维持神经元TDP-43的表达需要轴突溶酶体的转运。

IF 6.4 1区 生物学 Q1 BIOLOGY
eLife Pub Date : 2025-09-19 DOI:10.7554/eLife.104057
Veronica H Ryan, Sydney Lawton, Joel F Reyes, James Hawrot, Ashley M Frankenfield, Sahba Seddighi, Daniel M Ramos, Jacob Epstein, Faraz Faghri, Nicholas L Johnson, Jizhong Zou, Martin Kampmann, John Replogle, Yue Andy Qi, Hebao Yuan, Kory Johnson, Dragan Maric, Ling Hao, Mike A Nalls, Michael Emmerson Ward
{"title":"维持神经元TDP-43的表达需要轴突溶酶体的转运。","authors":"Veronica H Ryan, Sydney Lawton, Joel F Reyes, James Hawrot, Ashley M Frankenfield, Sahba Seddighi, Daniel M Ramos, Jacob Epstein, Faraz Faghri, Nicholas L Johnson, Jizhong Zou, Martin Kampmann, John Replogle, Yue Andy Qi, Hebao Yuan, Kory Johnson, Dragan Maric, Ling Hao, Mike A Nalls, Michael Emmerson Ward","doi":"10.7554/eLife.104057","DOIUrl":null,"url":null,"abstract":"<p><p>TDP-43 mislocalization and pathology occurs across a range of neurodegenerative diseases, but the pathways that modulate TDP-43 in neurons are not well understood. We generated a Halo-TDP-43 knock-in human induced pluripotent stem cell (iPSC) line and performed a genome-wide CRISPR interference FACS-based screen to identify modifiers of TDP-43 levels in neurons. A meta-analysis of our screen and publicly available screens identified both specific hits and pathways present across multiple screens, the latter likely responsible for generic protein level maintenance. We identified BORC, a complex required for anterograde lysosome transport, as a specific modifier of TDP-43 protein, but not mRNA, levels in neurons. BORC loss led to longer half-life of TDP-43 and other proteins, suggesting lysosome location is required for proper protein turnover. As such, lysosome location and function are crucial for maintaining TDP-43 protein levels in neurons.</p>","PeriodicalId":11640,"journal":{"name":"eLife","volume":"14 ","pages":""},"PeriodicalIF":6.4000,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12448747/pdf/","citationCount":"0","resultStr":"{\"title\":\"Maintenance of neuronal TDP-43 expression requires axonal lysosome transport.\",\"authors\":\"Veronica H Ryan, Sydney Lawton, Joel F Reyes, James Hawrot, Ashley M Frankenfield, Sahba Seddighi, Daniel M Ramos, Jacob Epstein, Faraz Faghri, Nicholas L Johnson, Jizhong Zou, Martin Kampmann, John Replogle, Yue Andy Qi, Hebao Yuan, Kory Johnson, Dragan Maric, Ling Hao, Mike A Nalls, Michael Emmerson Ward\",\"doi\":\"10.7554/eLife.104057\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>TDP-43 mislocalization and pathology occurs across a range of neurodegenerative diseases, but the pathways that modulate TDP-43 in neurons are not well understood. We generated a Halo-TDP-43 knock-in human induced pluripotent stem cell (iPSC) line and performed a genome-wide CRISPR interference FACS-based screen to identify modifiers of TDP-43 levels in neurons. A meta-analysis of our screen and publicly available screens identified both specific hits and pathways present across multiple screens, the latter likely responsible for generic protein level maintenance. We identified BORC, a complex required for anterograde lysosome transport, as a specific modifier of TDP-43 protein, but not mRNA, levels in neurons. BORC loss led to longer half-life of TDP-43 and other proteins, suggesting lysosome location is required for proper protein turnover. As such, lysosome location and function are crucial for maintaining TDP-43 protein levels in neurons.</p>\",\"PeriodicalId\":11640,\"journal\":{\"name\":\"eLife\",\"volume\":\"14 \",\"pages\":\"\"},\"PeriodicalIF\":6.4000,\"publicationDate\":\"2025-09-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12448747/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"eLife\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.7554/eLife.104057\",\"RegionNum\":1,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"eLife","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.7554/eLife.104057","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

TDP-43的错误定位和病理发生在一系列神经退行性疾病中,但神经元中调节TDP-43的途径尚不清楚。我们建立了一个Halo-TDP-43敲入的人诱导多能干细胞(iPSC)系,并进行了基于全基因组CRISPR干扰的facs筛选,以鉴定神经元中TDP-43水平的修饰因子。我们的筛选和公开可用的筛选的荟萃分析确定了在多个筛选中存在的特定hit和通路,后者可能负责一般蛋白质水平的维持。我们发现BORC是一种顺行溶酶体运输所需的复合物,是神经元中TDP-43蛋白的特异性修饰物,而不是mRNA的水平。BORC的丢失导致TDP-43和其他蛋白质的半衰期延长,这表明溶酶体的位置是适当的蛋白质周转所必需的。因此,溶酶体的位置和功能对于维持神经元中TDP-43蛋白的水平至关重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Maintenance of neuronal TDP-43 expression requires axonal lysosome transport.

TDP-43 mislocalization and pathology occurs across a range of neurodegenerative diseases, but the pathways that modulate TDP-43 in neurons are not well understood. We generated a Halo-TDP-43 knock-in human induced pluripotent stem cell (iPSC) line and performed a genome-wide CRISPR interference FACS-based screen to identify modifiers of TDP-43 levels in neurons. A meta-analysis of our screen and publicly available screens identified both specific hits and pathways present across multiple screens, the latter likely responsible for generic protein level maintenance. We identified BORC, a complex required for anterograde lysosome transport, as a specific modifier of TDP-43 protein, but not mRNA, levels in neurons. BORC loss led to longer half-life of TDP-43 and other proteins, suggesting lysosome location is required for proper protein turnover. As such, lysosome location and function are crucial for maintaining TDP-43 protein levels in neurons.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
eLife
eLife BIOLOGY-
CiteScore
12.90
自引率
3.90%
发文量
3122
审稿时长
17 weeks
期刊介绍: eLife is a distinguished, not-for-profit, peer-reviewed open access scientific journal that specializes in the fields of biomedical and life sciences. eLife is known for its selective publication process, which includes a variety of article types such as: Research Articles: Detailed reports of original research findings. Short Reports: Concise presentations of significant findings that do not warrant a full-length research article. Tools and Resources: Descriptions of new tools, technologies, or resources that facilitate scientific research. Research Advances: Brief reports on significant scientific advancements that have immediate implications for the field. Scientific Correspondence: Short communications that comment on or provide additional information related to published articles. Review Articles: Comprehensive overviews of a specific topic or field within the life sciences.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信