• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

鉴定核孔蛋白 Nup159 与纺锤体极体蛋白不对称定位的新型相互作用及其与自噬的关系。

Characterization of a novel interaction of the Nup159 nucleoporin with asymmetrically localized spindle pole body proteins and its link with autophagy.

机构信息

Centro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER) / Spanish National Research Council (CSIC) - University of Seville - University Pablo de Olavide, Sevilla, Spain.

出版信息

PLoS Biol. 2023 Aug 3;21(8):e3002224. doi: 10.1371/journal.pbio.3002224. eCollection 2023 Aug.

DOI:10.1371/journal.pbio.3002224
PMID:37535687
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10437821/
Abstract

Both the spindle microtubule-organizing centers and the nuclear pore complexes (NPCs) are convoluted structures where many signaling pathways converge to coordinate key events during cell division. Interestingly, despite their distinct molecular conformation and overall functions, these structures share common components and collaborate in the regulation of essential processes. We have established a new link between microtubule-organizing centers and nuclear pores in budding yeast by unveiling an interaction between the Bfa1/Bub2 complex, a mitotic exit inhibitor that localizes on the spindle pole bodies, and the Nup159 nucleoporin. Bfa1/Bub2 association with Nup159 is reduced in metaphase to not interfere with proper spindle positioning. However, their interaction is stimulated in anaphase and assists the Nup159-dependent autophagy pathway. The asymmetric localization of Bfa1/Bub2 during mitosis raises the possibility that its interaction with Nup159 could differentially promote Nup159-mediated autophagic processes, which might be relevant for the maintenance of the replicative lifespan.

摘要

纺锤体微管组织中心和核孔复合物(NPCs)都是卷曲结构,许多信号通路在那里汇聚,以协调细胞分裂过程中的关键事件。有趣的是,尽管它们具有不同的分子构象和总体功能,但这些结构具有共同的组成部分,并在调节基本过程中进行协作。我们通过揭示有丝分裂后期抑制剂 Bfa1/Bub2 复合物与核孔蛋白 Nup159 之间的相互作用,在芽殖酵母中建立了微管组织中心和核孔之间的新联系,该复合物定位于纺锤体极体上。Bfa1/Bub2 与 Nup159 的结合在中期减少,以不干扰纺锤体的正确定位。然而,它们的相互作用在后期被刺激,并协助 Nup159 依赖性自噬途径。Bfa1/Bub2 在有丝分裂期间的不对称定位提出了这样一种可能性,即其与 Nup159 的相互作用可能以不同的方式促进 Nup159 介导的自噬过程,这可能与维持复制寿命有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdab/10437821/f10686b59dda/pbio.3002224.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdab/10437821/854bfdd36364/pbio.3002224.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdab/10437821/d65b3ac76a2a/pbio.3002224.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdab/10437821/baba06752dbe/pbio.3002224.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdab/10437821/5cba5935d75b/pbio.3002224.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdab/10437821/31900684de62/pbio.3002224.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdab/10437821/f10686b59dda/pbio.3002224.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdab/10437821/854bfdd36364/pbio.3002224.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdab/10437821/d65b3ac76a2a/pbio.3002224.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdab/10437821/baba06752dbe/pbio.3002224.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdab/10437821/5cba5935d75b/pbio.3002224.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdab/10437821/31900684de62/pbio.3002224.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bdab/10437821/f10686b59dda/pbio.3002224.g006.jpg

