In vivo role of Escherichia coli single-strand exonucleases in SOS induction by gamma radiation

Abstract

Ionizing radiation causes different types of genetic damage, ranging from base modifications to single- and double-stranded DNA breaks, which may be deleterious or even lethal to the cell. There are different repair or tolerance mechanisms to counteract the damage. Among them is the Escherichia coli SOS system: a set of genes that becomes activated upon DNA damage to confer better opportunities for cell survival. However, since this response is triggered by single-stranded DNA regions, most lesions have to be processed or modified prior to SOS activation. Several genes such as recO, recB and recJ that seem to be required to induce the response have already been reported. The results of this work indicate that the four known E.coli single-strand exonucleases take part in processing gamma radiation damage, though RecJ and ExoI proved to be more important than ExoVII or ExoX. In addition, ExoV as well as glycosylases such as Nth and, to a lesser extent, Fpg are also required. A model intended to explain the role of all these genes in damage processing is presented.

The DNA Exonucleases of Escherichia coli

“…RecJ plays a redundant role with other single-strand DNA exonucleases for UV survival, particularly with fellow 5′ to 3′ ssdNA exonuclease ExoVII (248, 261). Either RecJ or ExoI are required to process lesions produced by gamma-irradiation to activate the regulatory SOS response to DNA damage (220). RecJ is also implicated, along with the other ssDNA exonucleases, in avoidance of a number of genetic rearrangements and recombination between short homologies.…”

Chromosome Segregation and Cell Division Defects in Escherichia coli Recombination Mutants Exposed to Different DNA-Damaging Treatments

“…Indeed, expression of the sulA gene in cells in which DNA has been damaged by I- Sce I nuclease is completely dependent on the RecBCD enzyme [ 36 ], while in cells exposed to UV radiation, maximal expression of the sulA gene depends dominantly on the RecFOR complex [ 48 ]. A mixed situation is present in γ-irradiated cells where both recombination pathways contribute significantly to the induction of the SOS response [ 49 ].…”

“…In γ-irradiated cells, some DSBs may arise when replication fork encounters a site of ongoing base excision repair or an unsealed ssDNA break. Some ssDNA breaks could be widened by ssExos into SSGs that could also cause collapse of the replication forks [ 49 ].…”

“…As mentioned above, in γ-irradiated cells, the induction of the SOS response depends on both RecA loading systems [ 49 ]. Therefore, a certain degree of SOS (SulA)-dependent filamentation can be expected in recB or recO single mutants after γ-irradiation, which is in agreement with our results ( Table 3 and Figure 7 , Figure 8 , Figure 9 and Figure 11 ).…”

Structural insights into the duplex DNA processing of TREX2

“…DEDDh exonucleases can be classified based on the in vitro activity assays (substrate preference) and the structural characteristic in binding to duplex DNA (the interaction to non-scissile strand of duplex DNA and the length requirement of double-stranded region). PARN, poly(A)-specific ribonuclease (43,45); ISG20, Interferon-stimulated gene 20-kDa protein (46); Exo I, Escherichia coli Exonuclease I (44,47); NP exonuclease, Lassa Virus NP Exonuclease (49,50); 3′hExo, human 3′-5′ exonuclease, also known as Eri-1 (18,51); Exo X, E. coli exonuclease X (22,39,52,53).…”