Rad4–Rad23 interaction with SWI/SNF links ATP-dependent chromatin remodeling with nucleotide excision repair

Gong, Feng; Fahy, Deirdre; Smerdon, Michael J.

doi:10.1038/nsmb1152

Cited by 136 publications

(148 citation statements)

References 32 publications

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“…This is expected since in vitro studies have suggested that SWI/SNF has an important role in chromatin remodeling and efficient NER of UV lesions (13,14). Studies in yeast as well as in mammalian cells also indicated that SWI/SNF is indispensable for NER (15,16). However, we found that Brg1 does not bind to another UV lesion 6-4PP and does not affect its repair.…”

Section: Brg1 Modulation Against Different Types Of Uv Lesions-wecontrasting

confidence: 48%

“…Evidence from yeast has shown that SNF5 and SNF6, two subunits of SWI/SNF, interact with XPC on the chromatin and are involved in NER (15). To determine if Brg1 directly interacts with the core NER factor XPC in mammalian cells, HeLa-XPC cells were UV irradiated at 20 J/m 2 , and the soluble chromatin was immunoprecipitated with anti-HA affinity gel.…”

Section: Brg1 Interacts With Xpc and Its Recruitment To Cpd Depends Omentioning

confidence: 99%

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Modulation of Nucleotide Excision Repair by Mammalian SWI/SNF Chromatin-remodeling Complex

Zhao

Wang

Ray

et al. 2009

Journal of Biological Chemistry

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Accessibility within chromatin is an important factor in the prompt removal of UV-induced DNA damage by nucleotide excision repair (NER). Chromatin remodeling by the SWI/SNF complex has been shown to play an important modulating role in NER in vitro and yeast in vivo. Nevertheless, the molecular basis of cross-talk between SWI/SNF and NER in mammalian cells is not fully understood. Here, we show that knockdown of Brg1, the ATPase subunit of SWI/SNF, negatively affects the elimination of cyclobutane pyrimidine dimers (CPD), but not of pyrimidine (6, 4)pyrimidone photoproducts (6-4PP) following UV irradiation of mammalian cells. Brg1-deficient cells exhibit a lower chromatin relaxation as well as impaired recruitment of downstream NER factors, XPG and PCNA, to UV lesions. However, the assembly of upstream NER factors, DDB2 and XPC, at the damage site was unaffected by Brg1 knockdown. Interestingly, Brg1 interacts with XPC within chromatin and is recruited to UV-damaged sites in a DDB2-and XPC-dependent manner. Also, postirradiation decrease of XPC levels occurred more rapidly in Brg1-deficient than normal cells. Conversely, XPC transcription remained unaltered upon Brg1 knockdown indicating that Brg1 affects the stability of XPC protein following irradiation. Thus, Brg1 facilitates different stages of NER by initially modulating UV-induced chromatin relaxation and stabilizing XPC at the damage sites, and subsequently stimulating the recruitment of XPG and PCNA to successfully culminate the repair.

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Section: Brg1 Modulation Against Different Types Of Uv Lesions-wecontrasting

confidence: 48%

Section: Brg1 Interacts With Xpc and Its Recruitment To Cpd Depends Omentioning

confidence: 99%

Modulation of Nucleotide Excision Repair by Mammalian SWI/SNF Chromatin-remodeling Complex

Zhao

Wang

Ray

et al. 2009

Journal of Biological Chemistry

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“…For example, a direct interaction between Rad4/Rad23 and components of the SWI/SNF complex was suggested to load the SWI/SNF complex in aiding NER in budding yeast (37). Thus, generation of accessible DNA for lesion removal requires coordination of remodeling complexes with distinct catalytic functions.…”

Section: Discussionmentioning

confidence: 99%

INO80 chromatin remodeling complex promotes the removal of UV lesions by the nucleotide excision repair pathway

