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Vol. 15, No. 13, pp. 1631-1636, July 1, 2001

RESEARCH COMMUNICATION
SOCS1 deficiency results in accelerated mammary gland development and rescues lactation in prolactin receptor-deficient mice

Geoffrey J. Lindeman,1 Sergio Wittlin,1 Hania Lada,1 Matthew J. Naylor,3 Margaret Santamaria,1 Jian-Guo Zhang,1,2 Robyn Starr,1,2 Douglas J. Hilton,1,2 Warren S. Alexander,1,2 Christopher J. Ormandy,3 and Jane Visvader1,4

1 The Walter and Eliza Hall Institute of Medical Research, Bone Marrow Research Laboratories, and 2 Cooperative Research Centre for Cellular Growth Factors, PO Royal Melbourne Hospital, VIC 3050, Australia; 3 Garvan Institute of Medical Research, Darlinghurst, NSW 2010, Australia

Prolactin is essential for proliferation and differentiation of the developing mammary gland. We have explored a role for Suppressor of Cytokine Signaling 1 (SOCS1) as a modulator of the prolactin response using mice deficient in SOCS1, which were rescued from neonatal death by deletion of the Interferon gamma (IFNgamma ) gene. SOCS1-/-/IFNgamma -/- mice exhibited accelerated lobuloalveolar development in the mammary gland during late pregnancy and precocious lactation. Significantly, the lactogenic defect in prolactin receptor heterozygous females could be rescued by deletion of a single SOCS1 allele. These findings establish a role for SOCS1 as a negative regulator of prolactin signaling and suggest that SOCS1 is required for the prevention of lactation prior to parturition.

[Key Words: Prolactin receptor; SOCS1; mammary gland]


4 Corresponding author.


GENES & DEVELOPMENT 15:1631-1636 © 2001 by Cold Spring Harbor Laboratory Press  ISSN 0890-9369/01 $5.00

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