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Interplay between three global regulatory proteins mediates oxygen regulation of the Escherichia coli cytochrome d oxidase ( cydAB ) operon
Author(s) -
Govantes Fernando,
Orjalo Arturo V.,
Gunsalus Robert P.
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.1365-2958.2000.02215.x
Subject(s) - operon , biology , psychological repression , repressor , promoter , transcription (linguistics) , escherichia coli , oxidase test , regulation of gene expression , gene , microbiology and biotechnology , transcription factor , gene expression , biochemistry , enzyme , linguistics , philosophy
The Escherichia coli cydAB operon, encoding the subunits of the high‐affinity cytochrome d oxidase, is maximally transcribed in microaerobiosis as a result of the combined action of the oxygen‐responsive regulators Fnr and ArcA. Here, we report that the histone‐like protein H‐NS is an aerobic repressor of cydAB expression. ArcA is shown to antagonize H‐NS action to render cydAB expression insensitive to H‐NS repression in anaerobiosis. The targets for H‐NS‐mediated aerobic repression are the four oxygen‐regulated promoters, designated P1, P2, P3 and P4. H‐NS control is the result of H‐NS binding to an extended region within the cydAB promoter element, including sequences upstream from and overlapping the four regulated promoters. We propose a regulatory model in which oxygen control of cydAB transcription is mediated by three alternative protein–DNA complexes that are assembled sequentially on the promoter region as the cells are shifted from aerobic to microaerobic and to anaerobic conditions. According to this model, ArcA‐P plays a central role in cydAB regulation by antagonizing H‐NS repression of cydAB transcription when oxygen becomes limiting. This allows peak gene expression and subsequent repression by Fnr under fully anaerobic conditions.