Stat5a is mandatory for adult mammary gland development and lactogenesis

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...

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Bibliographic Details
Published in:Genes & development 1997-01, Vol.11 (2), p.179-186
Main Authors: Liu, X, Robinson, G W, Wagner, K U, Garrett, L, Wynshaw-Boris, A, Hennighausen, L
Format: Article
Language:English
Subjects:
Animals
Cell Differentiation
DNA-Binding Proteins - analysis
DNA-Binding Proteins - genetics
DNA-Binding Proteins - physiology
Female
Gene Expression Regulation, Developmental
Gene Targeting
Homozygote
Lactation
Male
Mammary Glands, Animal - chemistry
Mammary Glands, Animal - cytology
Mammary Glands, Animal - growth & development
Mammary Glands, Animal - metabolism
Mice
Mice, Inbred C57BL
Mice, Inbred Strains
Milk Proteins - genetics
Milk Proteins - metabolism
Pregnancy
STAT5 Transcription Factor
Trans-Activators - analysis
Trans-Activators - genetics
Trans-Activators - physiology
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Summary: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.
ISSN:0890-9369
1549-5477
DOI:10.1101/gad.11.2.179