Stabilization of Ultraviolet (UV)-stimulated Scaffold Protein A by Interaction with Ubiquitin-specific Peptidase 7 Is Essential for Transcription-coupled Nucleotide Excision Repair*

@article{Higa2016StabilizationOU,
  title={Stabilization of Ultraviolet (UV)-stimulated Scaffold Protein A by Interaction with Ubiquitin-specific Peptidase 7 Is Essential for Transcription-coupled Nucleotide Excision Repair*},
  author={Mitsuru Higa and Xue Zhang and Kiyoji Tanaka and M. Saijo},
  journal={The Journal of Biological Chemistry},
  year={2016},
  volume={291},
  pages={13771 - 13779}
}
UV-sensitive syndrome is an autosomal recessive disorder characterized by hypersensitivity to UV light and deficiency in transcription-coupled nucleotide excision repair (TC-NER), a subpathway of nucleotide excision repair that rapidly removes transcription-blocking DNA damage. UV-sensitive syndrome consists of three genetic complementation groups caused by mutations in the CSA, CSB, and UVSSA genes. UV-stimulated scaffold protein A (UVSSA), the product of UVSSA, which is required for… Expand
Inhibition of UVSSA ubiquitination suppresses transcription‐coupled nucleotide excision repair deficiency caused by dissociation from USP7
TLDR
It is shown that UVSSA is mono‐ubiquitinated in vitro and identified a lysine residue (Lys414) in U VSSA as the target of ubiquitination and suppressed the deficiency in TC‐NER. Expand
FACT subunit Spt16 controls UVSSA recruitment to lesion-stalled RNA Pol II and stimulates TC-NER
TLDR
It is shown that UVSSA accumulates at TBLs independent of CSA and CSB, and Quantitative interaction proteomics showed that the Spt16 subunit of the histone chaperone FACT interacts with U VSSA, which is mediated by the DUF2043 domain. Expand
USP7-mediated deubiquitination differentially regulates CSB but not UVSSA upon UV radiation-induced DNA damage
TLDR
A role of USP7 as a CSB deubiquitinating enzyme for fine-tuning the process of TC-NER in human cells is revealed and is shown to be important for maintaining CSB levels after ultraviolet (UV)-induced DNA damage. Expand
Common TFIIH recruitment mechanism in global genome and transcription-coupled repair subpathways
TLDR
A common TFIIH recruitment mechanism is shared by UVSSA in TCR and XPC in GGR, highly resembling the interaction mechanism of XPC with p62. Expand
UVSSA, UBP12, and RDO2/TFIIS Contribute to Arabidopsis UV Tolerance
TLDR
The results indicate a conserved role for UVSSA, USP7 (UBP12), and TFIIS (RDO2) in TCR, which is consistent with a role in NER. Expand
Emerging Roles of Post-Translational Modifications in Nucleotide Excision Repair
Nucleotide excision repair (NER) is a versatile DNA repair pathway which can be activated in response to a broad spectrum of UV-induced DNA damage, such as bulky adducts, includingExpand
Disorders with Deficiency in TC-NER: Molecular Pathogenesis of Cockayne Syndrome and UV-Sensitive Syndrome
TLDR
This chapter will specifically describe the historical progress and recent findings of TC-NER and summarize the current understanding of the molecular pathogenesis of CS and UVSS. Expand
What happens at the lesion does not stay at the lesion: Transcription-coupled nucleotide excision repair and the effects of DNA damage on transcription in cis and trans.
TLDR
The diverse consequences of DNA damage on transcription, including transcription inhibition, induction of specific transcriptional programs and regulation of alternative splicing, are summarized and their consequences on the process of transcription restart are discussed. Expand
Mechanistic insights in transcription-coupled nucleotide excision repair of ribosomal DNA
TLDR
In mammals, the repair mechanism of rDNAs along with a specific behavior for RNAP1 after UV irradiation is identified, in mammals, and Nucleotide excision repair (NER) guarantees genome integrity against UV light-induced DNA damage. Expand
Timing of DNA lesion recognition: Ubiquitin signaling in the NER pathway
TLDR
Current knowledge of the ubiquitylation network that drives DNA repair in the NER pathway is summarized and the crosstalk of ubiquitin signaling with other prominent post-translational modfications that might be essential to time the DNA damage recognition step are discussed. Expand
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TLDR
Using exome sequencing, it is determined that mutations in the UVSSA gene (formerly known as KIAA1530) cause UVSS-A, which interacts with TC-NER machinery and stabilizes the ERCC6 complex; it also facilitates ubiquitination of RNA polymerase IIo stalled at DNA damage sites. Expand
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Findings indicate that UVSSA-USP7–mediated stabilization of ERCC6 represents a critical regulatory mechanism of TC-NER in restoring gene expression. Expand
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The predicted human gene UVSSA (formerly known as KIAA1530) corrects defective TCR in UVSS-A cells and is identified as the causative gene for this syndrome. Expand
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TLDR
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