Abstract
Prokaryotic toxin-antitoxin (TA) loci consist of two genes in an operon that encodes a metabolically stable toxin and an unstable antitoxin. The antitoxin neutralizes its cognate toxin by forming a tight complex with it. In all cases known, the antitoxin autoregulates TA operon transcription by binding to one or more operators in the promoter region while the toxin functions as a co-repressor of transcription. Interestingly, the toxin can also stimulate TA operon transcription. Here we analyse mechanistic aspects of how ReIE of Escherichia coli can function both as a co-repressor and as a derepressor of relBE transcription. When ROB was in excess to ReIE, two trimeric ReIB(2)center dot ReIE complexes bound cooperatively to two adjacent operator sites in the reIBE promoter region and repressed transcription. In contrast, ReIE in excess stimulated re/BE transcription and released the ReIB(2)center dot ReIE complex from operator DNA. A mutational analysis of the operator sites showed that ReIE in excess counteracted cooperative binding of the ReIB(2)center dot ReIE complexes to the operator sites. Thus, ReIE controls relBEtranscription by conditional cooperativity.
| Original language | English |
|---|---|
| Journal | Molecular Microbiology |
| Volume | 69 |
| Issue number | 4 |
| Pages (from-to) | 841-857 |
| Number of pages | 17 |
| ISSN | 0950-382X |
| DOIs | |
| Publication status | Published - 2008 |
| Externally published | Yes |