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Chinese hamster cells deficient in ornithine decarboxylase activity: Reversion by gene amplification and by azacytidine treatment

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Somatic Cell and Molecular Genetics

Abstract

A group of Chinese hamster ovary (CHO) cell mutants deficient in ornithine decarboxylase (ODC) activity are described and compared to the prototype mutant reported previously (21). Although all mutants belong to the same complementation group, they can be divided into two classes: those with some residual enzyme activity and those with no activity. All mutants are putrescine auxotrophs, but they differ in their ability to utilize the enzyme's substrate, ornithine, a property which correlates with the amount of residual enzyme activity. The mutants also differ in their frequency of reversion to prototrophy. The leaky mutants revert at a high rate by overproducing a partially defective enzyme by a gene amplification mechanism similar to that leading to the ornithine analog-resistant mutants which have elevated enzyme levels. Spontaneous reversion in the null mutants is rare. However, one null mutant, which was induced with ethyl methane sulfonate and which makes ODC mRNA but no active enzyme, is nevertheless revertible with 5-azacytidine. We conclude that CHO cells are at least diploid at the ODC locus, but that only one allele is active. Further studies suggest the possibility that ethyl methane sulfonate is not just a classical mutagen but may also induce gene inactivations that are revertible by 5-azacytidine.

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Author notes

  1. Carolyn Steglich

    Present address: Department of Microbiology, East Carolina University School of Medicine, 27834, Greenville, North Carolina

Authors and Affiliations

  1. Department of Biology, University of California San Diego, B-022, 92093, La Jolla, California

    Carolyn Steglich, Ann Grens & Immo E. Scheffler

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  1. Carolyn Steglich
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  2. Ann Grens
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  3. Immo E. Scheffler
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Steglich, C., Grens, A. & Scheffler, I.E. Chinese hamster cells deficient in ornithine decarboxylase activity: Reversion by gene amplification and by azacytidine treatment. Somat Cell Mol Genet 11, 11–23 (1985). https://doi.org/10.1007/BF01534730

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  • DOI: https://doi.org/10.1007/BF01534730

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