Abstract
Deinococcus bacteria are extremely resistant to radiation and able to repair a shattered genome in an essentially error-free manner after exposure to high doses of radiation or prolonged desiccation. An efficient, SOS-independent response mechanism to induce various DNA repair genes such as recA is essential for radiation resistance. This pathway, called radiation/desiccation response, is controlled by metallopeptidase IrrE and repressor DdrO that are highly conserved in Deinococcus. Among various Deinococcus species, Deinococcus radiodurans has been studied most extensively. Its genome encodes classical DNA repair proteins for error-free repair but no error-prone translesion DNA polymerases, which may suggest that absence of mutagenic lesion bypass is crucial for error-free repair of massive DNA damage. However, many other radiation-resistant Deinococcus species do possess translesion polymerases, and radiation-induced mutagenesis has been demonstrated. At least dozens of Deinococcus species contain a mutagenesis cassette, and some even two cassettes, encoding error-prone translesion polymerase DnaE2 and two other proteins, ImuY and ImuB-C, that are probable accessory factors required for DnaE2 activity. Expression of this mutagenesis cassette is under control of the SOS regulators RecA and LexA. In this paper, we review both the RecA/LexA-controlled mutagenesis and the IrrE/DdrO-controlled radiation/desiccation response in Deinococcus.
Highlights
Deinococcus bacteria are famous for their extreme resistance to high doses of ionizing radiation and other oxidative stress- and DNA damage-inducing conditions such as desiccation, and for their capacity to repair massive DNA damage including hundreds of double-strand breaks [1,2,3,4,5,6,7]
The radiation/desiccation response mechanism to induce these genes is essential for radiation resistance, because mutations abolishing this response are extremely sensitive to radiation [22,23,24,25]
Many years of studies with the model bacterium E. coli has provided a wealth of insight in many cellular processes including the SOS response
Summary
Deinococcus bacteria are famous for their extreme resistance to high doses of ionizing radiation and other oxidative stress- and DNA damage-inducing conditions such as desiccation, and for their capacity to repair massive DNA damage including hundreds of double-strand breaks [1,2,3,4,5,6,7]. In Deinococcus, induction of recA and other DNA repair genes occurs in an SOS-independent manner and is under control of two proteins called IrrE and DdrO [28]. The SOS regulon in E. coli comprises about 40 genes, encoding, amongst others, DNA repair proteins involved in homologous recombination (e.g., RecA), nucleotide excision repair (e.g., UvrA) and error-prone DNA translesion synthesis (DNA polymerases Pol II, Pol IV and Pol V). The SOS response is known for induction of DNA repair genes and SOS mutagenesis, SOS-induced dormancy (mediated by the toxin of one or more toxin-antitoxin systems) as well as LexA-regulated programmed cell death have been described in some bacteria [27,31,38,39,40]
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