RAD26, the functional S. cerevisiae homolog of the Cockayne syndrome B gene ERCC6.

Gool, Alain J. van; Verhage, Richard A.; Swagemakers, Sigrid; Putte, Pieter van de; Brouwer, Jaap; Troelstra, Christine; Bootsma, D.; Hoeijmakers, Jan H.J.

doi:10.1002/j.1460-2075.1994.tb06871.x

Cited by 234 publications

(217 citation statements)

References 56 publications

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“…Transcripts were shortened by 2, 6, and 10 nucleotides with additional bands in the 3-13 range appearing at lower frequencies. In contrast to predictions of TRC models (25)(26)(27), CSB counteracted the effect of TFIIS (Fig. 4A, lane 4).…”

Section: Biochemistry: Selby and Sancarcontrasting

confidence: 85%

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Cockayne syndrome group B protein enhances elongation by RNA polymerase II

Selby

Sancar²

1997

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

282

178

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Cockayne syndrome (CS) is characterized by impaired physical and mental development. Two complementation groups, CSA and CSB, have been identified. Here we report that the CSB gene product enhances elongation by RNA polymerase II. CSB stimulated the rate of elongation on an undamaged template by a factor of about 3. A thyminethymine cyclobutane dimer located in the template strand is known to be a strong block to transcription. Addition of CSB to the blocked polymerase resulted in addition of one nucleotide to the nascent transcript. Finally, addition of transcription factor IIS is known to cause polymerase blocked at a thymine-thymine cyclobutane dimer to digest its nascent transcript, and CSB counteracted this transcript shortening action of transcription factor IIS. Thus a deficiency in transcription elongation may contribute to the CS phenotype.

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Section: Biochemistry: Selby and Sancarcontrasting

confidence: 85%

“…It has been proposed that TFIIS acts as a TRC factor (25)(26)(27). TFIIS causes RNAPII stalled at a TϽϾT to digest its nascent transcript by several nucleotides (24).…”

Section: Biochemistry: Selby and Sancarmentioning

confidence: 99%

Cockayne syndrome group B protein enhances elongation by RNA polymerase II

Selby

Sancar²

1997

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

282

178

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“…The Mfd protein also termed TRCF (transcription-repair coupling factor) releases the RNA polymerase and the truncated transcript from the DNA in an ATP dependent manner allowing repair of the DNA damage by attracting NER factors particularly UvrA [26]. In the yeast S. cerevisiae, TC-NER involves the mfd counterpart encoded by the Rad26 gene [27]. Similar to the bacterial TC-NER, evidence has been presented in yeast that in some situations, a damage-arrested RNA polymerase might be released from the template by a mechanism that leads to its ubiquitylation and degradation [28].…”

Section: Transcription-coupled Nucleotide Excision Repair Requires Spmentioning

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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“…CSB gene is also known as ERCC6, which can complement the UV sensitivity of rodent UV-sensitive mutants belonging to complementation group 6 (6). General conservation of the core mechanisms of NER between mammalian cells and budding yeast prompted researchers to search for yeast counterparts of these TCR-related genes, and RAD28 and RAD26 have been identified as CSA and CSB homologs, respectively (7,8). Strangely, however, Rad26 but not Rad28 is involved in TCR of this organism.…”

mentioning

confidence: 99%

Transcription Dependence and the Roles of Two Excision Repair Pathways for UV Damage in Fission Yeast Schizosaccharomyces pombe

Yasuhira

Morimyo

Yasui

1999

Journal of Biological Chemistry

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Fission yeasts Schizosaccharomyces pombe possess two types of excision repair systems for UV-induced DNA damage, nucleotide excision repair (NER) and UVdamaged DNA endonuclease (UVDE)-dependent excision repair (UVER). Despite its high efficiency in damage removal, UVER defects have less effect on UV survival than NER defects. To understand the differential roles of two pathways, we examined strand-specific damage removal at the myo2 and rpb2 loci. Although NER removes cyclobutane pyrimidine dimers from the transcribed strand more rapidly than from the nontranscribed strand, UVER repairs cyclobutane pyrimidine dimers equally on both strands and at a much higher rate than NER. The low rate of damage removal from the nontranscribed strand in the absence of UVER indicates inefficient global genome repair (GGR) in this organism and a possible function of UVER as an alternative to GGR. Disruption of rhp26, the S. pombe homolog of CSB/ RAD26, eliminated the strand bias of NER almost completely and resulted in a significant increase of UV sensitivity of cells in a uvde⌬ background. We suggest that the combination of transcription-coupled repair of NER and rapid UVER contributes to UV survival in growing S. pombe cells, which is accomplished by transcriptioncoupled repair and GGR in other organisms.

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RAD26, the functional S. cerevisiae homolog of the Cockayne syndrome B gene ERCC6.

Cited by 234 publications

References 56 publications

Cockayne syndrome group B protein enhances elongation by RNA polymerase II

Cockayne syndrome group B protein enhances elongation by RNA polymerase II

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

Transcription Dependence and the Roles of Two Excision Repair Pathways for UV Damage in Fission Yeast Schizosaccharomyces pombe

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