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Title: Sister chromatid exchange, DNA repair, and single-gene mutation

Abstract

Sister chromatid exchange (SCE) has been studied in cultured mammalian cells with regard to the nature of the inducing lesion, mutation induction, and factors that modify the observed frequency following mutagen exposure, SCEs can be induced by a wide spectrum of DNA lesions and, for nine agents examined, the frequency of induced SCE is linearly related to induced single-gene mutation. Further, a deficiency in DNA repair may alter the expression of both SCE and mutation in a qualitatively similar manner. The frequency of SCE induced by mitomycin-C is suppressed in heterochromatic relative to euchromatin and, in nondividing lymphocytes, the lesions leading to the formation of SCEs may persist for several months.

Authors:
;
Publication Date:
Research Org.:
Lawrence Livermore National Lab., CA
OSTI Identifier:
6378885
DOE Contract Number:
W-7405-ENG-48
Resource Type:
Journal Article
Resource Relation:
Journal Name: UCLA Symp. Mol. Cell. Biol., New Ser.; (United States)
Country of Publication:
United States
Language:
English
Subject:
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.; ALKYLATING AGENTS; GENETIC EFFECTS; ANIMAL CELLS; SISTER CHROMATID EXCHANGES; BENZANTHRACENE; EMS; IONIZING RADIATIONS; MITOMYCIN; NITROSO COMPOUNDS; PROFLAVINE; ULTRAVIOLET RADIATION; BIOLOGICAL REPAIR; CELL CULTURES; CHROMATIN; DNA; EXPERIMENTAL DATA; GENE MUTATIONS; MUTANTS; UREA; ACRIDINES; AMIDES; AMINES; ANTI-INFECTIVE AGENTS; ANTIBIOTICS; ANTIMITOTIC DRUGS; ANTINEOPLASTIC DRUGS; AROMATICS; AZINES; BIOLOGICAL EFFECTS; BIOLOGICAL RECOVERY; CARBONIC ACID DERIVATIVES; CHROMOSOMAL ABERRATIONS; CONDENSED AROMATICS; DATA; DRUGS; ELECTROMAGNETIC RADIATION; ESTERS; FLAVINES; HETEROCYCLIC COMPOUNDS; HYDROCARBONS; INFORMATION; MUTAGENS; MUTATIONS; NUCLEIC ACIDS; NUMERICAL DATA; ORGANIC COMPOUNDS; ORGANIC NITROGEN COMPOUNDS; ORGANIC SULFUR COMPOUNDS; PYRIDINES; RADIATIONS; RECOVERY; REPAIR; SULFONIC ACID ESTERS; 560301* - Chemicals Metabolism & Toxicology- Cells- (-1987); 560121 - Radiation Effects on Cells- External Source- (-1987)

