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[P2.66]: Hedgehog signals received by retinal progenitor cells regulate cell cycle progression and neuronal fate specification in the embryonic mouse retina
Author(s) -
Sakagami K.,
Yang X.J.
Publication year - 2008
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2008.09.191
Subject(s) - embryonic stem cell , retina , progenitor cell , sonic hedgehog , neuroscience , hedgehog , citation , cell fate determination , biology , retinal , cell cycle , muller glia , library science , cell , stem cell , computer science , microbiology and biotechnology , genetics , signal transduction , botany , gene , transcription factor
asked whether Sema3A/F’s growth-suppressive actions required BDNF. Indeed, treatment with a function-blocking BDNF antibody suppressed Sema3A/F-induced growth cone collapse, suggesting that sempahorin requires ligand-induced activation of p75NTR for its biological activity. To identify the signaling pathway mediating Sema3A/F-p75NTR-induced growth cone collapse, we examined the role of the RhoA effector ROCK, which is required for the growth suppressive activity of p75NTR. Pharmacological inhibition of ROCK suppressed Sema3A/F-mediated axon growth collapse. We propose that BDNF-activated p75NTR and p75NTR-RhoAROCK signaling is necessary for semaphorin’s growth suppressive effects in sympathetic neurons. p75NTR may act either in a complex with semaphorin receptors, or as a ligand-activated receptor whose activity is required for semaphorin to induce its effects.