摘要：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
hoxd13aoverexpression 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.
