Molecular analysis of HPRT1(+) somatic cell hybrids derived from a carrier of an HPRT1 mutation responsible for Lesch-Nyhan syndrome

Am J Med Genet. 2001 Sep 15;103(1):48-55. doi: 10.1002/ajmg.1514.

Abstract

Heterozygous carriers of HPRT1 mutations responsible for Lesch-Nyhan syndrome can be detected by analysis of somatic cell hybrids derived from peripheral blood lymphocytes and Hprt1-negative cells of rodent origin followed by selection in culture medium containing hypoxanthine, aminopterine, and thymidine (HAT). The parental origin of the X chromosome containing the normal HPRT1 allele in HPRT1(+) hybrid cell lines can be determined by molecular haplotyping attributable to highly polymorphic X-linked markers. We used this procedure to study a presumed carrier whose paternal active X chromosome always segregated in the cell hybrids derived from her. Conversely, her maternal X chromosome was systematically absent in most cell hybrids, or when present, it was inactive and coexisted with an active, paternal X chromosome. These results clearly demonstrated that the proband was a heterozygous carrier of a mutation responsible for HPRT1 deficiency.

Publication types

  • Case Reports
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Animals
  • DNA / genetics
  • Family Health
  • Female
  • Genetic Carrier Screening / methods
  • Haplotypes
  • Heterozygote*
  • Humans
  • Hybrid Cells
  • Hypoxanthine Phosphoribosyltransferase / deficiency
  • Hypoxanthine Phosphoribosyltransferase / genetics*
  • Lesch-Nyhan Syndrome / enzymology
  • Lesch-Nyhan Syndrome / genetics*
  • Lesch-Nyhan Syndrome / pathology
  • Mutation
  • X Chromosome / genetics

Substances

  • DNA
  • Hypoxanthine Phosphoribosyltransferase