Overlapping functions for recF and priA in cell viability and UV‐inducible SOS expression are distinguished by dnaC809 in Escherichia coli K‐12

Overlapping functions for recF and priA in cell viability and UV‐inducible SOS expression are... The recF and priA genes have roles in DNA repair and homologous recombination. Mutations in these genes also cause decreases in cell viability and alterations in UV‐inducible sulAp–lacZ (SOS) expression. To find out if the two genes are in the same or different pathways for viability and SOS expression, the phenotypes of the double mutant strains were studied. The recF priA double mutant showed a lower viability and SOS expression level than either of the single mutants. In the case of cell viability, recF missense mutations decreased viability of a priA2::kan strain two to fivefold whereas recF null priA2::kan double mutants were not viable at all. dnaC809, a mutation that suppresses the UV‐sensitive (UVS) and Rec− phenotypes of priA2::kan, restored cell viability, but not UV‐inducible SOS expression, to a priA recF strain. Since recF is epistatic with recO and recR (recOR) for UV resistance, recOR mutations were also tested with priA2::kan. No overlap was found between recOR and priA for viability and SOS expression. It is concluded that priA and recF have two different overlapping functions in viability and SOS expression that are distinguishable by the effects of dnaC809. The role of recF in a priA2::kan strain in cell viability is a new function for recF and unlike recF 's other roles in DNA repair and recombination, is independent of recOR. A new role for priA in UV‐inducible SOS expression in a recF mutant is also defined. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Molecular Microbiology Wiley

Overlapping functions for recF and priA in cell viability and UV‐inducible SOS expression are distinguished by dnaC809 in Escherichia coli K‐12

Molecular Microbiology, Volume 19 (4) – Feb 1, 1996

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Publisher
Wiley
Copyright
Blackwell Science Ltd, Oxford
ISSN
0950-382X
eISSN
1365-2958
D.O.I.
10.1046/j.1365-2958.1996.429959.x
Publisher site
See Article on Publisher Site

Abstract

The recF and priA genes have roles in DNA repair and homologous recombination. Mutations in these genes also cause decreases in cell viability and alterations in UV‐inducible sulAp–lacZ (SOS) expression. To find out if the two genes are in the same or different pathways for viability and SOS expression, the phenotypes of the double mutant strains were studied. The recF priA double mutant showed a lower viability and SOS expression level than either of the single mutants. In the case of cell viability, recF missense mutations decreased viability of a priA2::kan strain two to fivefold whereas recF null priA2::kan double mutants were not viable at all. dnaC809, a mutation that suppresses the UV‐sensitive (UVS) and Rec− phenotypes of priA2::kan, restored cell viability, but not UV‐inducible SOS expression, to a priA recF strain. Since recF is epistatic with recO and recR (recOR) for UV resistance, recOR mutations were also tested with priA2::kan. No overlap was found between recOR and priA for viability and SOS expression. It is concluded that priA and recF have two different overlapping functions in viability and SOS expression that are distinguishable by the effects of dnaC809. The role of recF in a priA2::kan strain in cell viability is a new function for recF and unlike recF 's other roles in DNA repair and recombination, is independent of recOR. A new role for priA in UV‐inducible SOS expression in a recF mutant is also defined.

Journal

Molecular MicrobiologyWiley

Published: Feb 1, 1996

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