2010
DOI: 10.1128/jb.01489-09
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The Pneumococcal Cell Envelope Stress-Sensing System LiaFSR Is Activated by Murein Hydrolases and Lipid II-Interacting Antibiotics

Abstract: In the Firmicutes, two-component regulatory systems of the LiaSR type sense and orchestrate the response to various agents that perturb cell envelope functions, in particular lipid II cycle inhibitors. In the current study, we found that the corresponding system in Streptococcus pneumoniae displays similar properties but, in addition, responds to cell envelope stress elicited by murein hydrolases. During competence for genetic transformation, pneumococci attack and lyse noncompetent siblings present in the sam… Show more

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Cited by 54 publications
(93 citation statements)
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“…Homologs of the liaIH operon are absent in all Firmicutes cocci, indicating a functional diversification between the two groups of LiaFSRlike systems. These functional differences are also supported by the LiaR binding site of the Bacillus/Listeria group, which differs significantly from the consensus sequence determined for the Firmicutes cocci (16).…”
mentioning
confidence: 64%
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“…Homologs of the liaIH operon are absent in all Firmicutes cocci, indicating a functional diversification between the two groups of LiaFSRlike systems. These functional differences are also supported by the LiaR binding site of the Bacillus/Listeria group, which differs significantly from the consensus sequence determined for the Firmicutes cocci (16).…”
mentioning
confidence: 64%
“…2A and D). While the four core residues at the ends of the two repeats are conserved (boldface), only two more residues fit to the position weight matrix (capital letters) (16), and no additional complementary bases could be detected. To exactly map the LiaR binding site upstream of ydhE, two additional fragments (Ϫ74 and Ϫ71) were cloned and corresponding reporter strains (TMB676 and TMB769) constructed, and ␤-galactosidase activities were measured in the liaF mutant background.…”
Section: Resultsmentioning
confidence: 99%
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“…Disruption of this system in S. mutans led to augmented sensitivity to antibiotics interfering with lipid II cycling (442). A system homologous to LiaFSR has also been characterized for S. pneumoniae, in which it was shown to control the expression of at least 19 genes involved in protecting cells against murein hydrolases and lipid II-interacting antibiotics (449). In S. agalactiae, this system controls not only cell wall stress-related responses but also pilus expression and genes involved in the defense against host antimicrobial systems (440).…”
Section: Mechanosensitive Channelsmentioning
confidence: 99%