Abstract
BackgroundRepairing DNA damage begins with its detection and is often followed by elicitation of a cellular response. In E. coli, RecA polymerizes on ssDNA produced after DNA damage and induces the SOS Response. The RecA-DNA filament is an allosteric effector of LexA auto-proteolysis. LexA is the repressor of the SOS Response. Not all RecA-DNA filaments, however, lead to an SOS Response. Certain recA mutants express the SOS Response (recAC) in the absence of external DNA damage in log phase cells.Methodology/Principal FindingsGenetic analysis of two recAC mutants was used to determine the mechanism of constitutive SOS (SOSC) expression in a population of log phase cells using fluorescence of single cells carrying an SOS reporter system (sulAp-gfp). SOSC expression in recA4142 mutants was dependent on its initial level of transcription, recBCD, recFOR, recX, dinI, xthA and the type of medium in which the cells were grown. SOSC expression in recA730 mutants was affected by none of the mutations or conditions tested above.Conclusions/SignificanceIt is concluded that not all recAC alleles cause SOSC expression by the same mechanism. It is hypothesized that RecA4142 is loaded on to a double-strand end of DNA and that the RecA filament is stabilized by the presence of DinI and destabilized by RecX. RecFOR regulate the activity of RecX to destabilize the RecA filament. RecA730 causes SOSC expression by binding to ssDNA in a mechanism yet to be determined.
Highlights
Maintenance of genetic information is a priority for all organisms
All strains used in this study have the sulB103 allele that suppresses SOS cell division inhibition [29]
It has been known that the formation of a RecA-DNA filament is crucial to sensing DNA damage inflicted by externally added DNA damaging agents (i.e., UV irradiation or mitomycin C) and initiating the SOS Response
Summary
The RAD51-RecA family of proteins plays a critical role in the repair of DNA through the production of a proteinDNA helical filament [1]. In E. coli, RecA links these processes by its ability to detect and bind single-stranded DNA (ssDNA) produced by DNA damage to form a RecA-DNA helical filament. This structure transduces the information that DNA damage exists in the cell by increasing the rate of LexA auto-proteolysis [13]. Testing the single recX mutant in minimal medium above, showed no effect As indicated, this was expected since the ability to detect a recX-dependent change in the number of RecA filaments was dependent on rich medium [47]. Certain recA mutants express the SOS Response (recAC) in the absence of external DNA damage in log phase cells
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