相似文献

1
Characterization of a novel interaction of the Nup159 nucleoporin with asymmetrically localized spindle pole body proteins and its link with autophagy.鉴定核孔蛋白 Nup159 与纺锤体极体蛋白不对称定位的新型相互作用及其与自噬的关系。
PLoS Biol. 2023 Aug 3;21(8):e3002224. doi: 10.1371/journal.pbio.3002224. eCollection 2023 Aug.
2
Asymmetry of the budding yeast Tem1 GTPase at spindle poles is required for spindle positioning but not for mitotic exit.纺锤体极处出芽酵母Tem1 GTP酶的不对称性是纺锤体定位所必需的,但不是有丝分裂退出所必需的。
PLoS Genet. 2015 Feb 6;11(2):e1004938. doi: 10.1371/journal.pgen.1004938. eCollection 2015 Feb.
3
Cdc5-dependent asymmetric localization of bfa1 fine-tunes timely mitotic exit.Cdc5 依赖性的 bfa1 不对称定位精细调节适时有丝分裂退出。
PLoS Genet. 2012 Jan;8(1):e1002450. doi: 10.1371/journal.pgen.1002450. Epub 2012 Jan 12.
4
Disappearance of the budding yeast Bub2-Bfa1 complex from the mother-bound spindle pole contributes to mitotic exit.母本结合的纺锤极上出芽酵母Bub2-Bfa1复合物的消失有助于有丝分裂退出。
J Cell Biol. 2006 Jan 30;172(3):335-46. doi: 10.1083/jcb.200507162.
5
Coupling spindle position with mitotic exit in budding yeast: The multifaceted role of the small GTPase Tem1.在芽殖酵母中将纺锤体位置与有丝分裂退出相耦合:小GTP酶Tem1的多方面作用。
Small GTPases. 2015 Oct 2;6(4):196-201. doi: 10.1080/21541248.2015.1109023.
6
The N-Terminal Domain of Bfa1 Coordinates Mitotic Exit Independent of GAP Activity in .Bfa1 N 端结构域独立于 GAP 活性协调有丝分裂退出
Cells. 2022 Jul 12;11(14):2179. doi: 10.3390/cells11142179.
7
IBD2 encodes a novel component of the Bub2p-dependent spindle checkpoint in the budding yeast Saccharomyces cerevisiae.IBD2编码出芽酵母酿酒酵母中依赖Bub2p的纺锤体检查点的一种新组分。
Genetics. 2002 Jun;161(2):595-609. doi: 10.1093/genetics/161.2.595.
8
The Bfa1/Bub2 GAP complex comprises a universal checkpoint required to prevent mitotic exit.Bfa1/Bub2 GAP复合物包含一个防止有丝分裂退出所需的通用检查点。
Curr Biol. 2000 Nov 2;10(21):1379-82. doi: 10.1016/s0960-9822(00)00779-x.
9
Kin4 kinase delays mitotic exit in response to spindle alignment defects.Kin4激酶可响应纺锤体排列缺陷而延迟有丝分裂退出。
Mol Cell. 2005 Jul 22;19(2):209-21. doi: 10.1016/j.molcel.2005.05.030.
10
The Bub2-dependent mitotic pathway in yeast acts every cell cycle and regulates cytokinesis.酵母中依赖Bub2的有丝分裂途径在每个细胞周期发挥作用并调节胞质分裂。
J Cell Sci. 2001 Jun;114(Pt 12):2345-54. doi: 10.1242/jcs.114.12.2345.

本文引用的文献

1
Snx4-assisted vacuolar targeting of transcription factors defines a new autophagy pathway for controlling expression.Snx4 辅助的转录因子液泡靶向作用定义了一种新的自噬途径,用于控制 表达。
Autophagy. 2021 Nov;17(11):3547-3565. doi: 10.1080/15548627.2021.1877934. Epub 2021 Mar 8.
2
In-cell architecture of the nuclear pore and snapshots of its turnover.核孔的细胞内结构及其周转的快照。
Nature. 2020 Oct;586(7831):796-800. doi: 10.1038/s41586-020-2670-5. Epub 2020 Sep 2.
3
NPC-phagy: selective autophagy of the nuclear pore complexes.
NPC 自噬:核孔复合体的选择性自噬。
Autophagy. 2020 Oct;16(10):1735-1736. doi: 10.1080/15548627.2020.1798199. Epub 2020 Jul 27.
4
Stress eating: Autophagy targets nuclear pore complexes.压力进食:自噬靶向核孔复合物。
J Cell Biol. 2020 Jul 6;219(7). doi: 10.1083/jcb.202006007.
5
TORC1 inactivation stimulates autophagy of nucleoporin and nuclear pore complexes.TORC1 失活可刺激核孔蛋白和核孔复合物的自噬。
J Cell Biol. 2020 Jul 6;219(7). doi: 10.1083/jcb.201910063.
6
A guiding torch at the poles: the multiple roles of spindle microtubule-organizing centers during cell division.两极的指路明灯:纺锤体微管组织中心在细胞分裂中的多重作用。
Cell Cycle. 2020 Jun;19(12):1405-1421. doi: 10.1080/15384101.2020.1754586. Epub 2020 May 13.
7
Regulation of Mitotic Exit by Cell Cycle Checkpoints: Lessons From .细胞周期检查点对有丝分裂后期的调控:来自. 的启示。
Genes (Basel). 2020 Feb 12;11(2):195. doi: 10.3390/genes11020195.
8
Selective autophagy degrades nuclear pore complexes.选择性自噬降解核孔复合物。
Nat Cell Biol. 2020 Feb;22(2):159-166. doi: 10.1038/s41556-019-0459-2. Epub 2020 Feb 6.
9
DNA damage kinase signaling: checkpoint and repair at 30 years.DNA 损伤激酶信号转导:30 年来的检查点和修复。
EMBO J. 2019 Sep 16;38(18):e101801. doi: 10.15252/embj.2019101801. Epub 2019 Aug 8.
10
Age-dependent deterioration of nuclear pore assembly in mitotic cells decreases transport dynamics.有丝分裂细胞中核孔组装随年龄的退化降低了运输动力学。
Elife. 2019 Jun 3;8:e48186. doi: 10.7554/eLife.48186.