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 and E. Premkumar Reddy
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Antonio Toscani: Temple University School of Medicine
Richard V. Mettus: Temple University School of Medicine
Robert Coupland: Temple University School of Medicine
Henry Simpkins: Temple University School of Medicine
Judith Litvin: Temple University School of Medicine
Joanne Orth: Temple University School of Medicine
Kimi S. Hatton: Temple University School of Medicine
E. Premkumar Reddy: Temple University School of Medicine

Nature, 1997, vol. 386, issue 6626, 713-717

Abstract: Abstract The Myb gene family currently consists of three members, named A-, B- and c-myb1,2. 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 cells2,3. 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.

Date: 1997
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DOI: 10.1038/386713a0

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