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Life in protein‐rich environments: the relA ‐independent response of Streptococcus pyogenes to amino acid starvation
Author(s) -
Steiner Kerstin,
Malke Horst
Publication year - 2000
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.1365-2958.2000.02203.x
Subject(s) - biology , operon , response regulator , streptococcus pyogenes , downregulation and upregulation , amino acid , effector , mutant , psychological repression , regulation of gene expression , gene , stringent response , transcriptional regulation , gene expression , microbiology and biotechnology , biochemistry , genetics , bacteria , staphylococcus aureus
Considering that group A streptococci are multiple auxotrophs that may encounter shortage of amino acids during specific stages of the infectious process, we studied their adaptive response to amino acid deprivation. We found that, in addition to the (p)ppGpp‐mediated stringent response characterized previously, Streptococcus pyogenes exhibits a relA‐ independent response comprising transcriptional modulation of a specific subset of genes involved in pathogenesis. Genes/operons transcriptionally upregulated during starvation of both wild type and relA mutants included the two‐component signal transduction system covRS , the positive regulator ( ropB ) of the pyrogenic exotoxin B gene, speB , the oligopeptide ( opp ) and dipeptide ( dpp ) permease systems and the pepB gene putatively involved in the intracellular processing of oligopeptides. Upregulation of covRS was accompanied by downregulation of ska , one of the target genes of the negative CovR regulator, and the net effect of amino acid starvation also favoured repression of speB. A significant feature of upregulated opp expression was stimulated readthrough transcription of the operon‐internal oppA terminator, leading to increased mRNA levels for synthesis of the translocator complex relative to the substrate‐binding protein. Based on these and previous results, a stimulus–response network is proposed that counteracts the stringent response and may enable the pathogen to mount a dynamic response to the protein‐rich environment provided by its human host.