Scientific article

The DUF1013 protein TrcR tracks with RNA polymerase to control the bacterial cell cycle and protect against antibiotics

Published inProceedings of the National Academy of Sciences, vol. 118, no. 8, e2010357118
Publication date2021

How DNA-dependent RNA polymerase (RNAP) acts on bacterial cell cycle progression during transcription elongation is poorly investigated. A forward genetic selection for Caulobacter crescentus cell cycle mutants unearthed the uncharacterized DUF1013 protein (TrcR, transcriptional cell cycle regulator). TrcR promotes the accumulation of the essential cell cycle transcriptional activator CtrA in late S-phase but also affects transcription at a global level to protect cells from the quinolone antibiotic nalidixic acid that induces a multidrug efflux pump and from the RNAP inhibitor rifampicin that blocks transcription elongation. We show that TrcR associates with promoters and coding sequences in vivo in a rifampicin-dependent manner and that it interacts physically and genetically with RNAP. We show that TrcR function and its RNAP-dependent chromatin recruitment are conserved in symbiotic Sinorhizobium sp. and pathogenic Brucella spp Thus, TrcR represents a hitherto unknown antibiotic target and the founding member of the DUF1013 family, an uncharacterized class of transcriptional regulators that track with RNAP during the elongation phase to promote transcription during the cell cycle.

Citation (ISO format)
DELABY, Marie et al. The DUF1013 protein TrcR tracks with RNA polymerase to control the bacterial cell cycle and protect against antibiotics. In: Proceedings of the National Academy of Sciences, 2021, vol. 118, n° 8, p. e2010357118. doi: 10.1073/pnas.2010357118
Main files (1)
Article (Published version)
Secondary files (5)
ISSN of the journal0027-8424

Technical informations

Creation02/20/2021 8:50:00 AM
First validation02/20/2021 8:50:00 AM
Update time03/16/2023 12:11:15 AM
Status update03/16/2023 12:11:13 AM
Last indexation05/06/2024 6:45:11 AM
All rights reserved by Archive ouverte UNIGE and the University of GenevaunigeBlack