Topic: Mechanisms of Evolution:

[Nemesis]

For a long time evolution was presumed to be by means of mutation of genes. Over time this has been refined.  Added to it has been mutation of the timing/control mechanism of genes but no one really knew what it was.  One such mechanism has been seen to be the number of "inert" copies of various genes.  Change the number and you change (or at least may change) how the related gene functions.

Now a new mechanism may have been found.

Link to full article

Scientists have deciphered the three-dimensional structure of the human genome, paving the way for new insights into genomic function and expanding our understanding of how cellular DNA folds at scales that dwarf the double helix.

"Cells cleverly separate the most active genes into their own special neighborhood, to make it easier for proteins and other regulators to reach them," says Job Dekker, associate professor of biochemistry and molecular pharmacology at UMass Medical School and a senior author of the Science paper.

The folding pattern of the DNA is shown by this research to block or unblock genes from easy functioning.  Change the folding pattern and you will change how a gene expresses itself.  Not only can a change in the pattern block or inhibit a gene but a change could also reactivate an old long blocked gene or genes. 

The "inert genes" mentioned earlier could function as "spacers" moving the active copy into a more accessible or inaccessible region.  Changing their number changes the overall length of the chromosome and therefore affects the folding pattern at least slightly.  Which would explain how even an inactive area being added or removed from a chromosome could change how other apparently unrelated genes function by moving them to more or less accessible regions of the 3d folding pattern.

So this provides not only a mechanism of mutation but one that explains back mutations as well.

It might even explain aging.  As the telomeres at the ends of chromosomes get shorter the "packing" of the DNA gets looser changing how genes function and potentially activating normally inert genes that no longer function properly.

[Nemesis]

It might even explain aging.  As the telomeres at the ends of chromosomes get shorter the "packing" of the DNA gets looser changing how genes function and potentially activating normally inert genes that no longer function properly.

More telomere research.

Link to article

A team led by researchers at Albert Einstein College of Medicine of Yeshiva University has found a clear link between living to 100 and inheriting a hyperactive version of an enzyme that rebuilds telomeres -- the tip ends of chromosomes.

"Our findings suggest that telomere length and variants of telomerase genes combine to help people live very long lives, perhaps by protecting them from the diseases of old age," says Dr. Suh. "We're now trying to understand the mechanism by which these genetic variants of telomerase maintain telomere length in centenarians. Ultimately, it may be possible to develop drugs that mimic the telomerase that our centenarians have been blessed with."

Maintain the lenght of telomeres and thereby DNA strands and the folding pattern is maintained too.  Fewer genes have their functioning modified and aging is slowed.