Specific gene mutations in L5178Y cells in culture.

@article{Clive1983SpecificGM,
  title={Specific gene mutations in L5178Y cells in culture.},
  author={D. Clive and R. McCuen and J. Spector and C. Piper and K. Mavournin},
  journal={Mutation research},
  year={1983},
  volume={115 2},
  pages={
          225-51
        }
}
The predominant test system uses a near-diploid L5178Y mouse lymphoma cell line and is based on the quantitation of forward mutations occurring at the heterozygous thymidine kinase (TK) locus (TK+/- leads to TK-/-). (Other markers, such as ouabain- or methothrexate-resistance and alanine independence, in other L5178Y mouse lymphoma cells were also examined, but our criteria for the acceptability of data or the paucity of data considerably reduced the value of these mutagenesis test systems to… Expand
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References

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Evidence for chemically-induced structural gene mutations at the thymidine kinase locus in cultured L5178Y mouse lymphoma cells.
TLDR
Findings were incompatible with a non-mutational model for the production of these stable variants and, in conjunction with reversion-rate data, they tended to favor either direct structural gene modifications or mutations affecting the expression of adult and fetal enzymes. Expand
A mutational assay system for L5178Y mouse lymphoma cells, using hypoxanthine-guanine-phosphoribosyl-transferase (HGPRT) -deficiency as marker. The occurrence of a long expression time for mutations induced by X-rays and EMS.
TLDR
The development of a system for the detection of somatic cell mutation to hypoxanthine-guanine-phosphoribosyl-transferase (HGPRT) and the selection of mutant cells was not influenced by the concentration of the selective agent 6-thioguanine, and the optimal expression time for TGr-resistant mutants in L5178Y cells was 6 to 7 days. Expand
A mutational assay system using the thymidine kinase locus in mouse lymphoma cells.
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An estimate can be made of the relative mutagenicities of various treatments of the TK locus and the observed induced mutation rates with the spontaneous TK +/− → TK −/− mutation rate. Expand
Cytogenetic analysis of the L5178Y/TK+/− → TK−/− mouse lymphoma mutagenesis assay system
TLDR
It seems likely that λ and σ mutants result from 2 different mutational mechanisms that may be distinguished on the basis of mutant colony morphology, possibly related to the type of chromosomal damage sustained. Expand
Validation and characterization of the L5178Y/TK+/- mouse lymphoma mutagen assay system.
TLDR
Characterization of the TK-/- mutants suggests that two mutagenic mechanisms contribute to their final yield, and is consistent with the induction of slow-growing specific locus mutants by a chromosomal mechanism and their subsequent dilution during this long expression time. Expand
Ethyl methanesulphonate mutagenesis with L5178Y mouse lymphoma cells: a comparison of ouabain, thioguanine and excess thymidine resistance.
TLDR
Using induced mutation frequencies at optimum expression times, equal EMS treatments yielded substantially more variants resistant to thioguanine than to ouabain, suggested that this difference may have origin in possible constraints in the classes of mutants which are permissible in a vital function, maintenance of the Na+/K+ balance, when compared with a non-vital function, salvage purine biosynthesis. Expand
Detection of chemical mutagens using a host-mediated assay (L5178Y) mutagenesis system.
TLDR
Dose-response experiments showed that the increase in mutant frequency was a function of the levels of the mutagen employed, and Mutant induction in the host was obtained without loss of viability of target cells or weight loss of the animals. Expand
Chemically induced mutation of L-5178Y mouse leukemia cells from asparagine-dependence to asparagine-independence.
TLDR
The mutability of this easily assayed nutritional genetic marker in a cell line that can be grown either in vitro or in vivo may provide a useful system for assay of other agents of unknown mutagenic potential. Expand
Isolation of nutrient deficient mutants and quantitative mutation assay by reversion of alanine-requiring L5178Y cells.
TLDR
A quantitative mutation assay system for the reversion of L5178Y-Ala 32 cells from auxotrophy to prototropy was established and the system was applied to some known mutagens, MNNG, 4-NQO, UV and gamma-rays. Expand
Bromodeoxyuridine resistance induced in mouse lymphoma cells by microsomal activation of dimethylnitrosamine.
TLDR
The locus is extremely sensitive to mutagenesis by DMN compared with other known mutagens at similar levels of cell survival, but exerts both mutagenic and toxic effects when incubated in a microsome reaction mixture. Expand
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