PPM-2 regulates DLK-1 by acting on S874.

<p>(<i>A</i>) Quantitation of PLM axon termination defects (hook) caused by transgenic overexpression of DLK-1 and phosphomimetic DLK-1 point mutants. Note that coexpression of PPM-2 rescues defects caused by overexpression of DLK-1, but not defects caused by overexpression of DLK-1 <i>S874E S878E</i> and DLK-1 <i>S874E</i>. Shown are averages of data pooled from 5 or more transgenic lines for the indicated genotypes; young adult worms (16–20 hours post L4) grown at 23°C were analyzed. (<i>B</i>) CoIP from transgenic whole worm lysates showing that FLAG::DLK-1L <i>K162R</i> coprecipitates with GFP::DLK-1S, and binding of DLK-1L to DLK-1S is not altered in <i>ppm-2-/-</i> mutants (upper panel). (<i>C</i>) Quantitation of FLAG::DLK-1L <i>K162R</i> coIP with GFP::DLK-1S for the indicated genotypes normalized to amount of GFP::DLK-1S precipitated. Shown are the average levels of FLAG::DLK-1 <i>K162R</i> coprecipitating with GFP::DLK-1S acquired from 3 independently derived transgenic lines for each genotype. Error bars represent the standard error of the mean, and significance was determined using an unpaired <i>t</i>-test. **p<0.01, ***p<0.001, ns = not significant.