Dorsal/Ventral (DV) axis formation in the sea urchin embryo depends upon the expression of nodal on the ventral side, which behaves as a DV organizing centre. However, only fuzzy clues are known as to the early symmetry-breaking steps that lead to the positioning of such an organizer.An extremely interesting candidate for this role is the hbox12 homeobox-containing gene. In Paracentrotus lividus, hbox12 expression is antecedent and complementary with respect to that of nodal, being confined in prospective dorsal cells.We show that ectopic expression of Hbox12 provokes DV abnormalities and attenuates nodal as well as nodal-dependent gene transcription. By blastomere transplantation, we also establish that DV defects arise from hbox12 misexpression in the animal hemisphere.To impair Hbox12 function we expressed ubiquitously a truncated form of the protein, encoding for the homeodomain. Such a perturbation disrupts DV axis formation by allowing ectopic expression of nodal across the embryo. Moreover, clonal loss-of-function imposed by either blastomere transplantation or gene transfer assays highlights that Hbox12 action in prospective dorsal cells is necessary for DV polarization. Remarkably, the localized knock-down of nodal restores DV polarity of embryos lacking hbox12 function.Finally, we show that hbox12 is involved in the dorsal-specific inactivation of the p38 MAPK, which is known to be required for nodal expression.Altogether, our results indicate that Hbox12 prevents the ectopic activation of nodal transcription within the future dorsal side of the early sea urchin embryo.
|Number of pages||2|
|Publication status||Published - 2014|