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. 2016 Oct 31;205(1):273–293. doi: 10.1534/genetics.116.194464

Figure 9.

Figure 9

MLT and NEKL proteins control clathrin-mediated endocytosis. (A–L) Confocal images of GFP::CHC-1 apical epidermal expression. Normal punctate expression of GFP::CHC-1 (A) was not perturbed in qua-1(RNAi) animals (B), which showed penetrant molting defects. Whereas both mlt-2(RNAi) (C) and mlt-3(RNAi) (D, E) caused penetrant molting defects, mlt-3 depletion led to more severe alterations in GFP::CHC-1 expression, which varied from large accumulations (D) to diffuse expression at the apical surface (E). Abnormal accumulations and diffuse expression of GFP::CHC-1 were also observed in some nekl-2(RNAi) (F, G) and nekl-3(RNAi) (H, I) animals. Whereas hypomorphic alleles of nekl-2 (fd81) and nekl-3 (gk894345) did not perturb GFP::CHC-1 localization (J, K), nekl-2(fd81); nekl-3(gk894345) double mutants displayed extensive accumulation of the GFP signal (L). Bar, 5 µm