Structural characterization of transcription-coupled repair protein UVSSA and its interaction with TFIIH protein

Mistry, Hiral; Kumari, Shweta; Aswal, Vinod K.; Gupta, Gagan D.

doi:10.1016/j.ijbiomac.2023.125792

Cited by 4 publications

(1 citation statement)

References 37 publications

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“…Since the downstream repair proteins, XPA and ERCC1-XPF, were not detected with the RNA polymerase pulldowns, it is hypothesized that the RNA polymerase II and CSB-CSA-UVSSA complex may be shifted or possibly removed when TFIIH binds with XPA [69]. In support of these findings, Mistry et al found that there is a large structural change in UVSSA upon TFIIH binding that causes UVSSA to become more compact and may cause the dissociation of the CBS-CBA-UVSSA complex from DNA and/or RNA Polymerase II [71].…”

Section: Transcription-coupled Nucleotide Excision Repair (Tc-ner)mentioning

confidence: 95%

New Discoveries on Protein Recruitment and Regulation during the Early Stages of the DNA Damage Response Pathways

Waters,

Spratt

2024

IJMS

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Maintaining genomic stability and properly repairing damaged DNA is essential to staying healthy and preserving cellular homeostasis. The five major pathways involved in repairing eukaryotic DNA include base excision repair (BER), nucleotide excision repair (NER), mismatch repair (MMR), non-homologous end joining (NHEJ), and homologous recombination (HR). When these pathways do not properly repair damaged DNA, genomic stability is compromised and can contribute to diseases such as cancer. It is essential that the causes of DNA damage and the consequent repair pathways are fully understood, yet the initial recruitment and regulation of DNA damage response proteins remains unclear. In this review, the causes of DNA damage, the various mechanisms of DNA damage repair, and the current research regarding the early steps of each major pathway were investigated.

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Section: Transcription-coupled Nucleotide Excision Repair (Tc-ner)mentioning

confidence: 95%

New Discoveries on Protein Recruitment and Regulation during the Early Stages of the DNA Damage Response Pathways

Waters,

Spratt

2024

IJMS

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Unveiling potential inhibitors targeting the nucleocapsid protein of SARS-CoV-2: Structural insights into their binding sites

Kumari,

Mistry,

Bihani

et al. 2024

International Journal of Biological Macromolecules

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Coordination of transcription-coupled repair and repair-independent release of lesion-stalled RNA polymerase II

Zhu,

Zhang,

Gao

et al. 2024

Nat Commun

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Transcription-blocking lesions (TBLs) stall elongating RNA polymerase II (Pol II), which then initiates transcription-coupled repair (TCR) to remove TBLs and allow transcription recovery. In the absence of TCR, eviction of lesion-stalled Pol II is required for alternative pathways to address the damage, but the mechanism is unclear. Using Protein-Associated DNA Damage Sequencing (PADD-seq), this study reveals that the p97-proteasome pathway can evict lesion-stalled Pol II independently of repair. Both TCR and repair-independent eviction require CSA and ubiquitination. However, p97 is dispensable for TCR and Pol II eviction in TCR-proficient cells, highlighting repair’s prioritization over repair-independent eviction. Moreover, ubiquitination of RPB1-K1268 is important for both pathways, with USP7’s deubiquitinase activity promoting TCR without abolishing repair-independent Pol II release. In summary, this study elucidates the fate of lesion-stalled Pol II, and may shed light on the molecular basis of genetic diseases caused by the defects of TCR genes.

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Structural characterization of transcription-coupled repair protein UVSSA and its interaction with TFIIH protein

Cited by 4 publications

References 37 publications

New Discoveries on Protein Recruitment and Regulation during the Early Stages of the DNA Damage Response Pathways

New Discoveries on Protein Recruitment and Regulation during the Early Stages of the DNA Damage Response Pathways

Unveiling potential inhibitors targeting the nucleocapsid protein of SARS-CoV-2: Structural insights into their binding sites

Coordination of transcription-coupled repair and repair-independent release of lesion-stalled RNA polymerase II

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