Germ-line intrachromosomal recombination restores fertility in transgenic MyK-103 male mice

Thomas M Wilkie, Robert E. Braun, Walter J. Ehrman, Richard D. Palmiter, Robert E Hammer

Research output: Contribution to journalArticle

23 Scopus citations

Abstract

Males of the MyK-103 line of transgenic mice are fertile and sire litters of normal size, but they never transmit the transgene, whereas females transmit the transgene with normal frequency. The chromosome originally bearing the transgene can be transmitted through the male germ line, but only after the transgene is deleted or rearranged by intrachromosomal recombination. The transgene encodes a functional herpes simplex virus (HSV) thymidine kinase gene that causes sperm infertility when expressed in postmeiotic germ cells. Immunocytochemistry revealed clones of germ cells that fail to express HSV thymidine kinase. We postulate that these cells arose by transgene deletion in embryonic germ cells and postnatal spermatogonial stem cells and that they are responsible for the normal fertility of MyK-103 males. The frequency of recombination events at the integration locus suggests that it contains a hotspot for mitotic recombination.

Original languageEnglish (US)
Pages (from-to)38-48
Number of pages11
JournalGenes and Development
Volume5
Issue number1
DOIs
StatePublished - Jan 1 1991

Keywords

  • recombinational hotspot
  • spermatogonial stem cell
  • transmission ratio distortion

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

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