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epigenetic changes with alterations in the structure of the DNA and its associated proteins, histones, which affects the way that genes can behave in later life.

"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.

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.

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.