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First published online 11 July 2007
doi: 10.1242/dev.005066

Development 134, 2935-2945 (2007)
Published by The Company of Biologists 2007
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Semaphorin signaling facilitates cleft formation in the developing salivary gland

Ling Chung1, Tsung-Lin Yang1,*, Hsiu-Ru Huang1,*, Su-Ming Hsu1,2, Hwai-Jong Cheng3,{dagger} and Pei-Hsin Huang1,2,{dagger},{ddagger}

1 Graduate Institute of Pathology, College of Medicine, National Taiwan University, Taipei, Taiwan.
2 Department of Pathology, National Taiwan University Hospital, Taipei, Taiwan.
3 Center for Neuroscience, University of California, Davis, CA 95618, USA.

{ddagger} Author for correspondence (e-mail: phhuang{at}ntu.edu.tw)

Accepted 30 May 2007

Semaphorin signaling plays integral roles in multiple developmental processes. Branching morphogenesis is one such role that has not been thoroughly explored. Here, we show in mice that functional blockage of neuropilin 1 (Npn1) inhibits cleft formation in the developing submandibular gland (SMG) cultured ex vivo. This Npn1-dependent morphogenesis is mediated by Sema3A and Sema3C in an additive manner, and can be abolished by decreasing the expression of plexin A2 or plexin D1. VEGF, another known Npn1 ligand, has no apparent effects on SMG development. FGF signaling, which also mediates SMG branching morphogenesis, acts in parallel with semaphorin signaling. Finally, in contrast to the effect of FGF signaling, we find that semaphorins do not stimulate the proliferation of SMG epithelial cells. Instead, the semaphorin signals act locally on the epithelial cells to facilitate SMG cleft formation.

Key words: Branching morphogenesis, Salivary gland, Cleft formation, Class 3 semaphorin, Plexin, Neuropilin (Npn1; Nrp1), Mouse


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Branching through semaphorin

Development 2007 134: e1602. [Full Text]  



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© The Company of Biologists Ltd 2007