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This version published online on February 10, 2005
Molecular Endocrinology, doi:10.1210/me.2004-0254
Molecular Endocrinology Vol. 0, No. 2005 200402541-
doi:10.1210/me.2004-0254
Copyright © 2005 by the Endocrine Society.
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*Compound via MeSH
*Substance via MeSH
Medline Plus Health Information
*Dietary Proteins

Submitted on July 1, 2004
Accepted on February 2, 2005

Transcriptional Changes Underlying the Secretory Activation Phase of Mammary Gland Development

Matthew J. Naylor, Samantha R. Oakes, Margaret Gardiner-Garden, Jessica Harris, Katrina Blazek, Timothy W. C. Ho, Foo C. Li, David Wynick, Ameae M. Walker, and Christopher J. Ormandy*

Development Group, Cancer Research Program, Garvan Institute of Medical Research, St Vincent's Hospital, Sydney, NSW, 2010, Australia (M.J.N., S.R.O., M.G.-G., J.H. K.B. C.J.O.); Division of Biomedical Sciences, University of California, Riverside, California 92521 (T.W.C.H., A.M.W.) and University Research Centre Neuroendocrinology, Bristol University, Marlborough Street, Bristol BS2 8HW, United Kingdom (F.C.L., D.W.)

* To whom correspondence should be addressed. E-mail: c.ormandy{at}garvan.org.au.

The secretory activation stage of mammary gland development occurs after parturition and converts inactive lobuloalveoli to active milk secretion. This process is triggered by progestin withdrawal and depends upon augmented prolactin signaling. Little is known about the prolactin-induced transcriptional changes that occur in the mammary gland to drive this process. To examine changes in the mammary transcriptome responsible for secretory activation we have used transcript profiling of three mouse models that exhibit failure of secretory activation; knockout of galanin (a regulator of pituitary prolactin production and a mammary cell autonomous modulator of prolactin action), treatment with S179D prolactin (a phosphoprolactin mimic) and knockout of a single prolactin receptor allele. A significant reduction in expression was observed in genes belonging to 46 gene ontologies including those representing milk proteins, metabolism, lipid, cholesterol and fatty acid biosynthetic enzymes, immune response and key transcription factors. A key set of 35 genes, commonly regulated in all three models, was identified and their role in lactogenesis was validated by examining their expression in response to prolactin-stimulation or Stat5 knockdown in the HC11 mouse mammary cell culture model. The transcript profiles provided by these experiments identify 35 key genes (many for the first time) involved in the secretory activation phase of mammary gland development, show that S179D acts as an antagonist of prolactin action and provide insight into the partial penetrance of failed lactation in prolactin receptor heterozygous females.




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