Bmp-signaling and the finfold size in zebrafish: implications for the fin-to-limb transition.

In tetrapods, BMP signalling coordinates limb outgrowth, skeleton patterning, and apoptosis during the formation of their typical autopod structures, the digits. In addition, inhibition of BMP signalling during mouse limb development leads to the persistence and enlargement of an important signalling center, the apical ectodermal ridge (AER), and consequent digit defects. Interestingly, during fish fin development there is a natural elongation of the AER, rapidly converted into an apical finfold (FF), in which osteoblasts differentiate into dermal fin rays used in aquatic locomotion. Previous reports have led us to suggest that upregulation of Hox13 genes in the distal fin mesenchyme, caused by the origin of novel enhancer modules, may have caused an increment of the BMP signalling potentially leading to the apoptosis of these osteoblasts precursors of the fin-rays. To explore this hypothesis, we characterized the expression of several components of the BMP signalling in zebrafish lines with distinct finfold sizes (bmp2b, smad1, smoc1, smoc2, grem1a, msx1b, msx2b, Psamd1/5/9). Our data suggest that the BMP signalling is enhanced in shorter finfolds and inhibited in longer finfolds, as implied by the differential expression of several components of this network. In addition, we detected an earlier expression of several of these BMP-signalling components associated with the development of short finfolds and the opposite tendency during the development of longer finfolds. Thus, our results suggest that a heterochronic shift, involving enhanced Hox13 expression and BMP-signalling may have caused the reduction of the finfold size during the evolutionary transition from fish fins to tetrapod limbs.