The SMC-like RecN protein is at the crossroads of several genotoxic stress responses in Escherichia coli

DNA damage repair (DDR) is an essential process for living organisms and contributes to genome maintenance and evolution. DDR involves different pathways including Homologous recombination (HR), Nucleotide Excision Repair (NER) and Base excision repair (BER) for example. The activity of each pathway...

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Vydáno v:Frontiers in microbiology Ročník 14; s. 1146496
Hlavní autoři: Camus, Adrien, Espinosa, Elena, Zapater Baras, Pénélope, Singh, Parul, Quenech’Du, Nicole, Vickridge, Elise, Modesti, Mauro, Barre, François Xavier, Espéli, Olivier
Médium: Journal Article
Jazyk:angličtina
Vydáno: Switzerland Frontiers Media 24.04.2023
Frontiers Media S.A
Témata:
Bleomycin (BLM)
genotoxic
homologous recombination (HR)
Life Sciences
Microbiology
mitomycin C (Mit-C)
RecN
Tn-seq
mitomycin C (Mit-C)
sister chromatid cohesion
genotoxic
homologous recombination (HR)
uvrA
Tn-seq
Bleomycin (BLM)
RecN
ISSN:1664-302X, 1664-302X
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Shrnutí:DNA damage repair (DDR) is an essential process for living organisms and contributes to genome maintenance and evolution. DDR involves different pathways including Homologous recombination (HR), Nucleotide Excision Repair (NER) and Base excision repair (BER) for example. The activity of each pathway is revealed with particular drug inducing lesions, but the repair of most DNA lesions depends on concomitant or subsequent action of the multiple pathways. In the present study, we used two genotoxic antibiotics, mitomycin C (MMC) and Bleomycin (BLM), to decipher the interplays between these different pathways in . We combined genomic methods (TIS and Hi-SC2) and imaging assays with genetic dissections. We demonstrate that only a small set of DDR proteins are common to the repair of the lesions induced by these two drugs. Among them, RecN, an SMC-like protein, plays an important role by controlling sister chromatids dynamics and genome morphology at different steps of the repair processes. We further demonstrate that RecN influence on sister chromatids dynamics is not equivalent during the processing of the lesions induced by the two drugs. We observed that RecN activity and stability requires a pre-processing of the MMC-induced lesions by the NER but not for BLM-induced lesions. Those results show that RecN plays a major role in rescuing toxic intermediates generated by the BER pathway in addition to its well-known importance to the repair of double strand breaks by HR.
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Edited by: Tamara Basta, UMR 9198 Institut de Biologie Intégrative de la Cellule (I2BC), France
Reviewed by: Amar Deep, University of California, San Diego, United States; Johannes Stigler, Ludwig Maximilian University of Munich, Germany
ISSN:1664-302X
1664-302X
DOI:10.3389/fmicb.2023.1146496