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. 2014 Mar 15;141(6):1342–1353. doi: 10.1242/dev.102434

Fig. 2.

Fig. 2.

mig-2, ced-10 (Rac GTPases) and unc-34 (Ena/VASP) act downstream of UNC-40. (A) AC-specific overexpression of UNC-40 {qyEx259 [cdh-3 >unc-40::GFP (overexpressed)]} induced ectopic membrane protrusions (arrowheads) in wild-type ACs. (B-D) Loss of unc-34, mig-2 and ced-10 suppressed the protrusive phenotype induced by UNC-40 overexpression. Insets show the morphological changes in the AC membrane. (E-G) Quantification of UNC-40 overexpression phenotype in unc-34, mig-2 and ced-10 mutants (n≥15 for each stage per genotype). Error bars indicate s.e.m. Significant differences compared with wild-type animals are indicated (Student’s t-test). (H-J) DIC images (left), corresponding fluorescence (middle), and overlay (right). The polarized localization of UNC-40::GFP at the invasive cell membrane remained unchanged in ACs that failed to invade (arrowheads) in unc-34 mutants and mig-2 mutants treated with ced-10 RNAi. (K) Quantification of UNC-40 polarity in wild-type animals, unc-34 mutants and mig-2(mu28);ced-10(RNAi) animals (n≥15 for each stage per genotype). No significant differences relative to wild type were observed (Student’s t-test). Scale bars: 5 μm.