Fig. S4

Fig. S4

Figure S4. CRISPR-generated loss-of-function mutants of waslb and vav2 and their interaction with reph and wan, related to Figure 1

(A) Mutant alleles of wasla, waslb, and vav2 generated by CRISPR-Cas9 targeted gene editing. Shown is reference wild-type sequence as well as the sequence for the generated mutant alleles. Guide target positions are indicated in bold type surrounded by a blue box. (B) wasla; waslb double mutants at 3 dpf. Double mutants exhibit curvature of the body and severe reduction of the fin fold. Alcian Blue staining shows that the endoskeletal disc is largely unaffected. Immunolabelling of collagen reveals that the smaller fin fold is devoid of actinotrichia (asterisk). (C) Adult phenotypes of wasla, waslb, and vav2 mutants. Homozygous single mutants of each gene are phenotypically wild type and exhibit typical fin patterning (n = 10 for each mutant). waslb; vav2 double mutants exhibit loss of proximal radial 4 (n = 4). (D) Loss of wasla function does not affect expression of the reph phenotype. (E) Loss of wasla function does not affect expression of the wan phenotype, while loss of waslb rescues the wild-type phenotype in wan/+ mutants.