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. Author manuscript; available in PMC: 2015 Aug 3.
Published in final edited form as: Curr Opin Genet Dev. 2008 Jul 28;18(4):362–367. doi: 10.1016/j.gde.2008.06.006

Figure 1.

Figure 1

Retrograde trafficking affects Wnt signaling via multiple mechanisms in C. elegans. (A) WRM-1/β-catenin asymmetry is disrupted by loss of IPLA-1 function. In this hypothetical model, IPLA-1 is presumed to modify a lipid component that results in steady-state reduction in components at the cortex required for anterior localization of WRM-1. In ipla-1 mutants, misrouting of these components appears to require retrograde vesicle trafficking, since it is disrupted by knockdown of components of the retromer and retrograde trafficking machinery. (B) The retromer complex and AP-2 regulate MIG-14/ Wntless trafficking, which indirectly regulates Wnt secretion. MOM-1/Porcupine is required for an early step in Wnt ligand processing, presumably in the endoplasmic reticulum. Later steps in MIG-14 trafficking are affected by AP-2 and retromer. AP-2 knockdown presumably prevents endocytic reuptake of MIG-14, preventing its entry into recycling endosomes; the return of MIG-14 to the Golgi is regulated by retromer components. Their removal results in significant reduction, but not complete abrogation, of MIG-14 function, thereby reducing the amount of Wnt secretion. (A) is adapted from [12•]; (B) is adapted from [40].