Temporal regulation of LET-23 EGFR signaling by ERM-1.

<p>(A, B, C) Nomarski images and (A′, B′, C′) EGL-17::CFP expression in <i>erm-1(tm677)/+</i> controls versus (D through F′) homozygous <i>erm-1(tm677)</i> mutants at the Pn.p (A′, D′), Pn.px (B′, E′) and Pn.pxx (C′, F′) stages. The scale bar is 10 µm. (G) Quantification of nuclear EGL-17::CFP intensities in P6.p and its descendants. The numbers of animals analyzed are indicated in brackets. *Indicates p<0.01 as determined in a two tailed student's t-test - two-sample unequal variance. Error bars represent the standard error of the mean. (H) Two antagonistic complexes control LET-23 localization at the basolateral membrane of the VPCs. The ternary LIN-2/LIN-7/LIN-10 complex promotes receptor activation, while the ERM-1 complex (magenta) prevents LET-23 endocytosis and signaling from basolateral membrane. ERM-1 may sequester LET-23 in an actin-rich membrane compartment to prevent receptor activation. (I) In the absence of ERM-1, more LET-23 can be activated via the LIN-2/LIN-7/LIN-10 complex, resulting in enhanced receptor endocytosis and recycling, and ultimately an increased accumulation of LET-23 on the apical plasma membrane.