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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.

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

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.

"It's like a recipe book," Wray said. "It tells you how to make the meal. You need to know the amounts. You need to know the order. The noncoding DNA tells you how much to make, when to make it and under what circumstances."

common diseases are probably more influenced by regulatory differences, Harismendy said. These include Type 2 diabetes, Crohn's disease, Alzheimer's Disease and a variety of cancers, including breast, colon, ovarian, prostate and lung.

According to Wray, research has shown that diseases like bipolar syndrome and clinical depression may be associated with noncoding mutations that determine whether the brain is producing too much or not enough of a particular neurotransmitter. One noncoding mutation gives a person almost complete protection against the nasty malaria parasite, plasmodium vivax.

Another piece of noncoding DNA regulates the enzyme responsible for lactose tolerance, the ability to digest milk. Research by Wray and other scientists has shown that in four populations where dairy consumption is a vital part of the diet, new mutations have appeared that essentially keep the gene that produces the lactase enzyme from switching off.

And recent research done by evolutionary biologists suggests that differences in regulatory DNA may represent a major part of what separates us from chimpanzees.

reserved remains of a shaggy monster that lived in Siberia at -40°C 10,000 years ago have been uncovered;

Cloning the mammoth has been an aim of Japanese scientists for several years. They discovered almost intact bone marrow from a thigh bone in Yakutsk and hope to use a female elephant for what is obviously more than a simple experiment within the next 5 years.

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.