scholarly journals Comparative analyses of two primate species diverged by more than 60 million years show different rates but similar distribution of genome-wide UV repair events

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Umit Akkose ◽  
Veysel Ogulcan Kaya ◽  
Laura Lindsey-Boltz ◽  
Zeynep Karagoz ◽  
Adam D. Brown ◽  
...  
Keyword(s):  
Nucleotide Excision Repair ◽  
Cell Lines ◽  
Human Cell ◽  
Excision Repair ◽  
Mouse Lemur ◽  
Repair Mechanism ◽  
Damage Repair ◽  
Genome Wide ◽  
Repair Efficiency ◽  
Nucleotide Excision

Abstract Background Nucleotide excision repair is the primary DNA repair mechanism that removes bulky DNA adducts such as UV-induced pyrimidine dimers. Correspondingly, genome-wide mapping of nucleotide excision repair with eXcision Repair sequencing (XR-seq), provides comprehensive profiling of DNA damage repair. A number of XR-seq experiments at a variety of conditions for different damage types revealed heterogenous repair in the human genome. Although human repair profiles were extensively studied, how repair maps vary between primates is yet to be investigated. Here, we characterized the genome-wide UV-induced damage repair in gray mouse lemur, Microcebus murinus, in comparison to human. Results We derived fibroblast cell lines from mouse lemur, exposed them to UV irradiation, and analyzed the repair events genome-wide using the XR-seq protocol. Mouse lemur repair profiles were analyzed in comparison to the equivalent human fibroblast datasets. We found that overall UV sensitivity, repair efficiency, and transcription-coupled repair levels differ between the two primates. Despite this, comparative analysis of human and mouse lemur fibroblasts revealed that genome-wide repair profiles of the homologous regions are highly correlated, and this correlation is stronger for highly expressed genes. With the inclusion of an additional XR-seq sample derived from another human cell line in the analysis, we found that fibroblasts of the two primates repair UV-induced DNA lesions in a more similar pattern than two distinct human cell lines do. Conclusion Our results suggest that mouse lemurs and humans, and possibly primates in general, share a homologous repair mechanism as well as genomic variance distribution, albeit with their variable repair efficiency. This result also emphasizes the deep homologies of individual tissue types across the eukaryotic phylogeny.

scholarly journals Comparative analyses of two primate species diverged by more than 60 million years show different rates but similar distribution of genome-wide UV repair events

2020 ◽  
Author(s):  
Umit Akkose ◽  
Veysel Ogulcan Kaya ◽  
Laura Lindsey-Boltz ◽  
Zeynep Karagoz ◽  
Adam D. Brown ◽  
...  
Keyword(s):  
Nucleotide Excision Repair ◽  
Human Cell ◽  
Excision Repair ◽  
Mouse Lemur ◽  
Repair Mechanism ◽  
Damage Repair ◽  
Genome Wide ◽  
Repair Efficiency ◽  
Nucleotide Excision ◽  
Mouse Lemurs

AbstractNucleotide excision repair is the primary DNA repair mechanism that removes bulky DNA adducts such as UV-induced pyrimidine dimers. Correspondingly, genome-wide mapping of nucleotide excision repair with eXcision Repair sequencing (XR-seq), provides comprehensive profiling of DNA damage repair. A number of XR-seq experiments at a variety of conditions for different damage types revealed heterogenous repair in the human genome. Although human repair profiles were extensively studied, how repair maps vary between primates is yet to be investigated. Here, we characterized the genome-wide UV-induced damage repair in gray mouse lemur, Microcebus murinus, in comparison to human. Mouse lemurs are strictly nocturnal, are the world’s smallest living primates, and last shared a common ancestor with humans at least 60 million years ago. We derived fibroblast cell lines from mouse lemur, exposed them to UV irradiation. The following repair events were captured genome-wide through the XR-seq protocol. Mouse lemur repair profiles were analyzed in comparison to the equivalent human fibroblast datasets. We found that overall UV sensitivity, repair efficiency, and transcription-coupled repair levels differ between the two primates. Despite this, comparative analysis of human and mouse lemur fibroblasts revealed that genome-wide repair profiles of the homologous regions are highly correlated. This correlation is stronger for the highly expressed genes. With the inclusion of an additional XR-seq sample derived from another human cell line in the analysis, we found that fibroblasts of the two primates repair UV-induced DNA lesions in a more similar pattern than two distinct human cell lines do. Our results suggest that mouse lemurs and humans, and possibly primates in general, share a homologous repair mechanism as well as genomic variance distribution, albeit with their variable repair efficiency. This result also emphasizes the deep homologies of individual tissue types across the eukaryotic phylogeny.

