Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.ydbio.2008.02.034
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dc.titleHistone deacetylase 3 (hdac3) is specifically required for liver development in zebrafish
dc.contributor.authorFarooq, M.
dc.contributor.authorSulochana, K.N.
dc.contributor.authorPan, X.
dc.contributor.authorTo, J.
dc.contributor.authorSheng, D.
dc.contributor.authorGong, Z.
dc.contributor.authorGe, R.
dc.date.accessioned2014-10-27T08:30:36Z
dc.date.available2014-10-27T08:30:36Z
dc.date.issued2008-05-01
dc.identifier.citationFarooq, M., Sulochana, K.N., Pan, X., To, J., Sheng, D., Gong, Z., Ge, R. (2008-05-01). Histone deacetylase 3 (hdac3) is specifically required for liver development in zebrafish. Developmental Biology 317 (1) : 336-353. ScholarBank@NUS Repository. https://doi.org/10.1016/j.ydbio.2008.02.034
dc.identifier.issn00121606
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/100835
dc.description.abstractHistone deacetylases (HDACs) are key transcription regulators that function by deacetylating histones/transcription factors and modifying chromatin structure. In this work, we showed that chemical inhibition of HDACs by valproic acid (VPA) led to impaired liver development in zebrafish mainly by inhibiting specification, budding, and differentiation. Formation of exocrine pancreas but not endocrine pancreas was also inhibited. The liver defects induced by VPA correlate with suppressed total HDAC enzymatic activity, but are independent of angiogenesis inhibition. Gene knockdown by morpholino demonstrated that hdac3 is specifically required for liver formation while hdac1 is more globally required for multiple development processes in zebrafish including liver/exocrine pancreas formation. Furthermore, overexpression of hdac3 but not hdac1 partially rescued VPA induced small liver. One mechanism by which hdac3 regulates zebrafish liver growth is through inhibiting growth differentiation factor 11 (gdf11), a unique target of hdac3 and a member of the transforming growth factor β family. Simultaneous overexpression or morpholino knockdown showed that hdac3 and gdf11 function antagonistically in zebrafish liver development. These results revealed a novel and specific role of hdac3 in liver development and the distinct functions between hdac1 and hdac3 in zebrafish embryonic development. © 2008 Elsevier Inc. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.ydbio.2008.02.034
dc.sourceScopus
dc.subjectHistone deacetylase
dc.subjectLiver
dc.subjectOrganogenesis
dc.subjectPancreas
dc.subjectVPA
dc.subjectZebrafish
dc.typeArticle
dc.contributor.departmentBIOLOGICAL SCIENCES
dc.description.doi10.1016/j.ydbio.2008.02.034
dc.description.sourcetitleDevelopmental Biology
dc.description.volume317
dc.description.issue1
dc.description.page336-353
dc.description.codenDEBIA
dc.identifier.isiut000255628900028
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