Responses of hyperthermophilic crenarchaea to UV irradiation
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Background: DNA damage leads to cellular responses that include the increased expression of DNA repair genes, repression of DNA replication and alterations in cellular metabolism. Archaeal information processing pathways resemble those in eukaryotes, but archaeal damage response pathways remain poorly understood. Results: We analyzed the transcriptional response to UV irradiation in two related crenarchaea, Sulfolobus solfataricus and Sulfolobus acidocaldarius. Sulfolobus species encounter high levels of DNA damage in nature, as they inhabit high temperature, aerobic environments and are exposed to sunlight. No increase in expression of DNA repair genes following UV irradiation was observed. There was, however, a clear transcriptional response, including repression of DNA replication and chromatin proteins. Differential effects on the expression of the three transcription factor B ( tfb) genes hint at a mechanism for the modulation of transcriptional patterns in response to DNA damage. TFB3, which is strongly induced following UV irradiation, competes with TFB1 for binding to RNA polymerase in vitro, and may act as a repressor of transcription or an alternative transcription factor for certain promoters. Conclusion: A clear response to DNA damage was observed, with down-regulation of the DNA replication machinery, changes in transcriptional regulatory proteins, and up-regulation of the biosynthetic enzymes for beta-carotene, which has UV protective properties, and proteins that detoxify reactive oxygen species. However, unlike eukaryotes and bacteria, there was no induction of DNA repair proteins in response to DNA damage, probably because these are expressed constitutively to deal with increased damage arising due to high growth temperatures.
Gotz , D , Paytubi , S , Munro , S , Lundgren , M , Bernander , R & White , M F 2007 , ' Responses of hyperthermophilic crenarchaea to UV irradiation ' Genome Biology , vol 8 , no. 10 , pp. R220 . , 10.1186/gb-2007-8-10-r220
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This work was supported by a dedicated functional genomics grant from the Swedish Research Council and the Swedish Graduate Research School in Genomics and Bioinformatics to RB, and by grants from the Wellcome Trust and BBSRC to MFW.
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