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.
- 作者:NotionNext
- 链接:https://tangly1024.com/article/30548bd6-1f96-81e4-8a4b-c9a6645968b4
- 声明:本文采用 CC BY-NC-SA 4.0 许可协议,转载请注明出处。
相关文章
