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Dorsal/ventral (DV) patterning of the sea urchin embryo relies on a ventrally-localized organizer expressing Nodal, a pivotal regulator of the DV gene regulatory network. However, the inceptive mechanisms imposing the symmetry-breaking are incompletely understood. In  Paracentrotus lividus , the Hbox12 homeodomain-containing repressor is expressed by prospective dorsal cells, spatially facing and preceding the onset of  nodal  transcription. We report that Hbox12 misexpression provokes DV abnormalities, attenuating  nodal  and  nodal -dependent transcription. Reciprocally, impairing  hbox12  function disrupts DV polarity by allowing ectopic expression of  nodal . Clonal loss-of-function, inflicted by blastomere transplantation or gene-transfer assays, highlights that DV polarization requires Hbox12 action in dorsal cells. Remarkably, the localized knock-down of  nodal  restores DV polarity of embryos lacking  hbox12  function. Finally, we show that  hbox12  is a dorsal-specific negative modulator of the p38-MAPK activity, which is required for  nodal  expression. Altogether, our results suggest that Hbox12 function is essential for proper positioning of the DV organizer.

Early asymmetric cues triggering the dorsal/ventral gene regulatory network of the sea urchin embryo