An activating mutation in AGEF-1, a putative Arf GEF, causes yolk extrusion from C. elegans embryos
Clare FitzPatrick1,2, Olga Skorobogata1, Ali M Fazlollahi1,2
1Department of Anatomy and Cell Biology, McGill University, Montreal, QC, CA.
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C. elegans 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 agef-1 ( vh4 [E1028K]) allele and agef-1 (RNAi) suggested that agef-1 ( vh4 ) was a hypomorph. Here we report that agef-1 ( vh4 ) results in extrusion of yolk from the embryo. This is suppressed by RNAi of agef-1 , arf-1 , arf-5 but not AP-1. Based on structure of the yeast AGEF-1 ortholog, Sec7p, the E1028K change is predicted to activate AGEF-1 . Thus, Arf GTPase cycling is likely required to regulate trafficking with AP-1 but not with Arf effectors regulating yolk trafficking.


