Hoxd13/Bmp2-mediated mechanism involved in zebrafish finfold design

The overexpression of hoxd13a during zebrafish fin development causes distal endochondral expansion and simultaneous reduction of the finfold, mimicking the major events thought to have happened during the fin-to-limb transition in Vertebrates. We investigated the effect of hoxd13a overexpression on putative downstream targets and found it to cause downregulation of proximal fin identity markers (meis1 and emx2) and upregulation of genes involved in skeletogenesis/patterning (fbn1, dacha) and AER/Finfold maintenance (bmps). We then show that bmp2b overexpression leads to finfold reduction, recapitulating the phenotype observed in hoxd13a-overexpressing fins. In addition, we show that during the development of the long finfold in leo(t1)/lof(dt1) mutants, hoxd13a and bmp2b are downregulated. Our results suggest that modulation of the transcription factor Hoxd13 during evolution may have been involved in finfold reduction through regulation of the Bmp signalling that then activated apoptotic mechanisms impairing finfold elongation.

Automated summary

The study found that hoxd13a and bmp2b play important roles in zebrafish fin development by regulating the expression of genes involved in skeletogenesis and AER/Finfold maintenance. Hoxd13a may be involved in finfold reduction through modulation of the Bmp signaling pathway.