Please use this identifier to cite or link to this item:
|Title:||Class 3 Semaphorin Mediates Dendrite Growth in Adult Newborn Neurons through Cdk5/FAK Pathway||Authors:||Ng, T.
|Issue Date:||10-Jun-2013||Citation:||Ng, T., Ryu, J.R., Sohn, J.H., Tan, T., Song, H., Ming, G.-L., Goh, E.L.K. (2013-06-10). Class 3 Semaphorin Mediates Dendrite Growth in Adult Newborn Neurons through Cdk5/FAK Pathway. PLoS ONE 8 (6) : -. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0065572||Abstract:||Class 3 semaphorins are well-known axonal guidance cues during the embryonic development of mammalian nervous system. However, their activity on postnatally differentiated neurons in neurogenic regions of adult brains has not been characterized. We found that silencing of semaphorin receptors neuropilins (NRP) 1 or 2 in neural progenitors at the adult mouse dentate gyrus resulted in newly differentiated neurons with shorter dendrites and simpler branching in vivo. Tyrosine phosphorylation (Tyr 397) and serine phosphorylation (Ser 732) of FAK were essential for these effects. Semaphorin 3A and 3F mediate serine phosphorylation of FAK through the activation of Cdk5. Silencing of either Cdk5 or FAK in newborn neurons phenocopied the defects in dendritic development seen upon silencing of NRP1 or NRP2. Furthermore, in vivo overexpression of Cdk5 or FAK rescued the dendritic phenotypes seen in NRP1 and NRP2 deficient neurons. These results point to a novel role for class 3 semaphorins in promoting dendritic growth and branching during adult hippocampal neurogenesis through the activation of Cdk5-FAK signaling pathway. © 2013 Ng et al.||Source Title:||PLoS ONE||URI:||http://scholarbank.nus.edu.sg/handle/10635/109965||ISSN:||19326203||DOI:||10.1371/journal.pone.0065572|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
|10_1371_journal_pone_0065572.pdf||6.8 MB||Adobe PDF|
checked on Apr 7, 2020
WEB OF SCIENCETM
checked on Mar 30, 2020
checked on Mar 28, 2020
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.