Please use this identifier to cite or link to this item: https://doi.org/10.1038/srep04289
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dc.titleZebrafish yap1 plays a role in differentiation of hair cells in posterior lateral line
dc.contributor.authorLoh, S.-L.
dc.contributor.authorTeh, C.
dc.contributor.authorMuller, J.
dc.contributor.authorGuccione, E.
dc.contributor.authorHong, W.
dc.contributor.authorKorzh, V.
dc.date.accessioned2014-10-27T08:45:29Z
dc.date.available2014-10-27T08:45:29Z
dc.date.issued2014-03-06
dc.identifier.citationLoh, S.-L., Teh, C., Muller, J., Guccione, E., Hong, W., Korzh, V. (2014-03-06). Zebrafish yap1 plays a role in differentiation of hair cells in posterior lateral line. Scientific Reports 4 : -. ScholarBank@NUS Repository. https://doi.org/10.1038/srep04289
dc.identifier.issn20452322
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/102186
dc.description.abstractThe evolutionarily conserved Hippo signaling pathway controls organ size by regulating cell proliferation and apoptosis and this process involves Yap1. The zebrafish Yap1 acts during neural differentiation, but its function is not fully understood. The detailed analysis of yap1 expression in proliferative regions, revealed it in the otic placode that gives rise to the lateral line system affected by the morpholino-mediated knockdown of Yap1. The comparative microarray analysis of transcriptome of Yap1-deficient embryos demonstrated changes in expression of many genes, including the Wnt signaling pathway and, in particular, prox1a known for its role in development of mechanoreceptors in the lateral line. The knockdown of Yap1 causes a deficiency of differentiation of mechanoreceptors, and this defect can be rescued by prox1a mRNA. Our studies revealed a role of Yap1 in regulation of Wnt signaling pathway and its target Prox1a during differentiation of mechanosensory cells.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1038/srep04289
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentBIOLOGICAL SCIENCES
dc.description.doi10.1038/srep04289
dc.description.sourcetitleScientific Reports
dc.description.volume4
dc.description.page-
dc.identifier.isiut000332327400001
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