ABSTRACT
Bone morphogenetic proteins (Bmps) are signaling molecules that have been implicated in a variety of inductive processes. We report here that zebrafish Bmp7 is disrupted in snailhouse (snh) mutants. The allele snhst1 is a translocation deleting the bmp7 gene, while snhty68 displays a Val→Gly exhange in a conserved motif of the Bmp7 prodomain. The snhty68 mutation is temperature-sensitive, leading to severalfold reduced activity of mutant Bmp7 at 28°C and non-detectable activity at 33°C. This prodomain lesion affects secretion and/or stability of secreted mature Bmp7 after processing has occurred. Both snhst1 and snhty68 mutant zebrafish embryos are strongly dorsalized, indicating that bmp7 is required for the specification of ventral cell fates during early dorsoventral patterning. At higher temperature, the phenotype of snhty68 mutant embryos is identical to that caused by the amorphic bmp2b mutation swirl swrta72 and similar to that caused by the smad5 mutation somitabun sbndtc24 . mRNA injection studies and double mutant analyses indicate that Bmp2b and Bmp7 closely cooperate and that Bmp2b/Bmp7 signaling is transduced by Smad5 and antagonized by Chordino.
