Fig. S3

Synergistic interaction and compound mutant/morphant analyses. (A–T) Demonstration of synergistic interactions between itga3 and lama5 (A–D), fras1 and frem2a (E–H), hmcn1 and fbn2 (I–L), and fras1 and hmcn1 (M–P), but not hmcn1 and lama5 (Q–T). Images show lateral views of embryos tails at 30 hpf (I–L), 36 hpf (E–H) or 48 hpf (A–D; M–T) after injection of sub-phenotypic doses of morpholinos against itga3 (B), fras1 (F,N), frem2a (G), hmcn1 (J,O,S), fbn2 (K) or lama5 (C,R). All single morphants appear as their uninjected WT controls (A,E,I,M,Q). In contrast, a dysmorphogenic phenotype is seen upon itga3 and lama5 co-injection (D), whilst blisters are evident upon combined injection of fras1 and frem2a (H), hmcn1 and fbn2 (L) and fras1 and hmcn1 (P). Neither phenotype is seen upon co-injection of hmcn1 and lama5 (T). (U-X) Lateral views of the medial fins of pif^te262/te262 (V), nel^tq207/tq207 (W), pif^+/te262; nel^+/tq207 (U) and pif^te262/te262; nel^tq207/tq207 (X) embryos at 30 hpf, showing that blisters in the double mutant are more severe than in nel^tq207/tq207, but of equal severity to pif^te262/te262. (Y-AB) Lateral views on tails of embryos at 32 hpf, demonstrating that the defects due to triple loss of frem2a/2b/3 combined with loss of fras1 (AB) appears as severe as loss of either fras1 alone (Z) or combined loss of frem2a/2b/3 (AA). WT embryo is shown for comparison (Y). (AC-AF) Additive function of hmcn1 and fbn2 as assessed by generation of compound mutant/strong morphant embryos imaged at 32 hpf. Injection of strong doses of fbn2 MO into nel^tq207/tq207 (AF) generated embryos with stronger blistering than nel^tq207/tq207 (AD) or strong fbn2 morphants (AE) alone.