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  • 1
    Electronic Resource
    Electronic Resource
    The levels of repair of endonuclease III-sensitive sites, 6-4 photoproducts and cyclobutane pyrimidine dimers differ in a point mutant forRAD14, theSaccharomyces cerevisiae homologue of the human gene defective inXPA patients (1996)
    Springer
    Molecular genetics and genomics 250 (1996), S. 515-522 
    Details
    ISSN: 1617-4623
    Keywords: Saccharomyces cerevisiae ; Nucleotide excision repair ; RAD14 ; XPA homologue
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract In the accompanying paper we demonstrated that endonuclease III-sensitive sites in theMATα andHMLα loci ofSaccharomyces cerevisiae are repaired by the Nucleotide Excision Repair (NER) pathway. In the current report we investigated the repair of endonuclease III sites, 6-4 photoproducts and cyclobutane pyrimidine dimers (CPDs) in arad14-2 point mutant and in arad14 deletion mutant. TheRAD14 gene is the yeast homologue of the human gene that complements the defect in cells from xeroderma pigmentosum (XP) patients belonging to complementation group A. In the point mutant we observed normal repair of endonuclease III sites (i.e. as wild type), but no removal of CPDs at theMATα andHMLα loci. Similar experiments were undertaken using the recently createdrad14 deletion mutant. Here, neither endonuclease III sites nor CPDs were repaired inMAT a orHMR a. Thus the point mutant appears to produce a gene product that permits the repair of endonuclease III sites, but prevents the repair of CPDs. Previously it was found that, in the genome overall, repair of 6-4 photoproducts was less impaired than repair of CPDs in the point mutant. The deletion mutant repairs neither CPDs nor 6-4 photoproducts in the genome overall. This finding is consistent with the RAD14 protein being involved in lesion recognition in yeast. A logical interpretation is that therad14-2 point mutant produces a modified protein that enables the cell to repair endonuclease III sites and 6-4 photoproducts much more efficiently than CPDs. This modified protein may aid studies designed to elucidate the role of the RAD14 protein in lesion recognition.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02174040
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  • 2
    Electronic Resource
    Electronic Resource
    UV-induced endonuclease III-sensitive sites at the mating type loci inSaccharomyces cerevisiae are repaired by nucleotide excision repair: RAD7 and RAD16 are not required for their removal fromHMLα (1996)
    Springer
    Molecular genetics and genomics 250 (1996), S. 505-514 
    Details
    ISSN: 1617-4623
    Keywords: DNA repair ; Nucleotide excision repair ; Saccharomyces cerevisiae
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Ultraviolet irradiation of DNA induces cyclobutane pyrimidine dimers (CPDs), 6-4′-(pyrimidine 2′-one) pyrimidines and pyrimidine hydrates. The dimer is the major photoproduct, and is specifically recognized by endonuclease V of phage T4. Pyrimidine hydrates represent a small fraction of the total photoproducts, and are substrates for endonuclease III ofEscherichia coli. We used these enzymes to follow the fate of their substrates in the mating type loci ofSaccharomyces cerevisiae. In a RAD strain, CPDs in the transcriptionally activeMATα locus are preferentially repaired relative to the inactiveHMLα locus, whilst repair of endonuclease III-sensitive sites is not preferential. Therad1, 2, 3 and4 mutants, which lack factors that are essential for the incision step of nucleotide excision repair (NER), repair neither CPDs nor endonuclease III-sensitive sites, clearly showing that these lesions are repaired by the NER pathway. Previously it had been shown that the products of theRAD7 andRAD16 genes are required for the NER of CPDs from theHMLα locus. We show that, in the same locus, these gene products are not needed for removal of endonuclease III-sensitive sites by the same mechanism. This indicates that the components required for NER differ depending on either the type of lesion encountered or on the specific location of the lesion within the genome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02174039
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    Paper (German National Licenses)
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