Disease relevance of ssrA

• Excision and loss of the cryptic prophage apparently allow expression of the Alp protease by inactivating a small stable RNA (10Sa RNA) encoded by the ssrA gene [1].
• In E. coli, the adaptor SspB tethers ssrA-tagged substrates to the ClpXP protease, causing a modest increase in their rate of degradation [2].
• The PAI is 39.5 kb in size, has low %G+C (35%), contains putative integrase and transposase genes, is flanked by att sites, and inserts near a 10Sa RNA gene (ssrA), suggesting it may be of bacteriophage origin [3].

High impact information on ssrA

• Although A-site-cleaved mRNAs were not detected, tmRNA-mediated ssrA tagging after SecM glycine 165 was observed [4].
• Indeed, compensatory overexpression of tRNA(2)(Pro) readily inhibits ssrA tagging after glycine 165, but has no effect on the duration of SecM ribosome arrest [4].
• Inactivation of ssrA by insertional mutagenesis is sufficient to allow expression of the suppressing Alp protease, even in the presence of the cryptic prophage [1].
• Finally, the internalization involved a FimH-dependent process but did not require sipB, a gene essential for Salmonella-mediated invasion of mammalian epithelial cells [5].
• Conversely, a null mutation in ssrA enhances the temperature-sensitive phenotype of the pth(ts) strain [6].

References