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

Authors:
  • RMRichard V. Mettus
    Richard V. Mettus
  • RCRobert Coupland
    Robert Coupland
  • HSHenry Simpkins
    Henry Simpkins
  • JLJudith Litvin
    Judith Litvin
  • JOJoanne Orth
    Joanne Orth
  • KHKimi S. Hatton
    Kimi S. Hatton
  • ERE. Premkumar Reddy
    E. Premkumar Reddy
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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.
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