Open AccessSuppression of induction of SOS functions in an Escherichia coli tif-1 mutant by plasmid R100.1
Author(s) -
Michael Bagdasarian,
Richard D’Ari,
Witold Filipowicz,
Jacqueline George
Publication year - 1980
Publication title -
journal of bacteriology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.652
H-Index - 246
eISSN - 1067-8832
pISSN - 0021-9193
DOI - 10.1128/jb.141.2.464-469.1980
Subject(s) - lysogen , prophage , biology , escherichia coli , lambda phage , mutagenesis , plasmid , lysogenic cycle , mutant , microbiology and biotechnology , filamentation , mutation , gene , genetics , bacteriophage , physics , optics , laser
The tif-1 mutation in the recA gene of Escherichia coli caused, at 40 degrees C, lethal cell filamentation, induction of the recA protein, mutagenesis, and, in lambda lysogens, prophage induction. The presence of plasmid R100.1 in tif-1 strains suppressed tif-mediated cell filamentation and killing, recA protein induction, and prophage induction in lysogens. It also reduced mutagenesis in a tif-1 sfiA11(R100.1) strain. Plasmids F'lac, P1, and pMB9, in contrast, had little or no effect on tif-mediated induction of lambda. The presence of R100.1 did not inhibit the induction of the recA protein or of lambda by ultraviolet irradiation or mitomycin C treatment of tif-1(R100.1) or tif-1(lambda)(R100.1) strains.
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