Functional TFIIH Is Required for UV-Induced Translocation of CSA to the Nuclear Matrix

Saijo, Masafumi; Hirai, Takamasa; Ogawa, Akiko; Kobayashi, Aki; Kamiuchi, Shinya; Tanaka, Kiyoji

doi:10.1128/mcb.01288-06

Cited by 30 publications

(21 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Translocation of CSA to the nuclear matrix after UV irradiation is related to TC-NER and is dependent on CSB (20,21). Because the translocation did not occur with the deletion mutants (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Kps3 cells stably expressing FLAG-HA-UVSSA and CS3BESV cells stably expressing CSA-FLAG-HA have been generated previously (21,22). All cell lines were cultured in DMEM containing 10% FBS, 100 units/ml penicillin, and 100 g/ml streptomycin at 37°C in an incubator containing 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

“…Toranslocation of CSA to the Nuclear Matrix after UV Irradiation-UV light-induced translocation of CSA in a cellfree system was examined as described previously (21). CS1ANSV cells expressing CSB were irradiated with 20 J/m 2 UV light, incubated for 1 h, and then treated with CSK-Triton buffer to prepare the insoluble fractions (CSK-ppt fraction).…”

Section: Methodsmentioning

confidence: 99%

“…CSB is also needed for the translocation of CSA to the nuclear matrix after UV irradiation (20,21). This translocation is relevant to TC-NER.…”

Section: Uv Sensitivity and Recovery Of Rna Synthesis After Uv Irradimentioning

confidence: 99%

“…This translocation is relevant to TC-NER. Therefore, we next investigated the ability of each CSB mutant to translocate CSA to the nuclear matrix using a cell-free system (21). Mutant CSB cells were irradiated with UV light or not irradiated and incubated for 1 h. CSK-ppt fractions were prepared from the cells.…”

Section: Uv Sensitivity and Recovery Of Rna Synthesis After Uv Irradimentioning

confidence: 99%

See 4 more Smart Citations

The C-terminal Region and SUMOylation of Cockayne Syndrome Group B Protein Play Critical Roles in Transcription-coupled Nucleotide Excision Repair

Sin¹,

Tanaka

Saijo

2016

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

Cockayne syndrome (CS) is a recessive disorder that results in deficiencies in transcription-coupled nucleotide excision repair (TC-NER), a subpathway of nucleotide excision repair, and cells from CS patients exhibit hypersensitivity to UV light. CS group B protein (CSB), which is the gene product of one of the genes responsible for CS, belongs to the SWI2/SNF2 DNA-dependent ATPase family and has an ATPase domain and an ubiquitinbinding domain (UBD) in the central region and the C-terminal region, respectively. The C-terminal region containing the UBD is essential for the functions of CSB. In this study, we generated several CSB deletion mutants and analyzed the functions of the C-terminal region of CSB in TC-NER. Not only the UBD but also the C-terminal 30-amino acid residues were required for UV light resistance and TC-NER. This region was needed for the interaction of CSB with RNA polymerase II, the translocation of CS group A protein to the nuclear matrix, and the association of CSB with chromatin after UV irradiation. CSB was modified by small ubiquitin-like modifier 2/3 in a UV light-dependent manner. This modification was abolished in a CSB mutant lacking the C-terminal 30 amino acid residues. However, the substitution of lysine residues in this region with arginine did not affect SUMOylation or TC-NER. By contrast, substitution of a lysine residue in the N-terminal region with arginine decreased SUMOylation and resulted in cells with defects in TC-NER. These results indicate that both the most C-terminal region and SUMOylation are important for the functions of CSB in TC-NER.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…CSB is also needed for the translocation of CSA to the nuclear matrix after UV irradiation (20,21). This translocation is relevant to TC-NER.…”

Section: Uv Sensitivity and Recovery Of Rna Synthesis After Uv Irradimentioning

confidence: 99%

Section: Uv Sensitivity and Recovery Of Rna Synthesis After Uv Irradimentioning

confidence: 99%

See 3 more Smart Citations

The C-terminal Region and SUMOylation of Cockayne Syndrome Group B Protein Play Critical Roles in Transcription-coupled Nucleotide Excision Repair

Sin¹,

Tanaka

Saijo

2016

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

show abstract

Xeroderma Pigmentosum and Related Diseases

Schubert

Emmert

2019

Harper's Textbook of Pediatric Dermatology

View full text Add to dashboard Cite

Novel missense mutations in a conserved loop between ERCC6 (CSB) helicase motifs V and VI: Insights into Cockayne syndrome

Wilson

Lochan

Stark

et al. 2016

American J of Med Genetics Pt A

View full text Add to dashboard Cite

Cockayne syndrome is caused by biallelic ERCC8 (CSA) or ERCC6 (CSB) mutations and is characterized by growth restriction, microcephaly, developmental delay, and premature pathological aging. Typically affected patients also have dermal photosensitivity. Although Cockayne syndrome is considered a DNA repair disorder, patients with UV-sensitive syndrome, with ERCC8 (CSA) or ERCC6 (CSB) mutations have indistinguishable DNA repair defects, but none of the extradermal features of Cockayne syndrome. We report novel missense mutations affecting a conserved loop in the ERCC6 (CSB) protein, associated with the Cockayne syndrome phenotype. Indeed, the amino acid sequence of this loop is more highly conserved than the adjacent helicase motifs V and VI, suggesting that this is a crucial structural component of the SWI/SNF family of proteins, to which ERCC6 (CSB) belongs. These comprise two RecA-like domains, separated by an interdomain linker, which interact through helicase motif VI. As the observed mutations are likely to act through destabilizing the tertiary protein structure, this prompted us to re-evaluate ERCC6 (CSB) mutation data in relation to the structure of SWI/SNF proteins. Our analysis suggests that antimorphic mutations cause Cockayne syndrome and that biallelic interdomain linker deletions produce more severe phenotypes. Based on our observations, we propose that further investigation of the pathogenic mechanisms underlying Cockayne syndrome should focus on the effect of antimorphic rather than null ERCC6 (CSB) mutations.

show abstract

Functional TFIIH Is Required for UV-Induced Translocation of CSA to the Nuclear Matrix

Cited by 30 publications

References 50 publications

The C-terminal Region and SUMOylation of Cockayne Syndrome Group B Protein Play Critical Roles in Transcription-coupled Nucleotide Excision Repair

The C-terminal Region and SUMOylation of Cockayne Syndrome Group B Protein Play Critical Roles in Transcription-coupled Nucleotide Excision Repair

Xeroderma Pigmentosum and Related Diseases

Novel missense mutations in a conserved loop between ERCC6 (CSB) helicase motifs V and VI: Insights into Cockayne syndrome

Contact Info

Product

Resources

About