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Control of axon-axon attraction by Semaphorin reverse signaling.
Hsieh, Hsiao-Han; Chang, Wen-Tzu; Yu, Li; Rao, Yong.
Afiliação
  • Hsieh HH; McGill Centre for Research in Neuroscience, Department of Neurology and Neurosurgery,Department of Biology, McGill University Health Centre, Montreal, QC, Canada H3G 1A4.
  • Chang WT; McGill Centre for Research in Neuroscience, Department of Neurology and Neurosurgery.
  • Yu L; McGill Centre for Research in Neuroscience, Department of Neurology and Neurosurgery.
  • Rao Y; McGill Centre for Research in Neuroscience, Department of Neurology and Neurosurgery,Department of Medicine, and yong.rao@mcgill.ca.
Proc Natl Acad Sci U S A ; 111(31): 11383-8, 2014 Aug 05.
Article em En | MEDLINE | ID: mdl-25049408
ABSTRACT
Semaphorin family proteins are well-known axon guidance ligands. Recent studies indicate that certain transmembrane Semaphorins can also function as guidance receptors to mediate axon-axon attraction or repulsion. The mechanisms by which Semaphorin reverse signaling modulates axon-surface affinity, however, remain unknown. In this study, we reveal a novel mechanism underlying upregulation of axon-axon attraction by Semaphorin-1a (Sema1a) reverse signaling in the developing Drosophila visual system. Sema1a promotes the phosphorylation and activation of Moesin (Moe), a member of the ezrin/radixin/moesin family of proteins, and downregulates the level of active Rho1 in photoreceptor axons. We propose that Sema1a reverse signaling activates Moe, which in turn upregulates Fas2-mediated axon-axon attraction by inhibiting Rho1.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Axônios / Transdução de Sinais / Semaforinas / Drosophila melanogaster Limite: Animals Idioma: En Ano de publicação: 2014 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Axônios / Transdução de Sinais / Semaforinas / Drosophila melanogaster Limite: Animals Idioma: En Ano de publicação: 2014 Tipo de documento: Article