More research about the subject.
The ENCODE project have shown that at least 80% of the human genome is functionally active. Some try explaining it away by claiming that most of the activity is insignificant, but that away-explanation ignores several factors. One is that reading DNA is a job done by energy-expensive reading molecules, making any major amount of meaningless DNA activity extremely unlikely. Another factor is the missing heredity: protein-coding genes can only explain a minor fraction of the heredity shown by twin studies. Some explain away discoveries of functions in non-coding DNA by claiming that they are a minority case and that the vast majority is still junk, theoretically "supporting" it by reference to limitations of how many mutations natural selection can purge per generation. But they are overlooking the fact that hereditary diseases that cannot be explained by protein-coding DNA outnumbers those that can 20 to 1. That is patently not a "minor border revision". Rather, it is a massive expansion of the amount of functionally important genome that makes directed mutations necessary to avoid that literally everybody dies from genetic diseases. A possible mechanism for the directing is that working groups of proteins "feel" when one particular protein in the group does not do its job properly, and sends a signal that triggers unscrambling of the responsible parts of the genome. Experiments that supposedly prove that mutations are random, are in fact victims of false generalizations. Those experiments are really about introducing diseases or poisons that kills too fast for the organisms to have time to direct mutations. John Cairns experiments supporting directed mutations in the 1980s, on the other hand, were about malnutrition (only giving the bacteria food they lacked the genes to digest, in this case giving E.coli only lactose to eat), which gives more time to direct mutations. Not only must there be time to signal the error and change the gene(s), there must also be time to get the production of the modified protein up and going and distribute it to the relevant working groups of proteins. Several molecules are known to interact directly with specific locations in the genome, molecules chemically resembling ones known to affect the risk of cancer when intaken more diffusely. That mechanism should be able to locally alter mutation probabilities. Mechanical changes of the structure of the DNA spiral, a known part of epigenetics, also almost certainly affects the vulnerability of the DNA by making it more or less exposed. And as shown in "Bacteria evolved way to safeguard crucial genetic material", there is evidence that mutation rates do differ between parts of the genome, falsifying the dogma of mutation rates only being able to change over the whole genome and not locally. See Pure science Wiki, the pages "Self-organization" and "Inheritance of acquired characteristics". 220.127.116.11 (talk) 10:39, 7 December 2012 (UTC)Martin J Sallberg