Stat5a is mandatory for adult mammary gland development and lactogenesis

Xiuwen Liu, Gertraud W. Robinson, Kay Uwe Wagner, Lisa Garrett, Anthony Wynshaw-Boris, Lothar Hennighausen

Research output: Contribution to journalArticle

863 Scopus citations

Abstract

Prolactin (PRL) induces mammary gland development (defined as mammopoiesis) and lactogenesis. Binding of PRL to its receptor leads to the phosphorylation and activation of STAT (signal transducers and activators of transcription) proteins, which in turn promote the expression of specific genes. The activity pattern of two STAT proteins, Stat5a and Stat5b, in mammary tissue during pregnancy suggests an active role for these transcription factors in epithelial cell differentiation and milk protein gene expression. To investigate the function of Stat5a in mammopoiesis and lactogenesis we disrupted this gene in mice by gene targeting. Stat5a- deficient mice developed normally and were indistinguishable from hemizygous and wild-type littermates in size, weight, and fertility. However, mammary lobuloalveolar outgrowth during pregnancy was curtailed, and females failed to lactate after parturition because of a failure of terminal differentiation. Although Stat5b has a 96% similarity with Stat5a and a superimposable expression pattern during mammary gland development it failed to counterbalance for the absence of Stat5a. These results document that Stat5a is the principal and an obligate mediator of mammopoietic and lactogenic signaling.

Original languageEnglish (US)
Pages (from-to)179-186
Number of pages8
JournalGenes and Development
Volume11
Issue number2
DOIs
StatePublished - Jan 15 1997

Keywords

  • Stat5 proteins
  • epithelial cell differentiation
  • lactogenesis
  • mammopoiesis

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

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    Liu, X., Robinson, G. W., Wagner, K. U., Garrett, L., Wynshaw-Boris, A., & Hennighausen, L. (1997). Stat5a is mandatory for adult mammary gland development and lactogenesis. Genes and Development, 11(2), 179-186. https://doi.org/10.1101/gad.11.2.179