Mono-ubiquitination of histone H2B (H2B-Ub1) is a conserved modification that plays central role in regulating numerous biological processes including the DNA damage response, gene transcription, and DNA replication. Previous studies have revealed that H2B-Ub1 promotes recovery from replication stress by mediating Rad53 phosphorylation (Rad53-P), and activation of the intra-S replication checkpoint, in order to limit fork progression, and associated DNA damage. Since such mono-ubiquitination is a reversible process, we examined the role of H2B-Ub1 deubiquitination during replication stress. Using an experimental system in yeast which mimics H2B-Ub1 accumulation, we show that cells become sensitive to the replication stress induced by HU. This stress response was accompanied by Rad53-P accumulation, and delayed recovery from intra-S checkpoint arrest. Furthermore, we show that similar effects were recapitulated by the accumulation of endogenous H2B-Ub1, induced by the co-inactivation of the deubiquitinating enzyme, Ubp10, and Spt16, a FACT histone chaperone family member. While it has been well established that H2B mono-ubiquitination plays an essential role in recovering from replication stress, our data reveal that H2B-Ub1 deubiquitination is also essential for this process.
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Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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Site | Modification | Modifier | Source | Reference |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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