA into the targeted organelle. With these two modifications, a wide range of RNAs were targeted to and imported into the mitochondria, where they worked to repair defects in mitochondrial respiration and energy production in two different cell line models of human mitochondrial disease.