Fig. 1. Loss of the RhoGAP RGA-2 or MEL-11/MYPT induce similar defects in C. elegans. (A-F) DIC micrographs of (A) wild-type 3-fold, (B) rga-2(RNAi) and (C) 2-fold and (D) 3-fold rga-2(hd102) embryos, (E) mel-11(it26) embryo and (F) let-502(sb118ts) hatchling at the non-permissive temperature. Arrows, ventral bulge. (G) Physical map of Y53C10A.4/rga-2 with position of the hd102 deletion indicated. Predicted domains of the putative 908-residue RGA-2 protein along with its closest mammalian homologue, ARHGAP20. PH, Pleckstrin Homology; RhoGAP, GTPase-activator protein for Rho-family GTPases; RA, Ras-association (RalGDS/AF-6); ANXL, annexin-like. The percentages of identity and similarity are indicated (for alignments, see Fig. S1 in the supplementary material). (H) Elongation rates for the mutants presented in I-L based on at least four embryos per genotype. (I-L) Still images from DIC videos for wild-type (I), rga-2(hd102) (J), mel-11(it26) (K) and let-502(sb118ts) (L) embryos maintained at 25.5°C. Timing (in minutes) is shown above each column. Arrows point to areas where rga-2 and mel-11 embryos appear to rupture; double-headed arrows, failure to constrict the head. Most rga-2(hd102) embryos (18/21) ruptured before the 2.3-fold stage (5/21 embryos ruptured before the 2-fold stage) in the anterior ventral midline (17/21) or less frequently posteriorly (3/21). Consistent with previous findings (Wissmann et al., 1999), 12/13 mel-11(it26) embryos ruptured at about the 1.6-fold stage. For originals, see Movies 1-4 in the supplementary material. Scale bar: 10 µm.