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Enterococcus faecalis MalR acts as a repressor of the maltose operons and additionally mediates their catabolite repression via direct interaction with seryl‐phosphorylated‐HPr
Author(s) -
Grand Maxime,
Blancato Victor Sebastián,
Espariz Martín,
Deutscher Josef,
Pikis Andreas,
Hartke Axel,
Magni Christian,
Sauvageot Nicolas
Publication year - 2020
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.14431
Subject(s) - catabolite repression , repressor , biology , operon , lac repressor , enterococcus faecalis , ccpa , microbiology and biotechnology , biochemistry , gene , transcription factor , escherichia coli , mutant
Abstract Enterococci are gram‐positive pathogens and lead to cause hospital‐acquired infections worldwide. Central carbon metabolism was shown as highly induced in Enterococcus faecalis during infection context. Metabolism of α‐polysaccharides was previously described as an important factor for host colonisation and biofilm formation. A better characterisation of the adaptation of this bacterium to carbohydrate availabilities may lead to a better understanding of the link between carbohydrate metabolism and the infection process of E. faecalis . Here we show that MalR, a LacI/GalR transcriptional regulator, is the main factor in the regulation of the two divergent operons involved in maltose metabolism in this bacterium. The malR gene is transcribed from the malP promoter, but also from an internal promoter inside the gene located upstream of malR . In the absence of maltose, MalR acts as a repressor and in the presence of glucose, it exerts efficient CcpA‐independent carbon catabolite repression. The central PTS protein P‐Ser‐HPr interacts directly with MalR and enhances its DNA binding capacity, which allows E. faecalis to adapt its metabolism to environmental conditions.