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Characterization of RAT, an autolysis regulator in Staphylococcus aureus
Author(s) -
Ingavale S. S.,
Van Wamel W.,
Cheung A. L.
Publication year - 2003
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.1365-2958.2003.03503.x
Subject(s) - biology , autolysis (biology) , mutant , autolysin , transposable element , gene , regulator , open reading frame , microbiology and biotechnology , repressor , regulator gene , gene product , genetics , regulation of gene expression , peptide sequence , gene expression , biochemistry , enzyme
Summary In trying to identify genetic loci involved in the regulation of cap5 genes in Staphylococcus aureus , we isolated a transposon mutant that exhibited a growth defect, enhanced autolysis and increased sensitivity to Triton X‐100 and penicillin, attributable in part to increased murein hydrolase activity. Analysis of the chromosomal sequence flanking the transposon insertion site revealed that the gene disrupted in the mutant encodes an open reading frame of 147 amino acids. We named this gene rat , which stands for regulator of autolytic activity. Sequence analysis indicated that Rat is homologous to the MarR and, to a lesser extent, the SarA protein families. Mutations in rat resulted in decreased expression of known autolytic regulators lytSR , lrgAB and arlRS . Gel shift studies indicated that Rat binds to the lytRS and arlRS promoters, thus confirming Rat as a DNA‐binding protein to these known repressors of autolytic activity. As anticipated, rat appears to be a negative regulator of autolysin genes including lytM and lytN . These data suggest that the rat gene product is an important regulator of autolytic activity in S. aureus .