SOS genes are rapidly induced while translesion synthesis polymerase activity is temporally regulated.

Autor:	Bergum OET; Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway., Singleton AH; Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway., Røst LM; Department of Biotechnology and Food Science, Norwegian University of Science and Technology (NTNU), Trondheim, Norway., Bodein A; Department of Molecular Medicine, CHU de Québec Research Center, Université Laval, Québec, QC, Canada., Scott-Boyer MP; Department of Molecular Medicine, CHU de Québec Research Center, Université Laval, Québec, QC, Canada., Rye MB; Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.; Clinic of Surgery, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway.; Clinic of Laboratory Medicine, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway.; BioCore - Bioinformatics Core Facility, Norwegian University of Science and Technology (NTNU), Trondheim, Norway., Droit A; Department of Molecular Medicine, CHU de Québec Research Center, Université Laval, Québec, QC, Canada., Bruheim P; Department of Biotechnology and Food Science, Norwegian University of Science and Technology (NTNU), Trondheim, Norway., Otterlei M; Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.; Clinic of Laboratory Medicine, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway.
Jazyk:	angličtina
Zdroj:	Frontiers in microbiology [Front Microbiol] 2024 Mar 26; Vol. 15, pp. 1373344. Date of Electronic Publication: 2024 Mar 26 (Print Publication: 2024).
DOI:	10.3389/fmicb.2024.1373344
Abstrakt:	The DNA damage inducible SOS response in bacteria serves to increase survival of the species at the cost of mutagenesis. The SOS response first initiates error-free repair followed by error-prone repair. Here, we have employed a multi-omics approach to elucidate the temporal coordination of the SOS response. Escherichia coli was grown in batch cultivation in bioreactors to ensure highly controlled conditions, and a low dose of the antibiotic ciprofloxacin was used to activate the SOS response while avoiding extensive cell death. Our results show that expression of genes involved in error-free and error-prone repair were both induced shortly after DNA damage, thus, challenging the established perception that the expression of error-prone repair genes is delayed. By combining transcriptomics and a sub-proteomics approach termed signalomics, we found that the temporal segregation of error-free and error-prone repair is primarily regulated after transcription, supporting the current literature. Furthermore, the heterology index (i.e., the binding affinity of LexA to the SOS box) was correlated to the maximum increase in gene expression and not to the time of induction of SOS genes. Finally, quantification of metabolites revealed increasing pyrimidine pools as a late feature of the SOS response. Our results elucidate how the SOS response is coordinated, showing a rapid transcriptional response and temporal regulation of mutagenesis on the protein and metabolite levels. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2024 Bergum, Singleton, Røst, Bodein, Scott-Boyer, Rye, Droit, Bruheim and Otterlei.)
Databáze:	MEDLINE
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