Regulation of the Saccharomyces cerevisiae DNA repair gene RAD16

Bang, Dang Duong; Timmermans, V.; Verhage, Richard A.; Zeeman, Anne‐Marie; Putte, Pieter van de; Brouwer, Jaap

doi:10.1093/nar/23.10.1679

Cited by 26 publications

(21 citation statements)

References 44 publications

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“…The targets of the checkpoint that are responsible for this effect are not yet known, but potential candidates include the NER factors Rad2, Rad7, Rad16, and Rad23 (6,25,31,46). In contrast, the checkpoint appears to function in TC-NER primarily via modification of repair factors, since inhibition of new protein synthesis via cycloheximide treatment had little or no effect on this repair pathway.…”

Section: Discussionmentioning

confidence: 99%

A Role for Checkpoint Kinase-Dependent Rad26 Phosphorylation in Transcription-Coupled DNA Repair in Saccharomyces cerevisiae

Täschner

Harreman

Teng

et al. 2010

Molecular and Cellular Biology

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Section: Discussionmentioning

confidence: 99%

A Role for Checkpoint Kinase-Dependent Rad26 Phosphorylation in Transcription-Coupled DNA Repair in Saccharomyces cerevisiae

Täschner

Harreman

Teng

et al. 2010

Molecular and Cellular Biology

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“…The deletion mutants for these strains show an intermediate sensitivity to UV light and the gene products are thought to play an accessory role in NER (Prakash et al,1993). A number of studies show that the phenotypes of rad7 and rad16 mutants are almost indistinguishable, one of the few differences being the RAD16 gene's induction in response to heat shock (Bang et al, 1995). Terleth et al (1990) showed that both RAD7 and RAD16 were required for the repair of CPDs from the transcriptionally inactive HMLa locus.…”

Section: Discussionmentioning

confidence: 99%

Excision repair at the level of the nucleotide in the Saccharomyces cerevisiae MFA2 gene: mapping of where enhanced repair in the transcribed strand begins or ends and identification of only a partial rad16 requisite for repairing upstream control sequences

Teng

Waters

et al. 1997

Journal of Molecular Biology

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“…There is no homology between the RAD7 (565 codons) and RAD23 (398 codons) at the amino acid sequence level, however. Like the RAD2 gene, which is indispensable for NER, the RAD7, RAD16, and RAD23 genes (but not other RAD genes required for NER) are transcriptionally up-regulated when cells are exposed to UV radiation (1,12,13,23).The partial UV radiation-sensitive phenotype of rad7 and rad16 mutants may relate to the observation that these genes are uniquely required for NER in certain transcriptionally repressed regions of DNA. Both rad16 (2) and rad7 (28,36) mutants are defective in the excision of pyrimidine dimers from the transcriptionally silent HML␣ and HMRa matingtype locus, yet they support efficient repair of the transcriptionally active MAT␣ locus.…”

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The RAD7, RAD16, and RAD23 Genes of Saccharomyces cerevisiae: Requirement for Transcription-Independent Nucleotide Excision Repair In Vitro and Interactions between the Gene Products

Wang

Wei

Reed

et al. 1997

Molecular and Cellular Biology

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Nucleotide excision repair (NER) is a biochemical process required for the repair of many different types of DNA lesions. In the yeast Saccharomyces cerevisiae, the RAD7, RAD16, and RAD23 genes have been specifically implicated in NER of certain transcriptionally repressed loci and in the nontranscribed strand of transcriptionally active genes. We have used a cell-free system to study the roles of the Rad7, Rad16, and Rad23 proteins in NER. Transcription-independent NER of a plasmid substrate was defective in rad7, rad16, and rad23 mutant extracts. Complementation studies with a previously purified NER protein complex (nucleotide excision repairosome) indicate that Rad23 is a component of the repairosome, whereas Rad7 and Rad16 proteins were not found in this complex. Complementation studies with rad4, rad7, rad16, and rad23 mutant extracts suggest physical interactions among these proteins. This conclusion was confirmed by experiments using the yeast two-hybrid assay, which demonstrated the following pairwise interactions: Rad4 with Rad23, Rad4 with Rad7, and Rad7 with Rad16. Additionally, interaction between the Rad7 and Rad16 proteins was demonstrated in vitro. Our results show that Rad7, Rad16, and Rad23 are required for transcription-independent NER in vitro. This process may involve a unique protein complex which is distinct from the repairosome and which contains at least the Rad4, Rad7, and Rad16 proteins.Nucleotide excision repair (NER) in eukaryotic cells is a complex biochemical process involving multiple gene products (see references 8 and 9 for reviews). By using a cell-free system that faithfully mirrors the genetic requirements for NER in the yeast Saccharomyces cerevisiae, it has been directly demonstrated that at least nine proteins are indispensable for this process (25,30,31,34). Disruption or deletion of the RAD1, RAD2, RAD4, and RAD14 genes confers extreme sensitivity of cells to killing by UV radiation, and cell extracts of such mutants are defective in NER (reviewed in reference 9). Similarly, cells carrying mutations in the essential genes RAD3, SSL1, SSL2 (RAD25), TFB1, and TFB2, all of which encode subunits of the RNA polymerase II basal transcription factor IIH (TFIIH), which is required both for transcription and NER (6,7,10,25,30,31), are also defective in NER in vitro (6,30,31).Mutational inactivation of the RAD7, RAD16, or RAD23 genes confers partial sensitivity to UV radiation (20,22,37), and such cells have been reported to retain residual capacity for excision of pyrimidine dimers following exposure to UV light (16-18, 21, 28, 37). Strains carrying mutations in both the RAD7 and RAD16 genes are no more sensitive than either single mutant (28), suggesting that the Rad7 and Rad16 proteins operate in the same biochemical pathway. The RAD7 and RAD23 genes are located immediately adjacent to the highly conserved cytochrome c genes CYC1 (RAD7) and CYC7 (RAD23) on yeast chromosomes X and V, respectively, and it has been suggested that these regions may have arisen by gene duplication (...

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Regulation of the Saccharomyces cerevisiae DNA repair gene RAD16

Abstract: The RAD16 gene product has been shown to be essential for the repair of the silenced mating type loci [Bang et al. (1992)

Cited by 26 publications

References 44 publications

A Role for Checkpoint Kinase-Dependent Rad26 Phosphorylation in Transcription-Coupled DNA Repair in Saccharomyces cerevisiae

A Role for Checkpoint Kinase-Dependent Rad26 Phosphorylation in Transcription-Coupled DNA Repair in Saccharomyces cerevisiae

Excision repair at the level of the nucleotide in the Saccharomyces cerevisiae MFA2 gene: mapping of where enhanced repair in the transcribed strand begins or ends and identification of only a partial rad16 requisite for repairing upstream control sequences

The RAD7, RAD16, and RAD23 Genes of Saccharomyces cerevisiae: Requirement for Transcription-Independent Nucleotide Excision Repair In Vitro and Interactions between the Gene Products

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