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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.
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