Table 1.
stage | 30hpf | 55hpf | |||
---|---|---|---|---|---|
Phenotype | Blisters trunk | n | Blisters trunk | Fin defect | n |
MO | |||||
hmcn2 0.5 mM | 0% | 163 | 0% | 0% | 163 |
fbln1 0.1 mM | 0% | 176 | 0% | 0% | 176 |
fbln1c 0.125 mM | 0% | 97 | 0% | 0% | 97 |
fbln1d 0.125 mM | 0% | 98 | 0% | 0% | 98 |
hmcn2 0.5mM + fbln1 0.1 mM | 60,4% | 447 | 37% | 62,7% | 243 |
hmcn2 0.5 mM + fbln1c 0.125 mM |
0% | 93 | 0% | 74,2% | 93 |
hmcn2 0.5 mM + fbln1d 0.125 mM |
0% | 120 | 0% | 63,3% | 120 |
hmcn2 0.5 mM + fbln1c 0.125 mM+ fbln1d 0.125 mM |
61,3% | 132 | 41% | 84,8% | 132 |
Defects were analyzed via light microscopy at indicated stages. The reduction of trunk blistering frequency from 30 hpf to 55 hpf is caused by progressive healing of this phenotypic trait (see Figure 2 and Supplementary Fig. S5C,E for 72 hpf), whereas fin defects persist (see Supplementary Fig. S5D,F for 72 hpf). For testing of Fbln1 splice variants, note that fin defects were obtained both upon co-injection of fbln1c and hmcn2 MOs, and upon co-injection of fbln1d and hmcn2 MOs, whereas trunk blistering required triple injection of fbln1c, fbln1d and hmcn2 MOs. n, number of scored embryos (3 independent experiments).