Loss of srgp-1 function slows junction formation and enhances the embryonic lethality of α- or β-catenin hypomorphs. (A) Ventral enclosure visualized by HMP-1::GFP. In the first frame, the leading cells are ∼1 µm apart (arrows). Junctions form faster (arrowheads) in control versus srgp-1(RNAi) embryos. The boxes in the images on the left outline the areas that are shown in the time series from 0 to 6 min. (B) Time-lapse Nomarski of a developing wild-type embryo alongside an hmp-1(fe4) mutant, which develops lumps during elongation, and an hmp-1(fe4);srgp-1(RNAi) embryo, which fails to close the gastrulation cleft and then ruptures. WT, wild type. (C) Comparison of cell junctions using AJM-1::GFP in hmp-2(qm39) and hmp-2(qm39);srgp-1(RNAi) embryos demonstrates a gap between epidermal cells at the midline in the double mutant (arrows). (D) Rescue of embryonic lethality associated with the knockdown of endogenous srgp-1 in hmp-2(qm39) mutants by the expression of transgenic full-length srgp-1 or deletion constructs that contain the F-BAR and junctional targeting sequence. Error bars denote SEM (n > 250).