Mutations causing deficiency of APRT in fibroblasts cultured from human heterozygous for mutant APRT alleles

Somatic Cell Genet. 1982 Jan;8(1):115-41. doi: 10.1007/BF01538655.

Abstract

Frequent mutation to adenine analog resistance in diploid human cells reflected heterozygosity for recessive alleles affecting expression of the adenine phosphoribosyltransferase (APRT) locus. Cells from both parents of APRT-deficient sibs were heterozygous and had rates of spontaneous mutation to 2,6-diaminopurine (DAP) resistance of 6.0 x 10(-5) and 16 x 10(-5) per cell generation. Spontaneous DAP-resistant mutants were not observed in cultures of homozygous cells. Almost all mutants of proven heterozygous cultures were APRT deficient and could not use adenine for growth. Frequent DAP-resistant mutations identified heterozygous strain 438, which carried an allele encoding a partially defective form of APRT. All DAP-resistant mutants of strain 438 were partially APRT deficient and could use adenine for growth. The frequency of MNNG-induced DAP-resistant mutants in homozygous strains was approximately the square of the induced frequency in heterozygous strains.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 2-Aminopurine / analogs & derivatives
  • 2-Aminopurine / pharmacology
  • Adenine Phosphoribosyltransferase / deficiency
  • Adenine Phosphoribosyltransferase / genetics*
  • Drug Resistance
  • Humans
  • Methylnitronitrosoguanidine / pharmacology
  • Mutation
  • Pentosyltransferases / genetics*

Substances

  • Methylnitronitrosoguanidine
  • 2-Aminopurine
  • 2,6-diaminopurine
  • Pentosyltransferases
  • Adenine Phosphoribosyltransferase