Lactation failure in Src knockout mice is due to impaired secretory activation

Harriet Watkin1, Monica M Richert, Andrew Lewis

  • 1Department of Pathology, University of Colorado Health Sciences Center, Research Complex I, South Tower, Mail Stop 8104, 12801 East 17th Avenue, Aurora, CO 80045, USA. harriet.watkin@uchsc.edu

BMC Developmental Biology
|January 25, 2008
PubMed
Abstract

Insights

The Src tyrosine kinase is essential for successful lactation. Mice lacking Src show impaired mammary gland development, leading to lactation failure and early tissue regression, highlighting Src's role in milk production.

Area of Science:

  • Cellular signaling
  • Developmental biology
  • Biochemistry

Background:

  • Mammary gland development is crucial for lactation, involving complex signaling pathways.
  • Src family kinases are key regulators of intracellular signaling.
  • The role of Src in mammary gland development and lactation remained unclear.

Purpose of the Study:

  • To investigate the role of Src in mammary gland development and function.
  • To determine the impact of Src deficiency on pregnancy and lactation in mice.

Main Methods:

  • Generation and analysis of Src-deficient (Src-/-) mice.
  • Assessment of mammary gland development, lactation, and involution.
  • Analysis of prolactin receptor expression, STAT5 phosphorylation, and milk protein gene expression.

Main Results:

  • Src-/- mice exhibited severe lactation defects, with over 80% of litters dying.
  • Mammary gland development during pregnancy was normal, but secretory activation failed post-partum.
  • Reduced prolactin receptor expression, STAT5 phosphorylation, and milk protein production were observed in Src-/- mice.
  • Src deficiency led to precocious mammary gland involution, even during suckling.

Conclusions:

  • Src is essential for secretory activation during lactation.
  • Src signaling is required for proper prolactin receptor expression and downstream signaling.
  • Src plays a critical role in mammary gland development, lactation, and preventing premature involution.

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