Citation Formats

Carrano, A.V., and Thompson, L.H. Sister chromatid exchange, DNA repair, and single-gene mutation. United States: N. p., 1982. Web.
Carrano, A.V., & Thompson, L.H. Sister chromatid exchange, DNA repair, and single-gene mutation. United States.
Carrano, A.V., and Thompson, L.H. 1982. "Sister chromatid exchange, DNA repair, and single-gene mutation". United States. doi:.
@article{osti_6378885,
title = {Sister chromatid exchange, DNA repair, and single-gene mutation},
author = {Carrano, A.V. and Thompson, L.H.},
abstractNote = {Sister chromatid exchange (SCE) has been studied in cultured mammalian cells with regard to the nature of the inducing lesion, mutation induction, and factors that modify the observed frequency following mutagen exposure, SCEs can be induced by a wide spectrum of DNA lesions and, for nine agents examined, the frequency of induced SCE is linearly related to induced single-gene mutation. Further, a deficiency in DNA repair may alter the expression of both SCE and mutation in a qualitatively similar manner. The frequency of SCE induced by mitomycin-C is suppressed in heterochromatic relative to euchromatin and, in nondividing lymphocytes, the lesions leading to the formation of SCEs may persist for several months.},
doi = {},
journal = {UCLA Symp. Mol. Cell. Biol., New Ser.; (United States)},
number = ,
volume = ,
place = {United States},
year = 1982,
month = 1
}
  • Sister chromatid exchange (SCE) has been studied in cultured mammalian cells with regard to the nature of the inducing lesion, mutation induction, and factors that modify the observed frequency following mutagen exposure. SCEs can be induced by a wide spectrum of DNA lesions and, for nine agents examined, the frequency of induced SCE is linearly related to induced single-gene mutation. Further, a deficiency in DNA repair may alter the expression of both SCE and mutation in a qualitatively similar manner. The frequency of SCE induced by mitomycin-C is suppressed in heterochromatin relative to euchromatin and, in non-dividing lymphocytes, the lesionsmore » leading to the formation of SCEs may persist for several months.« less
  • The Chinese hamster cell line mutants EM9, which has a reduced ability to repair DNA strand breaks, is noted for its highly elevated frequency of sister chromatid exchange, a property shared with cells from individuals with Bloom's syndrome. The defect in EM9 cells was corrected by fusion hybridization with normal human fibroblasts and by transfection with DNA from hybrid cells. The transformants showed normalization of sister chromatid exchange frequency but incomplete correction of the repair defect in terms of chromosomal aberrations produced by 5-bromo-2-deoxyuridine. 28 references, 1 figure, 1 table.
  • Five UV-sensitive mutant strains of CHO cells representing different genetic complementation groups were analyzed for their ability to perform the incision step of nucleotide excision repair after UV exposure. The assay utilized inhibitors of DNA synthesis to accumulate the short-lived strand breaks resulting from repair incisions. After 6 J/m/sup 2/, each of the mutants showed < 10% of the incision rate of the parental AA8 cells. After 50 J/m/sup 2/, the rate in AA8 was similar to that at 6 J/m/sup 2/, but the rates in the mutants were significantly higher (approx. 20% of the rate of AA8). Thus bymore » this incision assay the mutants were phenotypically indistinguishable. Each of the mutants were hypersensitive to mutation induction at both the hprt and aprt loci by a factor of 10, and in the one strain tested ouabain resistance was induced sevenfold more efficiently than in AA8 cells. Sister chromatid exchange was also induced with sevenfold increased efficiency in the two mutant strains examined. Thus, here CHO mutants resemble xeroderma pigmentosum cells in terms of their incision defects and their hypersensitivity to DNA damage by UV.« less
  • The induction of sister chromatid exchanges (SCE) and mutation at the hypoxanthine-guanine phosphoribosyl transferase locus and toxicities of 40 different chemical and physical agents were examined on Chinese hamster V79 cells. These agents included mono-, di-, tri-, and polyfunctional alkylating agents, intercalators, gamma-rays, and UV light irradiation. Mutation was measured as resistance to 6-thioguanine and toxicity as loss of cell-plating efficiency. SCE were examined 29 hr after treatment. With the agents examined, a highly positive correlation existed between SCE-inducing and mutagenic potencies, when expressed as increase in the number per a unit dose over the control values. But the greatmore » difference of the ratios of mutagenic potencies versus SCE-inducing potencies among agents was observed, the maximal difference in the ratios being about 200-fold. The agents that showed the higher values of the ratio (agents producing more mutations than SCE) were bleomycin, cobalt-60 gamma-rays, all ethylating agents (N-ethyl-N-nitrosourea, N-ethyl-N'-nitro-N-nitrosoguanidine, ethyl methanesulfonate, and diethylsulfate), N-propyl-N-nitrosourea, N-butyl-N-nitrosourea, isopropyl methanesulfonate, intercalating acridine compounds (2-methoxy-6-chloro-9-(3-(ethyl-2-chloroethyl)aminopropylamino)-acridine X 2HCl and 2-methoxy-6-chloro-9-(3-(chloroethyl)-aminopropylamino)acridine 2HCl) and UV light at 254 nm.« less