Arrest of spermatogenesis and defective breast development in mice lacking A-myb

  • Antonio Toscani
  • , Richard V. Mettus
  • , Robert Coupland
  • , Henry Simpkins
  • , Judith Litvin
  • , Joanne Orth
  • , Kimi S. Hatton
  • , E. Premkumar Reddy

Research output: Contribution to journalArticlepeer-review

194 Scopus citations

Abstract

The Myb gene family currently consists of three members, named A-, B- and c-myb. These genes encode nuclear proteins that bind DNA in a sequence- specific manner and function as regulators of transcription. In adult male mice, A-myb is expressed predominantly in male germ cells. In female mice, A-myb is expressed in breast ductal epithelium, mainly during pregnancy- induced ductal branching and alveolar development. We report here that mice homozygous for a germline mutation in A-myb develop to term but show defects in growth after birth and male infertility due to a block in spermatogenesis. Morphological examination of the testes of A-myb(-/-) males revealed that the germ cells enter meiotic prophase and arrest at pachytene. In adult homozygous null A-myb female mice, the breast epithelial compartment showed underdevelopment of breast tissue following pregnancy and the female mice were unable to nurse their newborn pups. These results demonstrate that A-myb plays a critical role in spermatogenesis and mammary gland development.

Original languageEnglish
Pages (from-to)713-717
Number of pages5
JournalNature
Volume386
Issue number6626
DOIs
StatePublished - 17 Apr 1997
Externally publishedYes

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