Phenotypic heterogeneity in nucleotide excision repair mutants of rodent complementation groups 1 and 4 (Articolo in rivista)

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  • Phenotypic heterogeneity in nucleotide excision repair mutants of rodent complementation groups 1 and 4 (Articolo in rivista) (literal)
Anno
  • 1997-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1016/S0921-8777(96)00048-1 (literal)
Alternative label
  • Busch D.B.; Van Vuuren H.; De Wit J.; Collins A.; Zdzienicka M.Z.; Mitchell D.L.; Brookman K.W.; Stefanini M.; Riboni R.; Thompson L.H.; Albert R.B.; Van Gool A.J.; Hoeijmakers J. (1997)
    Phenotypic heterogeneity in nucleotide excision repair mutants of rodent complementation groups 1 and 4
    in Mutation research. DNA repair (Print)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Busch D.B.; Van Vuuren H.; De Wit J.; Collins A.; Zdzienicka M.Z.; Mitchell D.L.; Brookman K.W.; Stefanini M.; Riboni R.; Thompson L.H.; Albert R.B.; Van Gool A.J.; Hoeijmakers J. (literal)
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  • 91 (literal)
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  • 106 (literal)
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  • 383 (literal)
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  • 2 (literal)
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  • Scopu (literal)
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  • Dept. Environ. Toxicologic Pathol., Armed Forces Institute of Pathology, Washington, DC 20306-6000, United States; Afdeling Haematologie, Academisch Ziekenhuis Utrecht, Heidelberglaan 100, 3584 CX Utrecht, Netherlands; Dept. of Cell Biology and Genetics, MGC Erasmus University, PO Box 1738, 3000 DR Rotterdam, Netherlands; Boyd Orr Research Centre, University of Aberdeen, Rowett Research Institute, Greenburn Road, Bucksburn, Aberdeen AB2 9SB, United Kingdom; Dept. Genet., Radiat. Genet. C., MGC Leiden Univ. J.A. Cohen Inst., Interuniv. Res. Inst. R., Wassenaarseweg 72, 2300 RA Leiden, Netherlands; Science Park Research Division, MD Anderson Cancer Center, PO Box 389, Smithville, TX 78957, United States; Biomedical Sciences Division, Lawrence Livermore Natl. Laboratory, PO Box 5507, Livermore, CA 94550, United States; Cons. Natl. Ric.-Ist. Genet. B., via Abbiategrasso 207, 27100 Pavia, Italy; ICRF Claire Hall Laboratories, South Mimms, Herts EN6 3LD, United Kingdom (literal)
Titolo
  • Phenotypic heterogeneity in nucleotide excision repair mutants of rodent complementation groups 1 and 4 (literal)
Abstract
  • Rodent ultraviolet light (UV)-sensitive mutant cells in complementation groups (CGs) 1 and 4 normally are known for their extraordinary (~80-100 x) sensitivity to mitomycin C (MMC), although some CG1 mutants with reduced MMC sensitivity were previously reported (Stefanini et al. (1987) Cytotechnology 1, 91). We report here new CG1 and CG4 mutants with only 1.6-10 x wild-type MMC sensitivity despite low unscheduled DNA synthesis (UDS) levels. Mutant UV140, in UV CG4, has ~3.8 x the UV sensitivity of parental line AA8, ~1.6 x wild-type MMC sensitivity, wild-type X-ray and ethyl methanesulfonate (EMS) sensitivity, and is only slightly (~1.4 x) hypermutable to 8-azaadenine resistance by UV light, It has moderately decreased Incision of UV-damaged DNA, has moderately decreased removal of (6-4) photoproducts, and is profoundly deficient in UDS after UV. After UV, it shows abnormally decreased DNA synthesis and persistently decreased RNA synthesis. In addition a cell-free extract of this mutant displays strongly reduced nucleotide excision repair synthesis using DNA treated with N-acetoxy-acetyl-amino-fluorene (AAF). The extract selectively fails to complement extracts of group 1 and 4 mutants consistent with the notion that the affected proteins, ERCC1 and ERCC4, are part of the same complex and that mutations in one subunit also affect the other component. Mutant UV212 is a CG1 mutant with ~3.3 x wild-type UV and ~5-10 x wild-type MMC sensitivity, with profoundly deficient UDS and hypermutability (~5.8 x) by UV, Mutant UV201, probably in CG1, is only slightly (~1.5 x) UV-sensitive and has near wild-type (1.02 x) UV mutability. These unusual group 1 and 4 mutants demonstrate that the unique UV and MMC sensitivity phenotypes displayed by these groups can be separated and support the idea that they are the result of distinct repair functions of the corresponding ERCC1 and ERCC4 genes: nucleotide excision repair for UV lesions and a separate repair pathway for removal of interstrand crosslinks. (literal)
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