SOCS1 deficiency results in accelerated mammary gland development and rescues lactation in prolactin receptor–deficient mice

AUTOR(ES)

Lindeman, Geoffrey J.

FONTE

Cold Spring Harbor Laboratory Press

RESUMO

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 (IFNγ) gene. SOCS1−/−/IFNγ−/− 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.

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