Palmitoylation is required for Sept8‐204 and Sept5 to form vesicle‐like structure and colocalize with synaptophysin

Author:

Liu Huicong12,Tan Rong12,Tong Jia12,Wen Shuo12,Wu Can12,Rao Muding12ORCID,Zhu Jiangli3,Qi Shiqian3,Kong Eryan12ORCID

Affiliation:

1. The Second Affiliated Hospital of Xinxiang Medical University Xinxiang China

2. Xinxiang Key Laboratory of Protein Palmitoylation and Major Human Diseases, Henan Health Commission Key Laboratory of Gastrointestinal Cancer Prevention and Treatment, Institute of Psychiatry and Neuroscience Xinxiang Medical University Xinxiang China

3. State Key Laboratory of Biotherapy and Cancer Center, Department of Urology Sichuan University and National Collaborative Innovation Center Chengdu China

Abstract

AbstractSept8 is a vesicle associated protein and there are two typical transcriptional variants (Sept8‐204 and Sept8‐201) expressed in mice brain. Interestingly, the coexpression of Sept8‐204/Sept5 induces the formation of small sized vesicle‐like structure, while that of the Sept8‐201/Sept5 produces large puncta. Sept8 is previously shown to be palmitoylated. Here it was further revealed that protein palmitoylation is required for Sept8‐204/Sept5 to maintain small sized vesicle‐like structure and colocalize with synaptophysin, since either the expression of nonpalmitoylated Sept8‐204 mutant (Sept8‐204‐3CA) or inhibiting Sept8‐204 palmitoylation by 2‐BP with Sept5 produces large puncta, which barely colocalizes with synaptophysin (SYP). Moreover, it was shown that the dynamic palmitoylation of Sept8‐204 is controlled by ZDHHC17 and PPT1, loss of ZDHHC17 decreases Sept8‐204 palmitoylation and induces large puncta, while loss of PPT1 increases Sept8‐204 palmitoylation and induces small sized vesicle‐like structure. Together, these findings suggest that palmitoylation is essential for the maintenance of the small sized vesicle‐like structure for Sept8‐204/Sept5, and may hint their important roles in synaptic functions.

Funder

National Natural Science Foundation of China

Publisher

Wiley

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3