Jiang¹,

Wang²,

Bao³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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The creation of accessible DNA in the context of chromatin is a key step in many DNA functions. To reveal how ATP-dependent chromatin remodeling activities impact DNA repair, we constructed mammalian genetic models for the INO80 chromatin remodeling complex and investigated the impact of loss of INO80 function on the repair of UV-induced photo lesions. We showed that deletion of two core components of the INO80 complex, INO80 and ARP5, significantly hampered cellular removal of UV-induced photo lesions but had no significant impact on the transcription of nucleotide excision repair (NER) factors. Loss of INO80 abolished the assembly of NER factors, suggesting that prior chromatin relaxation is important for the NER incision process. Ino80 and Arp5 are enriched to UV-damaged DNA in an NER-incision-independent fashion, suggesting that recruitment of the remodeling activity likely takes place during the initial stage of damage recognition. These results demonstrate a critical role of INO80 in creating DNA accessibility for the NER pathway and provide direct evidence that repair of UV lesions and perhaps most bulky adduct lesions requires chromatin reconfiguration.DNA damage | DNA repair | chromatin | remodeling T he highly condensed nature of the chromatin assembly restricts the interaction of DNA with most nuclear factors. To create accessible DNA for various nuclear events, chromatin dynamics is regulated by the coordinated actions of two types of cellular mechanisms, posttranslational modifications of the core histones and ATP-dependent chromatin remodeling. Whereas covalent histone modifications, instigated mainly from regulation of yeast gene transcription, have been extensively studied, less is known about the chromatin remodeling process and how chromatin remodeling impacts various nuclear events.ATP-dependent chromatin remodeling is catalyzed by a distinct class of enzymes that comprises four families of structurally related ATP-dependent protein complexes (1). Biological activities of these complexes, defined by a variety of in vitro assays, include disruption of histone-DNA contact within nucleosomes, increased accessibility of nucleosomal DNA to transcription factors or restriction endonucleases, and cis and trans movement of histone octamers (2, 3). The INO80 chromatin remodeling complex was identified from the ino80-1 mutant defective in inositol/choline response (4-6). It contains the Ino80 ATPase, which belongs to the SNF/SWI2 superfamily (7). The Ino80 ATPase associates with 14 proteins to form a 1-MDa complex exhibiting 3′-5′ helicase activity (6,8). The INO80 complex also contains three actinrelated proteins (ARPs), of which ARP5 and ARP8 are specific to the INO80 complex. Deletion of either INO80-specific ARP compromises the ATPase activity of the remaining complex and gives rise to DNA-damage-sensitive phenotypes indistinguishable to the INO80 null mutant (9). Purification of human INO80 revealed a complex with virtually identical core components and a role in transcription (10, 11), indicating ...

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“…Recent studies in yeast revealed an enhanced association of subunits of the SWI/SNF chromatin-remodelling complex with Rad4-Rad23 (XPC-RAD23B in human), the principal DNA damage recognition factor in GG-NER [81]. Also histone acetyltransferases (HATs) are known to stimulate NER.…”

Section: Recruitment Of Chromatin Remodellers In Tc-nermentioning

confidence: 99%

Transcription-coupled nucleotide excision repair in mammalian cells: molecular mechanisms and biological effects

2008

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The encounter of elongating RNA polymerase II (RNAPIIo) with DNA lesions has severe consequences for the cell as this event provides a strong signal for P53-dependent apoptosis and cell cycle arrest. To counteract prolonged blockage of transcription, the cell removes the RNAPIIo-blocking DNA lesions by transcription-coupled repair (TC-NER), a specialized subpathway of nucleotide excision repair (NER). Exposure of mice to UVB light or chemicals has elucidated that TC-NER is a critical survival pathway protecting against acute toxic and long-term effects (cancer) of genotoxic exposure. Deficiency in TC-NER is associated with mutations in the CSA and CSB genes giving rise to the rare human disorder Cockayne syndrome (CS). Recent data suggest that CSA and CSB play differential roles in mammalian TC-NER: CSB as a repair coupling factor to attract NER proteins, chromatin remodellers and the CSA-E3-ubiquitin ligase complex to the stalled RNAPIIo. CSA is dispensable for attraction of NER proteins, yet in cooperation with CSB is required to recruit XAB2, the nucleosomal binding protein HMGN1 and TFIIS. The emerging picture of TC-NER is complex: repair of transcription-blocking lesions occurs without displacement of the DNA damage-stalled RNAPIIo, and requires at least two essential assembly factors (CSA and CSB), the core NER factors (except for XPC-RAD23B), and TC-NER specific factors. These and yet unidentified proteins will accomplish not only efficient repair of transcription-blocking lesions, but are also likely to contribute to DNA damage signalling events.

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Rad4–Rad23 interaction with SWI/SNF links ATP-dependent chromatin remodeling with nucleotide excision repair

Cited by 136 publications

References 32 publications

Modulation of Nucleotide Excision Repair by Mammalian SWI/SNF Chromatin-remodeling Complex

Modulation of Nucleotide Excision Repair by Mammalian SWI/SNF Chromatin-remodeling Complex

INO80 chromatin remodeling complex promotes the removal of UV lesions by the nucleotide excision repair pathway

Transcription-coupled nucleotide excision repair in mammalian cells: molecular mechanisms and biological effects

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