Premium
Mutational analysis of glucose transport regulation and glucose‐mediated virulence gene repression in Listeria monocytogenes
Author(s) -
Aké Francine M. D.,
Joyet Philippe,
Deutscher Josef,
Milohanic Eliane
Publication year - 2011
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 - 10.1111/j.1365-2958.2011.07692.x
Subject(s) - pep group translocation , derepression , glucose transporter , operon , biology , mutant , glut3 , snf3 , phosphotransferase , phosphoenolpyruvate carboxykinase , biochemistry , listeria monocytogenes , permease , virulence , complementation , catabolite repression , repressor , mannose , gene , glut1 , gene expression , psychological repression , genetics , bacteria , endocrinology , saccharomyces cerevisiae , insulin
Summary Listeria monocytogenes transports glucose/mannose via non‐PTS permeases and phosphoenolpyruvate:carbohydrate phosphotransferase systems (PTS). Two mannose class PTS are encoded by the constitutively expressed mpoABCD and the inducible manLMN operons. The man operon encodes the main glucose transporter because manL or manM deletion significantly slows glucose utilization, whereas mpoA deletion has no effect. The PTS Mpo mainly functions as a constitutively synthesized glucose sensor controlling man operon expression by phosphorylating and interacting with ManR, a LevR‐like transcription activator. EIIB Mpo plays a dual role in ManR regulation: P∼EIIB Mpo prevailing in the absence of glucose phosphorylates and thereby inhibits ManR activity, whereas unphosphorylated EIIB Mpo prevailing during glucose uptake is needed to render ManR active. In contrast to mpoA , deletion of mpoB therefore strongly inhibits man operon expression and glucose consumption. A Δ ptsI (EI) mutant consumes glucose at an even slower rate probably via GlcU‐like non‐PTS transporters. Interestingly, deletion of ptsI , manL , manM or mpoB causes elevated PrfA‐mediated virulence gene expression. The PTS Man is the major player in glucose‐mediated PrfA inhibition because the Δ mpoA mutant showed normal PrfA activity. The four mutants showing PrfA derepression contain no or only little unphosphorylated EIIAB Man (ManL), which probably plays a central role in glucose‐mediated PrfA regulation.