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Expression of the phosphotransferase system both mediates and is mediated by Mlc regulation in Escherichia coli
Author(s) -
Plumbridge Jacqueline
Publication year - 1999
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.1365-2958.1999.01462.x
Subject(s) - pep group translocation , biology , operon , glucose transporter , mutation , regulator , gene , regulation of gene expression , phosphotransferase , transcriptional regulation , transporter , biochemistry , escherichia coli , psychological repression , gene expression , microbiology and biotechnology , insulin , endocrinology
The ptsHIcrr operon encodes the cytoplasmic components of the phosphotransferase system (PTS). It is expressed from two major promoters, of which the upstream promoter has previously been shown to be induced by glucose and to be dependent upon cAMP/CAP. This promoter is now shown to be repressed by Mlc. Mlc is a transcriptional regulator controlling, among others, the gene ptsG , encoding EIICB Glc , the glucose‐specific transporter of the PTS. Transcription of ptsH p0 and ptsG are subject to the same regulatory pattern. In addition to induction by glucose and repression by Mlc, mutations in ptsHIcrr , which interrupt the PEP‐dependent phosphate transfer through the soluble components of the PTS, lead to high expression of both ptsH and ptsG , while mutations inactivating EIIBC Glc are non‐inducible. Mutations in mlc lead to high constitutive expression and are dominant, implying that Mlc is the ultimate regulator of ptsHI and ptsG expression. Growth on other PTS sugars, besides glucose, also induces ptsH and ptsG expression, suggesting that the target of Mlc regulation is the PTS. However, induction by these other sugars is only observed in the presence of ptsG + , thus confirming the importance of glucose and EIICB Glc in the regulation of the PTS. The ptsG22 mutation, although negative for glucose transport, shows a weak positive regulatory phenotype. The mutation has been sequenced and its effect on regulation investigated.