Figure 3.
cwn-2 regulates RMED/V neurite A/P outgrowth. (A)
xd1 is a C138Y missense mutation in the
cwn-2 locus. Black boxes are exons and grey boxes are UTRs. (B) Phenotypic quantification of RMED neurite A/P outgrowth defect in Wnt pathway receptor and ligand mutants. The average relative neurite length in wild type (
unc-30;juIs76) is set as 100. Error bars represent SEM. Note that
mig-1(
e1787);
cfz-2(
ok1201) double mutants mimic
cwn-2(
xd1). (C) Pcwn-2::mCherry expression pattern (Red) in different developmental stages. Green is RMED/V neurons highlighted by juIs76 marker. Top panels: fluorescence and bright field images of embryos with Pcwn-2::mCherry. In a 2-fold stage embryo,
cwn-2 is mainly expressed in the intestine (arrow). The highest level of mCherry signal is observed in the posterior pharyngeal bulb and the pharyngeal-intestine valve before hatching (arrowhead). After L1 stage, Pcwn-2::mCherry is expressed in the pharynx, body wall muscles and some ventral cord neurons. Asterisks point to the tips of RMED/V neurites. (D) Quantification analysis of the rescue activity of the
cwn-2 genomic fragment in
cwn-2(
xd1). The length of both RMED and RMEV were compared to wild-type controls (
unc-30;juIs76). The extent of RMED and RMEV extension was classified into three categories: ''WT'' stands for wild-type length in both RMED and RMEV neurites; ''no D, V'' stands for absence of both RMED and RMEV neurites (Class I phenotype); and ''short'' indicates an intermediate phenotype between ''WT'' and ''No D, V'' (including shorter processes and absence of either RMED or RMEV process). Results from two independent transgenic lines are presented.