Premium
Analysis of ssb mutations in vivo implicates SSB protein in two distinct pathways of SOS induction and in recombinational DNA repair
Author(s) -
Carlini Leslie E.,
Porter Ronald D.
Publication year - 1997
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.1997.3431694.x
Subject(s) - biology , sos response , dna repair , genetics , mutation , gene , escherichia coli , microbiology and biotechnology , dna damage , nucleotide excision repair , dna , dna mismatch repair
Site‐directed mutations in the Escherichia coli ssb gene were tested for the ability to complement a chromosomal ssb deletion for viability, and only the ssb W54→G mutation failed to do so at the pSC101 copy level. Non‐aromatic amino acid substitutions for SSB Trp‐54 ( ssb W54→L and ssb W54→S) produced the greatest effects on in vivo protein function including altered marker linkage subsequent to generalized transduction, extreme UV sensitivity, and a lack of ability to support SOS induction. Additionally, the ssb‐113 ( ssb P176→S) mutation demonstrated the existence of both uvrA ‐dependent and uvrA ‐independent components of SOS induction. Although nucleotide excision repair appeared unaffected by alterations in the SSB protein, the mutational analysis suggests a direct role for SSB in recombinational repair.