Semaphorin signaling facilitates cleft formation in the developing salivary gland

Ling Chung, Tsung Lin Yang, Hsiu Ru Huang, Su Ming Hsu, Hwai-Jong Cheng, Pei Hsin Huang

Research output: Contribution to journalArticlepeer-review

25 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)2935-2945
Number of pages11
Issue number16
StatePublished - Aug 2007


  • Branching morphogenesis
  • Class 3 semaphorin
  • Cleft formation
  • Mouse
  • Neuropilin (Npn; Nrp1)
  • Plexin
  • Salivary gland

ASJC Scopus subject areas

  • Anatomy
  • Cell Biology


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