Monday, June 1, 2009

SOS and mobile DNA

I'm catching up on some back reading this afternoon, and this paper was really interesting:

Guerin et al. 2009. The SOS response controls integron recombination. Science 324:1034.

There's a lot I could say about this, but let me try to boil it down to this: I've long argued that God must have made organisms truly adaptable. Creating organisms in some fragile state in which inevitable mutations irreversibly degrade them is just incompetent design. God's better than that. One could also argue that the amount of speciation after the Flood is too great to attribute to some kind of random variation/selection/drift mechanism; those speciation changes were designed. Likewise, some of the differences exhibited between species of the same baramin are adaptive, suggesting that they were also designed and not random. Since the genomic changes within baramins are sometimes extensive, standard Mendelian scenarios advocated by some creationists are not adequate. Critters were designed to change, and I suspect that they may have a mechanism to detect environmental stress and to respond accordingly.

Two things you'll need to know to appreciate this paper by Guerin et al.: (1) Integrons are bacterial mobile genetic elements that contain useful genes (often antibiotic resistance genes). (2) SOS (pronounced like "sauce") is a system in bacteria for detecting and responding to stress. Guerin et al. found that the mobilization of some integons is activated by the SOS response. Guerin et al. wrote,
The SOS response can be induced by several stresses, thus ensuring that the reordering of existing cassettes [mobile genetic elements] and the acquisition of exogenous cassettes occur under conditions when innovations are needed.

When they're needed? Barbara McClintock would be pleased. I know I am.

For those creationists making claims about antibiotic resistance, read carefully the last paragraph of Guerin et al.'s paper:
Current policies in the fight against antibiotic resistance rely on the assumption that resistance mechanisms are costly to the bacteria that host them, which thus gives these bacteria a selective disadvantage and leads to their loss in the absence of antibiotic exposure. However, the incorporation of responsive regulation in integrons indicates that antibiotic resistance genes can be silenced at no biological cost until needed....

That pretty much speaks for itself.