HOW DO HYPERTHERMOPHILIC ARCHAEA RESPOND TO DNA DAMAGE?

Measuring the effects of DNA damage provides basic information on the repair capabilities of micro-organisms. For example, survival curves (below, left) show that short-wave UV kills S. acidocaldarius with only about 2-fold greater efficiency than it kills E. coli. This provides evidence that S. acidocaldarius has reasonably high capacity for repairing UV photoproducts in the dark [publication 5].  Other experiments (below, right) show that S. acidocaldarius also has another way to repair UV-induced damage, namely photoreversal. When UV-treated cells are illuminated with white light, viability is restored in a dose-dependent manner, demonstrating the activity of a DNA photolyase [publication 3].  [For more genetic research on Sulfolobus, go here]

              (Sulfolobus strains vs.  E. coli strains)                                 (Illuminated Sulfolobus cells)

In addition to killing cells and inducing mutations, UV increases the formation of Sulfolobus recombinants by a conjugational mechanism. The yield of recombinants increases approximately exponentially with UV dose (graphs below) [publication 5].

The stimulatory effect on DNA transfer and recombination is transient, however. Incubation of the cells at physiological temperature after UV but before mating caused a rapid decay in the corresponding yield of recombinants (below). The properties of this decay are consistent with the formation of recombinogenic lesions from the initial UV photoproducts, and the subsequent enzymatic repair of those lesions in vivo [publication 10].

                Hours of Incubation before Mating

Finally, the genetic consequences of UV irradiation (mutation and recombination) are also observed with other agents that damage DNA in different ways. Gamma rays, chemicals that induce strand breaks, and chemicals that induce cross-links revealed some quantitative differences, but all were effective (graphs below). These results suggest that diverse DNA lesions manifest themselves in a few common genetic responses [see publication 15].