SATAY screen in a tdp1 Wss1 siz2 triple deletion strain
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB47156 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR6558455.fastq.gz | Fastqsanger.gz |
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2015-03-02 | PXD001681 | Pride
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Project description:In this study, the proteins SumoE1 and Fat10 or Fat10-AV mutant were crosslinked using the crosslinking reagent H12/D12 BS3 in order to determine specific interaction sites of Fat10 and SumoE1. Furthermore, quantitative chemical crosslinking coupled to mass spectrometry (q-XL-MS) was used to compare crosslink abundances of SumoE1 in presence of Sumo as well as Sumo and Fat10 versus crosslink abundances of SumoE1 in absence of Sumo and Fat10 in order to determine the influence of Sumo and Fat10 on the structural dynamics of SumoE1.
2019-10-08 | PXD012592 | Pride
Project description:The Fanconi Anemia (FA) repair pathway governs the repair of highly genotoxic DNA interstrand crosslinks (ICLs) with the assistance of translesion synthesis (TLS), that is facilitated by site-specific monoubiquitination of PCNA (PCNA-Ub) at lysine 164 (K164). Mutation at this residue (K164R) renders mammals hypersensitive to ICLs. Besides the FA pathway, alternative pathways have been associated with ICL repair However, the decision-making between the different pathways remains elusive. To study the dependence and relevance of PCNA-Ub in FA repair and pathway preference, we generated a germline Fancg-/- mouse and intercrossed PcnaK164R/+;Fancg-/+ mice. A compound mutation (KR;FGko) was embryonic lethal with the noted exception of very infrequent escapers. RNAseq of primary double mutant mouse embryonic fibroblasts (MEFs) revealed elevated levels of replication stress-induced checkpoints, which were rescued by Trp53 knockdown. Upon crosslink induction, KR and FGko MEFs displayed a similar phenotype regarding sensitivity, cell cycle arrest, fork progression and accumulation of single stranded DNA.Remarkably, PCNA-Ub excludes the mismatch recognition complex MSH2/MSH6 from being recruited. Our results implicate a dual function of PCNA-Ub in ICL repair: 1. Facilitate TLS opposite the unhooked ICL and 2. simultaneously exclude MSH2/MSH6 recruitment to channel the ICL towards canonical FA repair.
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Project description:BRCA1 functions independently of homologous recombination in DNA interstrand crosslink repair
| PRJNA152035 | ENA