Control of clathrin-mediated endocytosis by NIMA family kinases
Fig 2
Loss of fcho-1 activity suppresses nekl–mlt molting defects.
(A) DIC image of nekl-2(fd81); nekl-3(gk894345) adult worm containing the suppressor mutation fd131. Bar size in A = 100 μm. (B) Model of AP2 allosteric regulation by FCHO-1. (C) Gene structure diagram of fcho-1 including the locations of mutations. The point mutation fd131 is indicated by the arrow, indels (fd211, fd212) by the line ending in a small bracket, and deletions (ox477, fd262) by horizontal gray lines. (D) Protein domain diagram of FCHO-1 with corresponding allelic changes. The amino acid (aa) locations of the three domains are indicated. (E–G) Bar plots showing suppression of molting defects in nekl–mlt mutants by reduction of FCHO-1 activity. (E) Assays were carried out in nekl-2(fd81); nekl-3(gk894345) double mutants using the indicated fcho-1 alleles. (F) RNAi was carried out in the indicated backgrounds using injection methods; control indicates non-injected siblings. (G) Assays were carried out in strong/null nekl–mlt backgrounds using the null fcho-1(ox477) allele. (E–G) Error bars indicate 95% confidence intervals. p-Values were determined using Fischer’s exact test where proportions were compared to the wild-type allele (E,G) or to the RNAi control (F); ****p < 0.0001, ***p < 0.001. Raw data are available in S1 File.
