Fig. 5. DFer and Src42A cooperate during dorsal closure. (A-C) Late stage 16 Src42A^myri embryos (A) are closed but have an irregular arrangement of epidermal cells, whereas Src42A^myri;dfer^ex1 mutants (B) are still closing and Src42A^myri;dfer¹ mutants (C) are dorsally open (white, anti-phospho-tyrosine). (D-F) The F-actin cable (arrowheads) is slightly disrupted in Src42A^myri mutants (D, compare with Fig. 4D), further disrupted in Src42A^myri;dfer^ex1 mutants (E) and completely lost in Src42A^myri;dfer¹ embryos (F; white, Alexa568-Phalloidin). (G-I) P-Tyr staining (arrowheads) is progressively reduced in Src42A^myri (G), Src42A^myri;dfer^ex1 (H) and Src42A^myri;dfer¹ (I) mutants. (J) Wild-type cuticle preparation. (K,N) Src42A^myri;dfer^ex1 mutants typically show a small anterior hole (K; 95%, n=152; arrowhead), but are occasionally anterior open (N; 5%, arrowhead). (L,O) Src42A^myri;dfer¹ mutants have a small to medium anterior hole (L; 59%, n=102, down arrowhead), often with scabs along the dorsal midline (up arrowhead), or dorsal closure fails (O), yielding an anterior open phenotype (30%, down arrowhead). (M) Src42A^myri mutants fail to hatch (63%, n=191), with 37% showing a small anterior hole near the mouthparts (arrowhead).