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

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Vincenzo Cavalieri ◽  
Giovanni Spinelli
Keyword(s):  
Gene Regulatory Network ◽  
Sea Urchin ◽  
Regulatory Network ◽  
Ectopic Expression ◽  
Paracentrotus Lividus ◽  
Loss Of Function ◽  
Mapk Activity ◽  
Sea Urchin Embryo ◽  
Gene Regulatory ◽  
Dorsal Cells

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.

scholarly journals The tolerance to hypoxia is defined by a time-sensitive response of the gene regulatory network in sea urchin embryos

2020 ◽  
Author(s):  
Majed Layous ◽  
Lama Khalaily ◽  
Tsvia Gildor ◽  
Smadar Ben-Tabou de-Leon
Keyword(s):  
Gene Regulatory Network ◽  
Early Development ◽  
Sea Urchin ◽  
Regulatory Network ◽  
Normal Development ◽  
Oxygen Level ◽  
Sea Urchin Embryo ◽  
Tolerance To Hypoxia ◽  
Vegf Pathway ◽  
Gene Regulatory

AbstractDeoxygenation, the reduction of oxygen level in the oceans induced by global warming and anthropogenic disturbances, is a major threat to marine life. This change in oxygen level could be especially harmful to marine embryos that utilize endogenous hypoxia and redox gradients as morphogens during normal development. Here we show that the tolerance to hypoxic conditions changes between different developmental stages of the sea urchin embryo, due to the structure of the gene regulatory networks (GRNs). We demonstrate that during normal development, bone morphogenetic protein (BMP) pathway restricts the activity of the vascular endothelial growth factor (VEGF) pathway to two lateral domains and by that controls proper skeletal patterning. Hypoxia applied during early development strongly perturbs the activity of Nodal and BMP pathways that affect VEGF pathway, dorsal-ventral (DV) and skeletogenic patterning. These pathways are largely unaffected by hypoxia applied after DV axis formation. We propose that the use of redox and hypoxia as morphogens makes the sea urchin embryo highly sensitive to environmental hypoxia during early development, but the GRN structure provides higher tolerance to hypoxia at later stages.Summary statementThe use of hypoxia and redox gradients as morphogens makes sea urchin early development sensitive to environmental hypoxia. This sensitivity decreases later, due to the structure of the gene regulatory network.

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