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. 2019 Feb 20;146(4):dev171124. doi: 10.1242/dev.171124

Fig. 5.

Fig. 5.

Loss of FRM-2 enhances weak dyf-7 defects. (A) Schematic of genetic strategy used to isolate enhancers of the hypomorphic missense mutant dyf-7(ns117). Parental (P0) strain exhibits ∼35% short amphids (red) and ∼65% full-length amphids (green). Following mutagenesis, clonal third-generation (F3) progeny bearing additional mutations (mut) were visually screened for enhanced penetrance. (B) Schematic of the FRM-2 protein showing location of hmn162 nonsense mutation. FRM-2 is roughly 50-60% identical to human EPB41L5, zebrafish moe and Drosophila Yurt throughout the FERM B-lobe (FB), FERM C-lobe (FC) and FERM-adjacent (FA) domains, with a more divergent C-terminal sequence. (C) frm-2(hmn162) enhances the amphid dendrite extension defects of dyf-7(ns117). frm-2(+) transgene indicates animals bearing a transgene with a wild-type frm-2 genomic fragment. n≥100 amphids per genotype. Data are mean±s.e.m. (D) frm-2pro drives expression in sensory neurons (dyf-7pro, arrowheads) at the time of dendrite extension, as well as bright expression in pharynx and gut. (E) A rescuing FRM-2-GFP construct expressed by its endogenous promoter localizes to developing dendrite endings (arrow).