UV Stimulation of Chromosomal Marker Exchange in Sulfolobus acidocaldarius: Implications for DNA Repair, Conjugation and Homologous Recombination at Extremely High Temperatures

Abstract

The hyperthermophilic archaeon Sulfolobus acidocaldarius exchanges and recombines chromosomal markers by a conjugational mechanism, and the overall yield of recombinants is greatly increased by previous exposure to UV light. This stimulation was studied in an effort to clarify its mechanism and that of marker exchange itself. A variety of experiments failed to identify a significant effect of UV irradiation on the frequency of cell pairing, indicating that subsequent steps are primarily affected, i.e., transfer of DNA between cells or homologous recombination. The UV-induced stimulation decayed rather quickly in parental cells during preincubation at 75°, and the rate of decay depended on the incubation temperature. Preincubation at 75° decreased the yield of recombinants neither from unirradiated parental cells nor from parental suspensions subsequently irradiated. We interpret these results as evidence that marker exchange is stimulated by recombinogenic DNA lesions formed as intermediates in the process of repairing UV photoproducts in the S. acidocaldarius chromosome.

Horizontal Gene Transfer in Archaea—From Mechanisms to Genome Evolution

“…In both cases, other possible explanations, such as transduction by virus particles, cross-feeding, and genetic complementation by way of diploid heterozygous cell formation, were ruled out and in both cases cell-cell contact, including actual cell aggregation, was visible. Shortly after these observations it was noted that exposure to UV radiation greatly increases DNA exchange (117,155).…”

Integrated conjugative plasmid drives high frequency chromosomal gene transfer in Sulfolobus islandicus

“…Further work showed that selected marker transfer occurs in small discontinuous patches that are dependent on minimal homology ( Hansen et al, 2005 ). In most studies, ME is up-regulated with DNA damaging agent exposure leading to the current hypothesis that ME is a mechanism for DNA repair ( Schmidt et al, 1999 ; Ajon et al, 2011 ; van Wolferen et al, 2015 , 2016 , 2020 ; Feng et al, 2018 ; Schult et al, 2018 ; Sun et al, 2018 ). It has been experimentally shown that in Sulfolobus acidocaldarius , exposure to DNA damaging agents results in induced type IV pilin-mediated cell aggregation ( van Wolferen et al, 2016 ; Sun et al, 2018 ).…”