Selective repair of specific chromatin domains in UV-irradiated cells from xeroderma pigmentosum complementation group C

Kantor, George J.; Barsalou, Linda; Hanawalt, Philip C.

doi:10.1016/0921-8777(90)90071-c

Cited by 92 publications

(48 citation statements)

References 19 publications

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“…Venema and co-workers (34) found that the residual repair capacity in XP-C was highly selective for active genes. Similar results were obtained in our laboratory; we noted very rapid repair in the active ,-actin and DHFR genes but poor repair in a silent sequence from the inactive X chromosome (35). In contrast, the cells from CS patients are selectively deficient in the repair of active genes.…”

Section: Models To Explain Finestructure Heterogeneity In Dna Repairsupporting

confidence: 77%

Role of Transcription-Coupled DNA Repair in Susceptibility to Environmental Carcinogenesis

Hanawalt¹

1996

Environmental Health Perspectives

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Section: Models To Explain Finestructure Heterogeneity In Dna Repairsupporting

confidence: 77%

Role of Transcription-Coupled DNA Repair in Susceptibility to Environmental Carcinogenesis

Hanawalt¹

1996

Environmental Health Perspectives

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“…The reversed situation exists in rodent cells and in human XPC cell lines that remove dimers in only a relatively small part of the genome. In these cells, transcribed strands of active DNA are repaired efficiently, whereas dimers in the remainder of the genome are not removed, which results in only a modest UV sensitivity of these cell types (3,12,18,46,47). Preferential repair of the transcribed strand has been shown to exist in the yeast Saccharomyces cerevisiae for the URA3 gene on a minichromosome (33), for the chromosomal as well as episomal RPB2 gene (34), and for the transcriptionally induced GAL7 gene (13).…”

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confidence: 99%

The RAD7 and RAD16 genes, which are essential for pyrimidine dimer removal from the silent mating type loci, are also required for repair of the nontranscribed strand of an active gene in Saccharomyces cerevisiae.

Verhage¹,

Zeeman²,

Groot³

et al. 1994

Mol. Cell. Biol.

179

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Nucleic Acids Res. 20:3925-3931, 1992). Here we show that rad7 as well as rad7 rad16 double mutants have the same repair phenotype, indicating that the RAD7 and RAD16 gene products might operate in the same nucleotide excision repair subpathway. Dimer removal from the genome overall is essentially incomplete in these mutants, leaving about 20 to 30%Yo of the DNA unrepaired. Repair analysis of the transcribed RPB2 gene shows that the nontranscribed strand is not repaired at all in rad7 and radl6 mutants, whereas the transcribed strand is repaired in these mutants at a fast rate similar to that in RAD' cells. When the results obtained with the RPB2 gene can be generalized, the RAD7 and RAD16 proteins not only are essential for repair of silenced regions but also function in repair of nontranscribed strands of active genes in S. cerevisiae. The phenotype of rad7 and radl16 mutants closely resembles that of human xeroderma pigmentosum complementation group C (XP-C) cells, suggesting that RAD7 and RAD16 in S. cerevisiae function in the same pathway as the XPC gene in human cells. RAD4, which on the basis of sequence homology has been proposed to be the yeast XPC counterpart, seems to be involved in repair of both inactive and active yeast DNA, challenging the hypothesis that RAD4 and XPC are functional homologs.

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“…In normal human cells (2,3), Escherichia coli (4), and Saccharomyces cerevisiae (5)(6)(7)(8), both strands of active genes are repaired, but CPDs are removed more rapidly from the transcribed strands than from the nontranscribed strands. In rodent cell lines (2), in human xeroderma pigmentosum (XP) group C cell lines (3,9,10), and in mutant rad7 and radl6 S. cerevisiae strains (11), CPDs are removed from the transcribed strands of genes, while repair in nontranscribed DNA is inefficient. Conversely, mutations in the E. coli mfd gene (12), the human Cockayne syndrome (CS) group A and B genes (13), and the S. cerevisiae CS-B gene homolog (14) abolish transcription-coupled repair without significantly influencing repair of nontranscribed DNA; repair in transcribed and nontranscribed DNA occurs at similar rates.…”

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Products of DNA mismatch repair genes mutS and mutL are required for transcription-coupled nucleotide-excision repair of the lactose operon in Escherichia coli.

Mellon

Champe²

1996

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

160

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To improve our understanding of the mechanism that couples nucleotide-excision repair to transcription in expressed genes, we have examined the effects of mutations in several different DNA repair genes on the removal of cyclobutane pyrimidine dimers from the individual strands of the induced lactose operon in UV-irradiated Escherichia coli. As expected, we found little repair in either strand of the lactose operon in strains with mutations in established nucleotide excision-repair genes (uvrA, uvrB, uvrC, or uvrD). In contrast, we found that mutations in either of two genes required for DNA-mismatch correction (mutS and mutL) selectively abolish rapid repair in the transcribed strand and render the cells moderately sensitive to UV irradiation. Similar results were found in a strain with a mutation in the mfd gene, the product of which has been previously shown to be required for transcription-coupled repair in vitro. Our results demonstrate an association between mismatch-correction and nucleotide-excision repair and implicate components of DNAmismatch repair in transcription-coupled repair. In addition, they may have important consequences for human disease and may enhance our understanding of the etiology of certain cancers which have been associated with defects in mismatch correction.The selective removal of DNA damage from the transcribed strands of active genes, termed transcription-coupled nucleotide excision repair, may be ubiquitous and has been clearly demonstrated for the removal of UV light-induced cyclobutane pyrimidine dimers (CPDs) (1). In normal human cells (2, 3), Escherichia coli (4), and Saccharomyces cerevisiae (5-8), both strands of active genes are repaired, but CPDs are removed more rapidly from the transcribed strands than from the nontranscribed strands. In rodent cell lines (2), in human xeroderma pigmentosum (XP) group C cell lines (3, 9, 10), and in mutant rad7 and radl6 S. cerevisiae strains (11), CPDs are removed from the transcribed strands of genes, while repair in nontranscribed DNA is inefficient. Conversely, mutations in the E. coli mfd gene (12), the human Cockayne syndrome (CS) group A and B genes (13), and the S. cerevisiae CS-B gene homolog (14) abolish transcription-coupled repair without significantly influencing repair of nontranscribed DNA; repair in transcribed and nontranscribed DNA occurs at similar rates. Clearly, transcription can increase the efficiency of nucleotideexcision repair (NER), transcription-coupled repair can take place even in the absence of overall repair, and there appear to be additional factors that target components of NER to certain lesions present in the transcribed strands of genes.The precise mechanism of transcription-coupled repair in both prokaryotes and eukaryotes is unclear. Several studies indicate that an initial signal is provided by the RNA poly- (12,19) have demonstrated that it is required for transcription-coupled repair in an in vitro system, and the products of the CS genes in human cells are possible candidates for co...

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Selective repair of specific chromatin domains in UV-irradiated cells from xeroderma pigmentosum complementation group C

Cited by 92 publications

References 19 publications

Role of Transcription-Coupled DNA Repair in Susceptibility to Environmental Carcinogenesis

Role of Transcription-Coupled DNA Repair in Susceptibility to Environmental Carcinogenesis

The RAD7 and RAD16 genes, which are essential for pyrimidine dimer removal from the silent mating type loci, are also required for repair of the nontranscribed strand of an active gene in Saccharomyces cerevisiae.

Products of DNA mismatch repair genes mutS and mutL are required for transcription-coupled nucleotide-excision repair of the lactose operon in Escherichia coli.

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