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

Prolactin is essential for proliferation and differentiation of the develop ing mammary gland. We have explored a role for Suppressor of Cytokine Signa ling 1 (SOCS1) as a modulator of the prolactin response using mice deficien t in SOCS1, which were rescued from neonatal death by deletion of the Inter feron gamma (IFN gamma) gene. SOCS1(-/-)/IFN gamma (-/-) mice exhibited acc elerated lobuloalveolar development in the mammary gland during late pregna ncy and precocious lactation. Significantly, the lactogenic defect in prola ctin receptor heterozygous females could be rescued by deletion of a single SOCS1 allele. These findings establish a role for SOCS1 as a negative regu lator of prolactin signaling and suggest that SOCS1 is required for the pre vention of lactation prior to parturition.