Premium
Emergency derepression: stringency allows RNA polymerase to override negative control by an active repressor
Author(s) -
Kvint Kristian,
Hosbond Carsten,
Farewell Anne,
Nybroe Ole,
Nyström Thomas
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.1365-2958.2000.01714.x
Subject(s) - derepression , repressor , psychological repression , biology , rna polymerase , guanosine , sigma factor , enzyme repression , gene , rna , microbiology and biotechnology , genetics , gene expression
The uspA promoter, driving production of the universal stress protein A in response to diverse stresses, is demonstrated to be under dual control. One regulatory pathway involves activation of the promoter by the alarmone guanosine 3′,5′‐bisphosphate, via the β‐subunit of RNA polymerase, whereas the other consists of negative control by the FadR repressor. In contrast to canonical dual control by activation and repression circuits, which depends on concomitant activation and derepression for induction to occur, the ppGpp‐dependent activation of the uspA promoter overrides repression by an active FadR under conditions of severe cellular stress (starvation). The ability of RNA polymerase to overcome repression during stringency depends, in part, on the strength of the FadR operator. This emergency derepression is operative on other FadR‐regulated genes induced by starvation and is argued to be an essential regulatory mechanism operating during severe stress.