Open AccessInvolvement of the activated form of RecA protein in SOS mutagenesis and stable DNA replication in Escherichia coli.
Author(s) -
Evelyn M. Witkin,
Tokio Kogoma
Publication year - 1984
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.81.23.7539
Subject(s) - repressor lexa , sos response , repressor , biology , dna replication , regulon , mutagenesis , dna , microbiology and biotechnology , gene , dna damage , escherichia coli , genetics , mutation , gene expression
DNA damage activates RecA protein of E. coli to a form (RecA*) that promotes proteolytic cleavage of LexA protein, the repressor of at least 17 DNA damage-inducible genes, resulting in expression of the SOS response. In addition to this known role, RecA* performs another function necessary for expression of SOS mutagenesis [Blanco, M., Herrera, G., Collado, P., Rebollo, J. & Botella, L. M. (1982) Biochimie 64, 633-636]. The additional role of RecA* could be (i) cleavage of another repressor, (ii) proteolytic processing of one or more proteins, or (iii) mechanistic interaction with DNA or with one or more other proteins. We describe experiments designed to test the first possibility. Our results suggest that neither SOS mutator activity nor ultraviolet mutagenesis requires induction by RecA* of any gene(s) outside the LexA regulon and that the additional role of RecA* is not cleavage of another repressor. We show that stable DNA replication, another DNA damage-inducible function [Kogoma, T., Torrey, T. A. & Connaughton, M. J. (1979) Mol. Gen. Genet. 176, 1-9], shares with SOS mutagenesis the requirement for RecA* activity, even in a strain constitutively expressing all LexA-controlled genes. In this strain, conditions that activate RecA initiate expression of stable DNA replication in the presence of chloramphenicol, without an intervening period of protein synthesis. We conclude that the additional function of RecA* in stable DNA replication is not another antirepressor activity.