RPM-1 Uses Both Ubiquitin Ligase and Phosphatase-Based Mechanisms to Regulate DLK-1 during Neuronal Development
Figure 4
PPM-2 negatively regulates the MAP3K DLK-1.
PLM axon termination defects (hook) were quantified for the indicated genotypes using the transgene muIs32. (A) Loss of function in dlk-1 suppresses the axon termination defects in ppm-2-/- single mutants and glo-4-/-; ppm-2-/- double mutants. Shown are averages for data collected from 5–8 independent counts of 20–30 PLM neurons from young adult worms (16–20 hours post L4) grown at 23°C for each genotype. (B) Transgenic overexpression of the MAP3K DLK-1, or the MAP2K MKK-4 results in PLM axon termination defects (hook). Coexpression of PPM-2 rescues defects caused by overexpression of DLK-1, but not MKK-4. Shown are averages for data pooled from 5 or more transgenic lines for the indicated genotypes; young adult worms grown at 23°C were analyzed. For A and B, error bars represent the standard error of the mean, and significance was determined using an unpaired t-test. **p<0.005, ***p<0.001 and ns = not significant.
