Arf6将Cdr2节点锚定在细胞皮层,以控制细胞分裂时的大小

Hannah Opalko, K. E. Miller, Hyun-Soo Kim, Cesar Vargas-Garcia, Abhyudai Singh, M. Keogh, J. Moseley
{"title":"Arf6将Cdr2节点锚定在细胞皮层,以控制细胞分裂时的大小","authors":"Hannah Opalko, K. E. Miller, Hyun-Soo Kim, Cesar Vargas-Garcia, Abhyudai Singh, M. Keogh, J. Moseley","doi":"10.1101/2021.08.17.456680","DOIUrl":null,"url":null,"abstract":"Fission yeast cells prevent mitotic entry until a threshold cell surface area is reached. The protein kinase Cdr2 contributes to this size control system by forming multiprotein nodes that inhibit Wee1 at the medial cell cortex. Cdr2 node anchoring at the cell cortex is not fully understood. Through a genomic screen, we identified the conserved GTPase Arf6 as a component of Cdr2 signaling. Cells lacking Arf6 failed to divide at a threshold surface area and instead shifted to volume-based divisions at increased overall size. Arf6 stably localized to Cdr2 nodes in its GTP-bound but not GDP-bound state, and its GEF (guanine nucleotide exchange factor) Syt22 was required for both Arf6 node localization and proper size at division. In arf6Δ mutants, Cdr2 nodes detached from the membrane and exhibited increased dynamics. These defects were enhanced when arf6Δ was combined with other node mutants. Our work identifies a regulated anchor for Cdr2 nodes that is required for cells to sense surface area.","PeriodicalId":343306,"journal":{"name":"The Journal of Cell Biology","volume":"29 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2021-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"7","resultStr":"{\"title\":\"Arf6 anchors Cdr2 nodes at the cell cortex to control cell size at division\",\"authors\":\"Hannah Opalko, K. E. Miller, Hyun-Soo Kim, Cesar Vargas-Garcia, Abhyudai Singh, M. Keogh, J. Moseley\",\"doi\":\"10.1101/2021.08.17.456680\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Fission yeast cells prevent mitotic entry until a threshold cell surface area is reached. The protein kinase Cdr2 contributes to this size control system by forming multiprotein nodes that inhibit Wee1 at the medial cell cortex. Cdr2 node anchoring at the cell cortex is not fully understood. Through a genomic screen, we identified the conserved GTPase Arf6 as a component of Cdr2 signaling. Cells lacking Arf6 failed to divide at a threshold surface area and instead shifted to volume-based divisions at increased overall size. Arf6 stably localized to Cdr2 nodes in its GTP-bound but not GDP-bound state, and its GEF (guanine nucleotide exchange factor) Syt22 was required for both Arf6 node localization and proper size at division. In arf6Δ mutants, Cdr2 nodes detached from the membrane and exhibited increased dynamics. These defects were enhanced when arf6Δ was combined with other node mutants. Our work identifies a regulated anchor for Cdr2 nodes that is required for cells to sense surface area.\",\"PeriodicalId\":343306,\"journal\":{\"name\":\"The Journal of Cell Biology\",\"volume\":\"29 1\",\"pages\":\"0\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2021-08-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"7\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The Journal of Cell Biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1101/2021.08.17.456680\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Journal of Cell Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/2021.08.17.456680","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 7

摘要

分裂酵母细胞阻止有丝分裂进入,直到达到一个阈值细胞表面积。蛋白激酶Cdr2通过在内侧细胞皮层形成抑制Wee1的多蛋白节点来参与这个大小控制系统。Cdr2节点锚定在细胞皮层尚不完全清楚。通过基因组筛选,我们确定了保守的GTPase Arf6是Cdr2信号传导的一个组成部分。缺乏Arf6的细胞不能在阈值表面积上分裂,而是在整体大小增加的情况下转向基于体积的分裂。Arf6以gtp结合而非gdp结合状态稳定定位于Cdr2节点,Arf6节点定位和分裂时合适的大小都需要其GEF(鸟嘌呤核苷酸交换因子)Syt22。在arf6Δ突变体中,Cdr2节点从膜上分离并表现出增加的动态。当arf6Δ与其他节点突变体结合时,这些缺陷增强。我们的工作确定了细胞感知表面积所需的Cdr2节点的调节锚点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Arf6 anchors Cdr2 nodes at the cell cortex to control cell size at division
Fission yeast cells prevent mitotic entry until a threshold cell surface area is reached. The protein kinase Cdr2 contributes to this size control system by forming multiprotein nodes that inhibit Wee1 at the medial cell cortex. Cdr2 node anchoring at the cell cortex is not fully understood. Through a genomic screen, we identified the conserved GTPase Arf6 as a component of Cdr2 signaling. Cells lacking Arf6 failed to divide at a threshold surface area and instead shifted to volume-based divisions at increased overall size. Arf6 stably localized to Cdr2 nodes in its GTP-bound but not GDP-bound state, and its GEF (guanine nucleotide exchange factor) Syt22 was required for both Arf6 node localization and proper size at division. In arf6Δ mutants, Cdr2 nodes detached from the membrane and exhibited increased dynamics. These defects were enhanced when arf6Δ was combined with other node mutants. Our work identifies a regulated anchor for Cdr2 nodes that is required for cells to sense surface area.
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
自引率
0.00%
发文量
0
×
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:481959085
Book学术官方微信