Control of clathrin-mediated endocytosis by NIMA family kinases
Fig 3
Excess open AP2 enhances nekl–mlt molting defects.
(A) Model depicting the allosteric regulation of AP2 by FCHO-1 and NCAP-1. DPY-23/μ open mutants cause AP2 to remain in the open/active state. (B,D,E) Bar plots showing enhancement of molting defects by mutations in ncap-1 (B) and dpy-23/μ open mutants (D,E). RNAi feeding was carried out for the indicated genes; control RNAi feeding targeted GFP. (C) Bar plot showing partial reversion of suppression in nekl-2(fd81); fcho-1(fd131); nekl-3(gk894345) triple mutants after ncap-1(RNAi) was carried out using injection methods. Control indicates non-injected siblings. (B–E) Error bars indicate 95% confidence intervals. p-Values were determined using Fischer’s exact test where proportions were compared to the RNAi controls; ****p < 0.0001, ***p < 0.001. Raw data are available in S1 File.
