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

bioRxiv (Cold Spring Harbor Laboratory) 2026 Preprint Open access

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Authors: Clare K. Fitzpatrick, Olga Skorobogata, Ali M Fazlollahi, Kimberley D. Gauthier, Christian E. Rocheleau
DOI: 10.64898/2026.02.10.705107
Cited by: 1
References: 29

Abstract

Abstract 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. We propose that Arf GTPase cycling is required to regulate trafficking with AP-1 but not with Arf effectors regulating yolk trafficking.

Fields of Study & Subjects

Cellular transport and secretion Genetics Aging and Longevity in Model Organisms Nuclear Structure and Function

Publication details

Journal / source
bioRxiv (Cold Spring Harbor Laboratory)
Publisher
openRxiv
Publication date
11 February 2026
Language
EN
Document type
Preprint