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Published 12 November 2001. doi:10.1083/jcb.200107065
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© The Rockefeller University Press, 0021-9525/2001/11/531 $5.00
The Journal of Cell Biology, Volume 155, Number 4, November 12, 2001 531-542

Article

Signal transducer and activator of transcription (Stat) 5 controls the proliferation and differentiation of mammary alveolar epithelium



Keiko Miyoshi1,5, Jonathan M. Shillingford1, Gilbert H. Smith2, Sandra L. Grimm3, Kay-Uwe Wagner1,4, Takami Oka1, Jeffrey M. Rosen3, Gertraud W. Robinson1 and Lothar Hennighausen1

1 Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases
2 Laboratory of Tumor Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892
3 Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030
4 University of Nebraska Medical Center, Omaha, NE 68198
5 Department of Biochemistry, School of Dentistry, The University of Tokushima, Tokushima, Japan 770-8504

Address correspondence to Keiko Miyoshi, Laboratory of Genetics and Physiology NIDDK, National Institutes of Health Bldg. 8, Rm. 101, Bethesda, MD 20892-0822. Tel.: (301) 496-2716. Fax: (301) 480 7312. E-mail: mammary{at}nih.gov

Functional development of mammary epithelium during pregnancy depends on prolactin signaling. However, the underlying molecular and cellular events are not fully understood. We examined the specific contributions of the prolactin receptor (PrlR) and the signal transducers and activators of transcription 5a and 5b (referred to as Stat5) in the formation and differentiation of mammary alveolar epithelium. PrlR- and Stat5-null mammary epithelia were transplanted into wild-type hosts, and pregnancy-mediated development was investigated at a histological and molecular level. Stat5-null mammary epithelium developed ducts but failed to form alveoli, and no milk protein gene expression was observed. In contrast, PrlR-null epithelium formed alveoli-like structures with small open lumina. Electron microscopy revealed undifferentiated features of organelles and a perturbation of cell–cell contacts in PrlR- and Stat5-null epithelia. Expression of NKCC1, an Na-K-Cl cotransporter characteristic for ductal epithelia, and ZO-1, a protein associated with tight junction, were maintained in the alveoli-like structures of PrlR- and Stat5-null epithelia. In contrast, the Na-Pi cotransporter Npt2b, and the gap junction component connexin 32, usually expressed in secretory epithelia, were undetectable in PrlR- and Stat5-null mice. These data demonstrate that signaling via the PrlR and Stat5 is critical for the proliferation and differentiation of mammary alveoli during pregnancy.

Key Words: prolactin receptor; Stat5; mammary gland; cell specification; epithelia


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