6533b7d7fe1ef96bd1267bdc
RESEARCH PRODUCT
Ectopic hbox12 Expression Evoked by Histone Deacetylase Inhibition Disrupts Axial Specification of the Sea Urchin Embryo
Giovanni SpinelliVincenzo Cavalierisubject
Embryo NonmammalianNodal Proteinlcsh:MedicineRepressorSettore BIO/11 - Biologia MolecolareHydroxamic AcidsHistone DeacetylasesGene expressionAnimalsEpigeneticsPromoter Regions Geneticlcsh:ScienceBody PatterningHomeodomain ProteinsMultidisciplinarybiologylcsh:RGene Expression Regulation DevelopmentalAcetylationhistone deacetylase axial specification transcription repressor sea urchin embryoMolecular biologyChromatinChromatinHistone Deacetylase InhibitorsHistoneSea Urchinsbiology.proteinlcsh:QEctopic expressionHistone deacetylaseNODALResearch Articledescription
Dorsal/ventral patterning of the sea urchin embryo depends upon the establishment of a Nodal-expressing ventral organizer. Recently, we showed that spatial positioning of this organizer relies on the dorsal-specific transcription of the Hbox12 repressor. Building on these findings, we determined the influence of the epigenetic milieu on the expression of hbox12 and nodal genes. We find that Trichostatin-A, a potent and selective histone-deacetylases inhibitor, induces histone hyperacetylation in hbox12 chromatin, evoking broad ectopic expression of the gene. Transcription of nodal concomitantly drops, prejudicing dorsal/ventral polarity of the resulting larvae. Remarkably, impairing hbox12 function, either in a spatially-restricted sector or in the whole embryo, specifically rescues nodal transcription in Trichostatin-A-treated larvae. Beyond strengthen the notion that nodal expression is not allowed in the presence of functional Hbox12 in the same cells, these results highlight a critical role of histone deacetylases in regulating the spatial expression of hbox12.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2015-11-30 |