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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| Vydané v: | Frontiers in microbiology Ročník 14; s. 1146496 |
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| Hlavní autori: | , , , , , , , , |
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| Jazyk: | English |
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Frontiers Media
24.04.2023
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| Abstract | 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. |
|---|---|
| AbstractList | IntroductionDNA 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.MethodsIn the present study, we used two genotoxic antibiotics, mitomycin C (MMC) and Bleomycin (BLM), to decipher the interplays between these different pathways in E. coli. We combined genomic methods (TIS and Hi-SC2) and imaging assays with genetic dissections.ResultsWe 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.DiscussionThose 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. Introduction 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. Methods In the present study, we used two genotoxic antibiotics, mitomycin C (MMC) and Bleomycin (BLM), to decipher the interplays between these different pathways in E. coli . We combined genomic methods (TIS and Hi-SC2) and imaging assays with genetic dissections. Results 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. Discussion 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. 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.IntroductionDNA 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 E. coli. We combined genomic methods (TIS and Hi-SC2) and imaging assays with genetic dissections.MethodsIn the present study, we used two genotoxic antibiotics, mitomycin C (MMC) and Bleomycin (BLM), to decipher the interplays between these different pathways in E. coli. 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.ResultsWe 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.DiscussionThose 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. 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. |
| Author | Zapater Baras, Pénélope Camus, Adrien Singh, Parul Barre, François Xavier Espéli, Olivier Quenech’Du, Nicole Espinosa, Elena Vickridge, Elise Modesti, Mauro |
| AuthorAffiliation | 2 Institute for Integrative Biology of the Cell (I2BC), Université Paris-Saclay, CEA, CNRS , Gif-sur-Yvette , France 1 CIRB, Collège de France, INSERM U1050, CNRS UMR 7241, Université PSL , Paris , France 3 Goodman Cancer Research Centre, McGill University , Montreal, QC , Canada 4 Cancer Research Center of Marseille, Department of Genome Integrity, CNRS UMR 7258, INSERM U1068, Institut Paoli-Calmettes, Aix Marseille University , Marseille , France |
| AuthorAffiliation_xml | – name: 2 Institute for Integrative Biology of the Cell (I2BC), Université Paris-Saclay, CEA, CNRS , Gif-sur-Yvette , France – name: 4 Cancer Research Center of Marseille, Department of Genome Integrity, CNRS UMR 7258, INSERM U1068, Institut Paoli-Calmettes, Aix Marseille University , Marseille , France – name: 1 CIRB, Collège de France, INSERM U1050, CNRS UMR 7241, Université PSL , Paris , France – name: 3 Goodman Cancer Research Centre, McGill University , Montreal, QC , Canada |
| Author_xml | – sequence: 1 givenname: Adrien surname: Camus fullname: Camus, Adrien – sequence: 2 givenname: Elena surname: Espinosa fullname: Espinosa, Elena – sequence: 3 givenname: Pénélope surname: Zapater Baras fullname: Zapater Baras, Pénélope – sequence: 4 givenname: Parul surname: Singh fullname: Singh, Parul – sequence: 5 givenname: Nicole surname: Quenech’Du fullname: Quenech’Du, Nicole – sequence: 6 givenname: Elise surname: Vickridge fullname: Vickridge, Elise – sequence: 7 givenname: Mauro surname: Modesti fullname: Modesti, Mauro – sequence: 8 givenname: François Xavier surname: Barre fullname: Barre, François Xavier – sequence: 9 givenname: Olivier surname: Espéli fullname: Espéli, Olivier |
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| Keywords | mitomycin C (Mit-C) sister chromatid cohesion genotoxic homologous recombination (HR) uvrA Tn-seq Bleomycin (BLM) RecN |
| Language | English |
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| Title | The SMC-like RecN protein is at the crossroads of several genotoxic stress responses in Escherichia coli |
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