category
bioRxiv
date
Feb 11, 2026
slug
status
Published
summary
发现AGEF-1的E1028K突变具有激活作用,揭示其通过调控AP-1适配体与Arf GTPase循环相互作用,控制卵黄运输的分子机制。该研究首次明确AGEF-1在胚胎发育中维持卵黄膜稳定的关键功能。
tags
基因编辑
type
Post

📄 原文题目

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

🔗 原文链接

💡 AI 核心解读

发现AGEF-1的E1028K突变具有激活作用,揭示其通过调控AP-1适配体与Arf GTPase循环相互作用,控制卵黄运输的分子机制。该研究首次明确AGEF-1在胚胎发育中维持卵黄膜稳定的关键功能。

📝 英文原版摘要

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.
剪接旁系同源蛋白SNRPB和SNRPN调控差异代谢状态病毒样颗粒递送实现体外和体内正交基因编辑
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