In a previous essay, I highlighted the manner in which bacteria exert control over their own evolution. ScienceDaily reports on another study that echoes this same theme. This time, Dr. Susan Rosenberg, professor of molecular and human genetics at Baylor College of Medicine, found that the stress of starvation causes some bacteria to enhance their mutation rate.
According to the report in ScienceDaily:
When graduate student Rebecca G. Ponder set up a system so that she could control where the break in DNA occurred, 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.” (emphasis added)
Rosenberg’s lab found that only some members of a bacterial population undergo this enhanced mutation rate. This is smart. If a population is being starved, there is always the chance it will eventually encounter a fresh supply of nutrients, thus it makes sense for most to wait. However, if the food supply is not reacquired after some critical time, the newly made mutants might be needed to carry the population forward, as they may be able to make use of a new food source. As the ScienceDaily reports:
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.
Given that bacteria organize their genes into operons, where genes that are functionally related are clustered in a linear order, the ability to focus the mutations in discrete spots is clearly a clever strategy. So once again, we see that bacteria are not passive entities in the flow of evolution. On the contrary, they help natural selection along.
ScienceDaily also reports on a related study from 2003, where it was found that the expression of DNA polymerase IV was increased during times of starvation. Pol IV synthesizes pieces of DNA, but it is highly prone to introducing mutations.
Finally, there is another study that indicates an increase in the rate of mutation in turn increases the chance the mutation will persist in a population:
For more than three decades, molecular evolutionists have thought that no matter how many genetic mutations show up on a specific gene, whether or not those mutations become fixed in the species is determined primarily by natural selection. The new study shows that the speed at which these new mutations arrive also affects whether the mutations become fixed.
Not only does the study undercut one the primary measurements used to detect whether selection has played a crucial role in past evolution, it challenges the way we think about evolution:
The new data show that if more mutations show up at a gene, that gene tends to accept a higher percentage of those mutations. “A gene under strong mutational pressure succumbs to that pressure,” Lahn said. “For genes that have a high mutation rate, somehow selection appears to become less stringent.”
I have already spelled out some of the teleological implications of studies such as these. But let me add some more.
First, as it becomes more and more clear that organisms take control of their evolution, many arguments against design have become weaker:
Bad Design. It would be tempting to argue that Pol IV is a klugy design given that it is highly prone to error. But this is a myopic perspective that fails to appreciate the benefit of sloppy copying as seen from the perspective of adaptive mutation. From that perspective, the inability to enhance the mutation rate would be “bad design.”
Multiple Designers. It would be tempting to argue that because Pol IV is error-prone, while Pol I, II, and III are extremely accurate, two different designers are indicated. But this is another myopic perspective. From the larger perspective of evolvability and homeostasis, the dual-approach to fidelity is quite coherent – you faithfully propagate a design but, when needed, you also tweak it in a search for a better fit.
Secondly, a common complaint from the non-teleological perspective would argue that these mutations remain “random with regard to fitness.” This perspective assumes the teleological perspective would predict the cell would specifically target the right type of mutations to the right genes in order to meet the specific environmental challenge. Those who expect such a process from the teleological perspective are misguided (as I will explain in a future essay).
Thirdly, and most importantly, these type of findings are expected from the hypothesis of Front Loaded Evolution. This hypothesis entails that the future is designed through the present. To do this, designs at one point in time must be carried across deep time. To design in this manner, we would thus predict that evolution is dependent on biotic context, as it is this context that houses the design. In other words, if evolution was purely a function of random happenstance propagated only because such events happened to elicit greater fitness against the backdrop of haphazard environmental conditions, we would predict that the ability to design the future through the present would be quickly be swamped by noise. But if there is a strong, intrinsic component to evolution, the designs are buffered against such loss.
The non-teleological perspective tends to focus on the ‘natural selection’ component of evolution to explain form. Random variation is random variation, and it is selection that is supposed to impose the form on evolution (“the frozen accident”). While the teleologist can easily accomodate this perspective, he/she is also interested in the nature of this “random variation,” especially as it is not really random (apart from the “regard to fitness” mantra). If there is a form to this random variation, then we can draw from the biological/engineering criterion of the form-function relationship. And from there, it is not a big leap from function to design.