Monday, November 14, 2005
DNA Polymerase for Genetic Change
- Escherichia coli DNA Polymerase IV Mutator Activity: Genetic Requirements and Mutational Specificity by Wagner and Nohmi.
- General Stress Response Regulator RpoS in Adaptive Mutation and Amplification in Escherichia coli by Lombardo, Aponyi, and Rosenberg.
These are both fascinating articles. What they are showing is that, in stress situations, E. Coli is actively modifying its genome on a specific plasmid. This means that the cell can (a) sense trouble, and (b) activate specific change mechanisms to accomplish changes. It has a high degree of specificity as to both the activation of the mutations as well as where the mutations occur. This is natural genetic engineering at work.
As per the creation model, the cell is not a passive bystander of happenstance changes and "hoping for the best", but is in control of the changes that occur.
Basically, what these articles are saying is that a specific stress response factor, called RpoS, is produced when E. Coli cells are in trouble. This causes the cell to switch from using its standard DNA Polymerase (the enzyme which copies the DNA) to using a new type called DNA Polymerase IV (or DNA PolIV for short) when copying a specific plasmid. This polymerase is used to induce mutations within the strand -- both point mutations and frame-shifts.
Note that while this may seem like random mutation it is in fact not -- it includes random factors, but is not entirely random. It seems to be a non-deterministic computation (i.e. - randomized within specified limits). This information shows that the cell acts as a "database administrator" over its genome, and can induce changes when needed, in the specific place that they are needed.
Note that the authors of the articles are very likely not creationists, though their data is very interesting and beneficial to creationists and others who use a telic approach to biology.
UPDATE: Upon closer reading of the second article, it seems that the authors do not feel that the mutation is directed, just a rate increase. The only reason for suspecting this listed in the article itself is that there were mutations on other genes. However, I don't see how that means that the mutation rate was globally changed. I think perhaps they are excluding the possibility of adaptive mutagenesis too early, based on data that is not necessarily in conflict with the idea. Rosenberg herself seems to be trying to push the hypermutation model past the adaptive mutation model, but I don't think the data supports that conclusion (see also here). It seems that their requirement for being "adaptive mutations" is that the mutation must be in exactly one gene. This is an absurd requirement. There is no reason that adaptive mutagenesis cannot be applied to a _set_ of genes. In fact, the F plasmid would be perfect for this to occur, as the plasmid does not even need to exist for the cell to function under normal circumstances.