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Publication : Dystroglycan controls signaling of multiple hormones through modulation of STAT5 activity.

First Author  Leonoudakis D Year  2010
Journal  J Cell Sci Volume  123
Issue  Pt 21 Pages  3683-92
PubMed ID  20940259 Mgi Jnum  J:182923
Mgi Id  MGI:5317086 Doi  10.1242/jcs.070680
Citation  Leonoudakis D, et al. (2010) Dystroglycan controls signaling of multiple hormones through modulation of STAT5 activity. J Cell Sci 123(Pt 21):3683-92
abstractText  Receptors for basement membrane (BM) proteins, including dystroglycan (DG), coordinate tissue development and function by mechanisms that are only partially defined. To further elucidate these mechanisms, we generated a conditional knockout of DG in the epithelial compartment of the mouse mammary gland. Deletion of DG caused an inhibition of mammary epithelial outgrowth and a failure of lactation. Surprisingly, loss of DG in vivo did not disrupt normal tissue architecture or BM formation, even though cultured Dag1-null epithelial cells failed to assemble laminin-111 at the cell surface. The absence of DG was, however, associated with a marked loss in activity of signal transducer and activator of transcription 5 (STAT5). Loss of DG perturbed STAT5 signaling induced by either prolactin or growth hormone. We found that DG regulates signaling by both hormones in a manner that is dependent on laminin-111 binding, but independent of the DG cytoplasmic domain, suggesting that it acts via a co-receptor mechanism reliant on DG-mediated laminin assembly. These results demonstrate a requirement for DG in the growth and function of a mammalian epithelial tissue in vivo. Moreover, we reveal a selective role for DG in the control of multiple STAT5-dependent hormone signaling pathways, with implications for numerous diseases in which DG function is compromised.
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