Structural inhibition and reactivation of Escherichia coli septation by elements of the SOS and TER pathways
Open Access
- 1 April 1987
- journal article
- research article
- Published by American Society for Microbiology in Journal of Bacteriology
- Vol. 169 (4) , 1772-1776
- https://doi.org/10.1128/jb.169.4.1772-1776.1987
Abstract
The inhibition of cell division caused by induction of the SOS pathway in Escherichia coli structurally blocks septation, as deduced from two sets of results. Potential septation sites active at the time of SOS induction became inactivated, while those initiated during the following doubling time were active. Penicillin resistance increased in wild-type UV light-irradiated cells, a behavior similar to that observed in mutants in which structural blocks were introduced by inactivation of FtsA. Potential septation sites that have been structurally blocked by either the SOS division inhibitor, furazlocillin inhibition of PBP3, or inactivation of a TER pathway component, FtsA3, could be reactivated one doubling time after removal of the inhibitory agent in the presence of an active lon gene product. Reactivation of potential septation sites blocked by the presence of an inactivated FtsA3 was significantly lower when the lon protease was not active, suggesting that Lon plays a role in the removal of inactivated TER pathway products from the blocked potential septation sites.This publication has 38 references indexed in Scilit:
- Identification, Mapping, Cloning and Characterization of a Gene (sbmA) Required for Microcin B17 Action on Escherichia coli K12Microbiology, 1986
- Overproduction of FtsZ induces minicell formation in E. coliCell, 1985
- The ftsA Gene Product: a Possible Connection between DNA Replication and Septation in Escherichia coliMicrobiology, 1985
- Two pathways of division inhibition in UV-irradiated E. coliMolecular Genetics and Genomics, 1983
- Protein degradation in Escherichia coli: the lon gene controls the stability of sulA protein.Proceedings of the National Academy of Sciences, 1983
- The SOS regulatory system of Escherichia coliCell, 1982
- The frequency of P1 transduction of the genes of Escherichia coli as a function of chromosomal position: Preferential transduction of the origin of replicationMolecular Genetics and Genomics, 1977
- Cell length, cell growth and cell divisionNature, 1976
- Bacterial Mutants Defective in Plasmid Formation: Requirement for the lon + AlleleProceedings of the National Academy of Sciences, 1971
- Radiation sensitivity in Escherichia coli some properties of the radiation-sensitive Hfr K12 mutant, PAM 401Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 1965