Genetic instability at the adenine phosphoribosyltransferase locus in mouse L cells

J. A. Tischfield, J. J. Trill, Y. I. Lee, K. Coy, M. W. Taylor

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

Abstract

Resistance to adenine analogs such as 2,6-diaminopurine occurs at a rate of H~ 10-3 per cell per generation in mouse L cells. This resistance is associated with a loss of detectable adenine phosphoribosyltransferase activity. Other genetic loci in L cells have the expected mutation frequency (~10-6). Transformation of L cell mutants with Chinese hamster ovary cell DNA results in transformants with adenine phosphoribosyltransferase activity characteristic of Chinese hamster ovary cells. No activation of the mouse gene occurs on hybridization with human fibroblasts. That this high frequency event is the result of mutation rather than an epigenetic event is supported by antigenic and reversion studies of the 2,6-diaminopurine-resistant clones. These results are consistent with either a mutational hot-spot, a locus specific mutator gene, or a site of integration of an insertion sequence.

Original languageEnglish (US)
Pages (from-to)250-257
Number of pages8
JournalUnknown Journal
Volume2
Issue number3
DOIs
StatePublished - 1982
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

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