dia RNAi defects can be modified by decreasing or increasing Par-1 kinase activity. (A and B) Heterozygosity for the kinase-null allele par-1^w3 has no furrow effects (top). For embryos expressing a weaker dia shRNA construct, par-1^w3 heterozygosity enhanced furrow defects relative to sibling embryos heterozygous for a balancer chromosome (quantified in B as in Fig. S3 A). (C) Embryos expressing the weaker dia shRNA constructs display only punctate cap F-actin with GFP coexpression, bundle-like (arrows) plus punctate cap F-actin with GFP–Par-1 coexpression, and only punctate cap F-actin with coexpression of Par-1–KD. Both Par-1 constructs localize to the cortex. The active Par-1 construct is enriched along actin bundles (arrows). Images deconvolved. (D and E) Actin organization quantified as in Fig. 4 C (embryo numbers indicated). Asterisks indicate significant differences versus GFP control.