Analysis of ssb mutations in vivo implicates SSB protein in two distinct pathways of SOS induction and in recombinational DNA 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.
Carlini
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Department of Biochemistry and Molecular Biology, Pennsylvania State University, University Park 16802, USA.
Porter
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D017101:Bacteriophage P1 / Q000378:metabolism; D003001:Cloning, Molecular; D003227:Conjugation, Genetic; D004260:DNA Repair; D004268:DNA-Binding Proteins / Q000235:genetics*; D005816:Genetic Complementation Test; D007763:Lac Operon; D016297:Mutagenesis, Site-Directed; D011938:Rec A Recombinases / Q000235:genetics; D011995:Recombination, Genetic; D013014:SOS Response, Genetics; D013696:Temperature; D014161:Transduction, Genetic; D014466:Ultraviolet Rays
D004268:DNA-Binding Proteins; D011938:Rec A Recombinases