An activating mutation in AGEF-1, a putative Arf GEF, causes yolk extrusion from <i>C. elegans</i> embryos

<i>C. elegans</i> AGEF-1, an ortholog of human ARFGEF1 and ARFGEF2, functions with ARF-1, ARF-5 and the AP-1 clathrin adaptor to regulate membrane trafficking. Similar phenotypes induced by the <i>agef-1(vh4[E1028K])</i> allele and <i>agef-1(RNAi)</i> suggested that <i>agef-1(vh4)</i> was a hypomorph. Here we report that <i>agef-1(vh4)</i> results in extrusion of yolk from the embryo. This is suppressed by RNAi of <i>agef-1, arf-1, arf-5</i> but not AP-1. Based on structure of the yeast AGEF-1 ortholog, Sec7p, the E1028K change is predicted to activate AGEF-1. We propose that Arf GTPase cycling is required to regulate trafficking with AP-1 but not with Arf effectors regulating yolk trafficking.