This has been a controversial idea in the past year or so. An article in Science Daily gives us some more info on the subject that clears up some of the controversy:
It all begins with the way that the cell repairs breaks in the double strands of DNA that are its genetic blue print. Usually, when this happens, special protein machinery in the cell copies the missing DNA from another chromosome and rejoins the broken ends around the newly synthesized genetic material.
“It fixes the hole in the DNA by copying similar information,” said Rosenberg. However, when the process goes wrong, the repair process introduces errors into the DNA.
Researcher Rebecca Ponder set up experiments to control where the break occurred and examined where the increased mutations were located:
“…she found that errors occurred right next to the break in the stressed cells, and that the rate of errors was 6,000 fold higher than in cells whose DNA was not broken. “It’s really about local repair,” said Rosenberg. Not only that, but subsequent experiments proved that this mechanism of increased mutation at sites of DNA repair occurs only in the cells under stress. “Even if you get a break in a cell, it won’t process it in a mutagenic way,” said Rosenberg. “The cell repairs it, but does not make mutations unless the cell is stressed.”
Not all cells increase their mutation rates in this fashion when stressed. Not being a geneticist my guess would be that somehow stress interferes with repair mechanisms in some cells – which might be the next step in investigating the issue.
Among the small percentage that do increase mutations, most of the errors are neutral, not affecting cells at all. Many are deleterious, resulting in cell death. But a small percentage is advantageous, allowing the cells to survive in an adverse environment.
The fact that the changes in the rate of mutation occur only in a certain physical space at a certain time gives the cells advantage because it reduces the risk to the whole colony. DNA breaks occur only rarely in each individual cell. If the mutations are restricted in time and space, it reduces the risk that the mistakes in repair will affect some other gene. It can also enhance the likelihood of two mutations occurring in the same gene or neighboring genes.
Normally, in discussions of natural selection an entire organism is being talked about. I think the idea of selection between cell lines or even individual cells is fascinating – though I don’t know much about it.
At any rate, the article ends with two statements that give no comfort to intelligent design advocates:
“This can speed evolution of complex protein machines.”
The implications of this statement for intelligent design are obvious.
There is a second statement that affects the argument some are making for intelligent design. Namely the argument that evolutionary theory contibutes nothing to modern medicine. Well:
“…which was supported by grants from the U.S. Department of Defense Breast Cancer Research Program and the National Institutes of Health.”
Now why would the U.S. Department of Defense Breast Cancer Research Program and the National Institutes of Health support research into evolutionary theory when it contributes nothing to modern medicine??
I’ll eagerly await the response from the intelligent design community…