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Article: Phosphorylation of Sox9 is required for neural crest delamination and is regulated downstream of BMP and canonical Wnt signaling

TitlePhosphorylation of Sox9 is required for neural crest delamination and is regulated downstream of BMP and canonical Wnt signaling
Authors
KeywordsBasement membrane
In ovo electroporation
Issue Date2013
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings of the National Academy of Sciences, 2013, v. 110 n. 8, p. 2882-2887 How to Cite?
AbstractCoordination of neural crest cell (NCC) induction and delamination is orchestrated by several transcription factors. Among these, Sry-related HMG box-9 (Sox9) and Snail2 have been implicated in both the induction of NCC identity and, together with phoshorylation, NCC delamination. How phosphorylation effects this function has not been clear. Here we show, in the developing chick neural tube, that phosphorylation of Sox9 on S64 and S181 facilitates its SUMOylation, and the phosphorylated forms of Sox9 are essential for trunk neural crest delamination. Both phosphorylation and to a lesser extent SUMOylation, of Sox9 are required to cooperate with Snail2 to promote delamination. Moreover, bone morphogenetic protein and canonical Wnt signaling induce phosphorylation of Sox9, thereby connecting extracellular signals with the delamination of NCCs. Together the data suggest a model in which extracellular signals initiate phosphorylation of Sox9 and its cooperation with Snail2 to induce NCC delamination.
Persistent Identifierhttp://hdl.handle.net/10722/188870
ISSN
2017 Impact Factor: 9.504
2015 SCImago Journal Rankings: 6.883
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLiu, AJ-
dc.contributor.authorWu, MH-
dc.contributor.authorYan, HC-
dc.contributor.authorChau, KHB-
dc.contributor.authorSo, H-
dc.contributor.authorNg, A-
dc.contributor.authorChan, A-
dc.contributor.authorCheah, KSE-
dc.contributor.authorBriscoe, J-
dc.contributor.authorCheung, MCH-
dc.date.accessioned2013-09-17T14:18:46Z-
dc.date.available2013-09-17T14:18:46Z-
dc.date.issued2013-
dc.identifier.citationProceedings of the National Academy of Sciences, 2013, v. 110 n. 8, p. 2882-2887-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://hdl.handle.net/10722/188870-
dc.description.abstractCoordination of neural crest cell (NCC) induction and delamination is orchestrated by several transcription factors. Among these, Sry-related HMG box-9 (Sox9) and Snail2 have been implicated in both the induction of NCC identity and, together with phoshorylation, NCC delamination. How phosphorylation effects this function has not been clear. Here we show, in the developing chick neural tube, that phosphorylation of Sox9 on S64 and S181 facilitates its SUMOylation, and the phosphorylated forms of Sox9 are essential for trunk neural crest delamination. Both phosphorylation and to a lesser extent SUMOylation, of Sox9 are required to cooperate with Snail2 to promote delamination. Moreover, bone morphogenetic protein and canonical Wnt signaling induce phosphorylation of Sox9, thereby connecting extracellular signals with the delamination of NCCs. Together the data suggest a model in which extracellular signals initiate phosphorylation of Sox9 and its cooperation with Snail2 to induce NCC delamination.-
dc.languageeng-
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org-
dc.relation.ispartofProceedings of the National Academy of Sciences-
dc.rightsProceedings of the National Academy of Sciences. Copyright © National Academy of Sciences.-
dc.subjectBasement membrane-
dc.subjectIn ovo electroporation-
dc.titlePhosphorylation of Sox9 is required for neural crest delamination and is regulated downstream of BMP and canonical Wnt signaling-
dc.typeArticle-
dc.identifier.emailLiu, AJ: jessie11@hku.hk-
dc.identifier.emailWu, MH: ronmhwu@hkucc.hku.hk-
dc.identifier.emailCheah, KSE: hrmbdkc@hku.hk-
dc.identifier.emailCheung, MCH: mcheung9@hku.hk-
dc.identifier.authorityLiu, AJ=rp02546-
dc.identifier.authorityCheah, KSE=rp00342-
dc.identifier.authorityCheung, MCH=rp00245-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1073/pnas.1211747110-
dc.identifier.pmid23382206-
dc.identifier.pmcidPMC3581920-
dc.identifier.scopuseid_2-s2.0-84874247173-
dc.identifier.hkuros223791-
dc.identifier.hkuros213613-
dc.identifier.volume110-
dc.identifier.issue8-
dc.identifier.spage2882-
dc.identifier.epage2887-
dc.identifier.isiWOS:000315954400060-
dc.publisher.placeUnited States-

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