Figure S2. Requirements for the DMAP1 binding and AFD domains for DIP-2 neuronal development and protein localization. (A and B) EndogenousGFP::DIP-2 (
zy70) shows cytoplasmic localization in mechanosensory neurons (A) and membrane localization in epidermal cells (B) indistinguishable fromthose expressed in transgenic (zyEx78 and zyIs47) animals. Shown are confocal images of PLM neurons marked by Pmec-4-mKate2 (juSi329) in young adults(A) and L3 stage epidermal seam cells (B, bottom) and wide-field images of embryonic epidermal cells (B, top left) and L2 stage seam cells (B, top right).(C) Schematics of FL, DMAP1-binding, and AFD domain-deleted DIP-2 proteins. (D and E) ALM neuronal morphology and HSN migration defects in
dip-2mutants were rescued with transgenes expressing FL and DMAP1-binding domain-deleted but not AFD-deleted DIP-2 proteins. Error bars indicate SEM of proportion with number of neurons (n = 60-150; D) or animals (n = 27-46; E) indicated above. Significance compared between transgene-negative andtransgene-positive siblings using two-tailed t tests. ***, P < 0.001. (F and G) Representative images of
dip-2 promoter-driven FL DIP-2::GFP and domaindeleted DIP-2::GFP proteins expressed in L4-stage tail neurons and embryonic epidermal cells. FL and DMAP1 and AFD domain deleted DIP-2::GFP proteins show similar localization patterns in late-stage neuronal cells. However, in contrast with FL and DMAP1-deleted DIP-2::GFP, AFD1- and AFD2-deletedDIP-2::GFP proteins displayed a partial or complete loss, respectively, of membrane localization in epidermal cells. Bars: 10 um (A); 20 um (B, F, and G).