Transformation of the Hprt gene with DNA from spermatogenic cells. Implications for the evolution of X chromosome inactivation.
DNA-mediated transformation of hypoxanthine guanine phosphoribosyl transferase (HPRT)-deficient cells was used to assess the state of the chromosome Hprt gene in spermatogenic cells. It had been shown previously that DNA from the inactive X chromosome of somatic cells functions poorly or not at all in HPRT transformation, indicating that DNA modification is involved in somatic cell X chromosome inactivation (XCI). In contrast, DNA from mature sperm does function in HPRT transformation suggesting that DNA modification may not be the basis of XCI in mature sperm. In this paper, transformation of HPRT- mouse and hamster cells has been performed to test the nature of XCI during earlier stages of spermatogenesis. DNA from these developing murine germ cells was shown to be capable of HPRT transformation, extending the observation that XCI in sperm does not appear to involve a DNA modification. We also show here that DNA from mature sperm of marsupials functions in HPRT transformation, a result consistent with a role for sperm XCI in the evolution of somatic X inactivation.
D000818:Animals; D004247:DNA / Q000235:genetics / Q000302:isolation & purification; D004274:DNA, Recombinant / Q000378:metabolism*; D005260:Female; D005796:Genes; D007041:Hypoxanthine Phosphoribosyltransferase / Q000172:deficiency / Q000235:genetics*; D007739:L Cells / Q000201:enzymology; D008099:Liver / Q000201:enzymology; D008297:Male; D008394:Marsupialia; D051379:Mice; D013090:Spermatocytes / Q000201:enzymology*; D013091:Spermatogenesis; D014960:X Chromosome / Q000502:physiology*
D004274:DNA, Recombinant; D004247:DNA; D007041:Hypoxanthine Phosphoribosyltransferase