O V A.1 Nucleotide excision repair mechanism in human cells: Analysis by in vitro assays

1997 ◽  
Vol 379 (1) ◽  
pp. S33
Author(s):  
Bernard Salles ◽  
Patrick Calsou ◽  
Philippe Frit ◽  
Ruo-Ya Li ◽  
Catherine Muller ◽  
...  
Keyword(s):  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Human Cells ◽  
In Vitro Assays ◽  
Repair Mechanism ◽  
Nucleotide Excision

scholarly journals Inefficient Nucleotide Excision Repair in Human Cell Extracts of theN-(Deoxyguanosin-8-yl)-6-aminochrysene and 5-(Deoxyguanosin-N2-yl)-6-aminochrysene Adducts Derived from 6-Nitrochrysene

2011 ◽  
Vol 24 (1) ◽  
pp. 65-72 ◽  
Author(s):  
Jacek Krzeminski ◽  
Konstantin Kropachev ◽  
Marina Kolbanovskiy ◽  
Dara Reeves ◽  
Alexander Kolbanovskiy ◽  
...  
Keyword(s):  
Nucleotide Excision Repair ◽  
Human Cell ◽  
Excision Repair ◽  
Cell Extracts ◽  
Nucleotide Excision

scholarly journals Genome-wide role of Rad26 in promoting transcription-coupled nucleotide excision repair in yeast chromatin

2020 ◽  
Vol 117 (31) ◽  
pp. 18608-18616 ◽  
Author(s):  
Mingrui Duan ◽  
Kathiresan Selvam ◽  
John J. Wyrick ◽  
Peng Mao
Keyword(s):  
Nucleotide Excision Repair ◽  
Transcription Initiation ◽  
Excision Repair ◽  
Elongation Factor ◽  
Cockayne Syndrome ◽  
Proximal Half ◽  
Genome Wide ◽  
Nucleotide Excision ◽  
Nucleotide Resolution

Transcription-coupled nucleotide excision repair (TC-NER) is an important DNA repair mechanism that removes RNA polymerase (RNAP)-stalling DNA damage from the transcribed strand (TS) of active genes. TC-NER deficiency in humans is associated with the severe neurological disorder Cockayne syndrome. Initiation of TC-NER is mediated by specific factors such as the human Cockayne syndrome group B (CSB) protein or its yeast homolog Rad26. However, the genome-wide role of CSB/Rad26 in TC-NER, particularly in the context of the chromatin organization, is unclear. Here, we used single-nucleotide resolution UV damage mapping data to show that Rad26 and its ATPase activity is critical for TC-NER downstream of the first (+1) nucleosome in gene coding regions. However, TC-NER on the transcription start site (TSS)-proximal half of the +1 nucleosome is largely independent of Rad26, likely due to high occupancy of the transcription initiation/repair factor TFIIH in this nucleosome. Downstream of the +1 nucleosome, the combination of low TFIIH occupancy and high occupancy of the transcription elongation factor Spt4/Spt5 suppresses TC-NER in Rad26-deficient cells. We show that deletion ofSPT4significantly restores TC-NER across the genome in arad26∆mutant, particularly in the downstream nucleosomes. These data demonstrate that the requirement for Rad26 in TC-NER is modulated by the distribution of TFIIH and Spt4/Spt5 in transcribed chromatin and Rad26 mainly functions downstream of the +1 nucleosome to remove TC-NER suppression by Spt4/Spt5.

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