| Abstrakt: |
In tetrapods, BMP-signaling coordinates limb outgrowth, skeleton patterning, and apoptosis during the formation of their typical autopod structures, the digits. In addition, inhibition of BMP signaling during mouse limb development leads to the persistence and enlargement of an important signaling 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 signaling 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 signaling in zebrafish lines with distinct FF sizes (bmp2b , smad1 , smoc1 , smoc2, grem1a, msx1b, msx2b, Psamd1/5/9). Our data suggest that the BMP signaling is enhanced in shorter FFs and inhibited in longer FFs, as implied by the differential expression of several components of this network. In addition, we detected an earlier expression of several of these BMP-signaling components associated with the development of short FFs and the opposite tendency during the development of longer FFs. Thus, our results suggest that a heterochronic shift, involving enhanced Hox13 expression and BMP signaling may have caused the reduction of the FF size during the evolutionary transition from fish fins to tetrapod limbs. [ABSTRACT FROM AUTHOR] |
