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The orphan regulator ReiD of S almonella enterica is essential for myo ‐inositol utilization
Author(s) -
Rothhardt Johannes E.,
Kröger Carsten,
Broadley Steven P.,
Fuchs Thilo M.
Publication year - 2014
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/mmi.12788
Subject(s) - biology , regulon , regulator , repressor , mutant , promoter , transcription (linguistics) , transcription factor , gene , genetics , microbiology and biotechnology , gene expression , linguistics , philosophy
Summary In S almonella enterica serovar T yphimurium ( S . T yphimurium), the genomic island GEI 4417/4436 is responsible for the utilization of myo ‐inositol ( MI ) as carbon and energy source. Here, we report the characterization of a novel, island‐encoded positive autoregulator termed ReiD ( STM 4423) that is specific to certain S . enterica strains and E scherichia coli strain ED 1a able to use MI . ReiD was essential for growth with this polyol and also contributed to S . T yphimurium proliferation in swine caecum content. Providing higher copy numbers of ReiD reduced the long lag phase of 2 days during growth of S . T yphimurium in MI medium by 50%. In a heterologous host, expression of ReiD activated the transcription from the promoter of iolE / iolG , whose products catalyse the initial two steps in MI degradation. Episomal expression of iolE / iolG1 rescued the otherwise zero growth phenotype of a reiD deletion mutant in MI medium. Gel mobility shift assays with purified ReiD demonstrated directed interaction of ReiD with its own promoter and that of iolE . The repressor IolR bound the reiD promoter, implying that reiD is part of the IolR regulon. Taken together, the regulator ReiD is a trigger to accelerate the switch from more easily accessible nutrients to MI utilization by S . T yphimurium.