RPM-1 Uses Both Ubiquitin Ligase and Phosphatase-Based Mechanisms to Regulate DLK-1 during Neuronal Development
Figure 3
ppm-2 functions cell autonomously downstream of rpm-1.
The PLM axon termination defects (hook) were quantified for all genotypes shown using the transgene muIs32. (A) A cell specific promoter (Pmec-7) was used to transgenically express wild-type PPM-2, phosphatase-dead PPM-2 D59N, or PPM-2 G2A that was not N-myristoylated in the PLM neurons of ppm-2-/- fsn-1-/- double mutants. (B) A cell specific promoter (Pmec-7) was used to transgenically express PPM-2 or phosphatase-dead PPM-2 D59N in rpm-1-/- single mutants. Averages are shown for data collected from 5 or more transgenic lines for each genotype. In all experiments, young adult worms (16–20 hours post L4) grown at 23°C were analyzed. Error bars represent the standard error of the mean, and significance was determined using an unpaired t-test. ***p<0.001 and ns = not significant.
