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DdrO is an essential protein that regulates the radiation desiccation response and the apoptotic‐like cell death in the radioresistant D einococcus radiodurans bacterium
Author(s) -
Devigne Alice,
Ithurbide Solenne,
Bouthier de la Tour Claire,
Passot Fanny,
Mathieu Martine,
Sommer Suzanne,
Servant Pascale
Publication year - 2015
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.12991
Subject(s) - biology , regulon , dna damage , gene , deinococcus radiodurans , dna repair , repressor , repressor lexa , microbiology and biotechnology , genetics , sos response , programmed cell death , deinococcus , radioresistance , dna fragmentation , apoptosis , mutant , dna , gene expression , cell culture
Summary D einococcus radiodurans is known for its extreme radioresistance. Comparative genomics identified a radiation‐desiccation response ( RDR ) regulon comprising genes that are highly induced after DNA damage and containing a conserved motif ( RDRM ) upstream of their coding region. We demonstrated that the RDRM sequence is involved in cis ‐regulation of the RDR gene ddrB in vivo . Using a transposon mutagenesis approach, we showed that, in addition to ddrO encoding a predicted RDR repressor and irrE encoding a positive regulator recently shown to cleave DdrO in D einococcus deserti , two genes encoding α‐keto‐glutarate dehydrogenase subunits are involved in ddrB regulation. In wild‐type cells, the DdrO cell concentration decreased transiently in an IrrE ‐dependent manner at early times after irradiation. Using a conditional gene inactivation system, we showed that DdrO depletion enhanced expression of three RDR proteins, consistent with the hypothesis that DdrO acts as a repressor of the RDR regulon. DdrO ‐depleted cells loose viability and showed morphological changes evocative of an apoptotic‐like response, including membrane blebbing, defects in cell division and DNA fragmentation. We propose that DNA repair and apoptotic‐like death might be two responses mediated by the same regulators, IrrE and DdrO , but differently activated depending on the persistence of IrrE ‐dependent DdrO cleavage.