RapB Regulates Cell Adhesion and Migration in Dictyostelium, Similar to RapA.

IF 3.3 4区 生物学 Q2 MICROBIOLOGY
Journal of Microbiology Pub Date : 2024-08-01 Epub Date: 2024-06-17 DOI:10.1007/s12275-024-00143-y
Uri Han, Nara Han, Byeonggyu Park, Taeck Joong Jeon
{"title":"RapB Regulates Cell Adhesion and Migration in Dictyostelium, Similar to RapA.","authors":"Uri Han, Nara Han, Byeonggyu Park, Taeck Joong Jeon","doi":"10.1007/s12275-024-00143-y","DOIUrl":null,"url":null,"abstract":"<p><p>Ras small GTPases act as molecular switches in various cellular signaling pathways, including cell migration, proliferation, and differentiation. Three Rap proteins are present in Dictyostelium; RapA, RapB, and RapC. RapA and RapC have been reported to have opposing functions in the control of cell adhesion and migration. Here, we investigated the role of RapB, a member of the Ras GTPase subfamily in Dictyostelium, focusing on its involvement in cell adhesion, migration, and developmental processes. This study revealed that RapB, similar to RapA, played a crucial role in regulating cell morphology, adhesion, and migration. rapB null cells, which were generated by CRISPR/Cas9 gene editing, displayed altered cell size, reduced cell-substrate adhesion, and increased migration speed during chemotaxis. These phenotypes of rapB null cells were restored by the expression of RapB and RapA, but not RapC. Consistent with these results, RapB, similar to RapA, failed to rescue the phenotypes of rapC null cells, spread morphology, increased cell adhesion, and decreased migration speed during chemotaxis. Multicellular development of rapB null cells remained unaffected. These results suggest that RapB is involved in controlling cell morphology and cell adhesion. Importantly, RapB appears to play an inhibitory role in regulating the migration speed during chemotaxis, possibly by controlling cell-substrate adhesion, resembling the functions of RapA. These findings contribute to the understanding of the functional relationships among Ras subfamily proteins.</p>","PeriodicalId":16546,"journal":{"name":"Journal of Microbiology","volume":" ","pages":"627-637"},"PeriodicalIF":3.3000,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Microbiology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s12275-024-00143-y","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/6/17 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"MICROBIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Ras small GTPases act as molecular switches in various cellular signaling pathways, including cell migration, proliferation, and differentiation. Three Rap proteins are present in Dictyostelium; RapA, RapB, and RapC. RapA and RapC have been reported to have opposing functions in the control of cell adhesion and migration. Here, we investigated the role of RapB, a member of the Ras GTPase subfamily in Dictyostelium, focusing on its involvement in cell adhesion, migration, and developmental processes. This study revealed that RapB, similar to RapA, played a crucial role in regulating cell morphology, adhesion, and migration. rapB null cells, which were generated by CRISPR/Cas9 gene editing, displayed altered cell size, reduced cell-substrate adhesion, and increased migration speed during chemotaxis. These phenotypes of rapB null cells were restored by the expression of RapB and RapA, but not RapC. Consistent with these results, RapB, similar to RapA, failed to rescue the phenotypes of rapC null cells, spread morphology, increased cell adhesion, and decreased migration speed during chemotaxis. Multicellular development of rapB null cells remained unaffected. These results suggest that RapB is involved in controlling cell morphology and cell adhesion. Importantly, RapB appears to play an inhibitory role in regulating the migration speed during chemotaxis, possibly by controlling cell-substrate adhesion, resembling the functions of RapA. These findings contribute to the understanding of the functional relationships among Ras subfamily proteins.

Abstract Image

RapB 在竹荪中调控细胞粘附和迁移,与 RapA 相似。
Ras 小 GTP 酶是各种细胞信号通路的分子开关,包括细胞迁移、增殖和分化。竹荪中有三种 Rap 蛋白:RapA、RapB 和 RapC。据报道,RapA 和 RapC 在控制细胞粘附和迁移方面具有相反的功能。在这里,我们研究了竹荪中 Ras GTPase 亚家族成员 RapB 的作用,重点关注其在细胞粘附、迁移和发育过程中的参与。这项研究发现,RapB与RapA类似,在调控细胞形态、粘附和迁移方面发挥着关键作用。通过CRISPR/Cas9基因编辑产生的RapB无效细胞在趋化过程中表现出细胞大小改变、细胞与基质粘附性降低和迁移速度增加。通过表达 RapB 和 RapA,而不是 RapC,可以恢复 rapB 空细胞的这些表型。与这些结果一致的是,RapB 与 RapA 类似,都无法挽救 rapC null 细胞的表型、扩散形态、细胞粘附性增加以及趋化过程中迁移速度降低。rapB无效细胞的多细胞发育仍未受到影响。这些结果表明,RapB 参与控制细胞形态和细胞粘附。重要的是,RapB似乎在趋化过程中对迁移速度起抑制调节作用,可能是通过控制细胞与基质的粘附,这与RapA的功能类似。这些发现有助于理解 Ras 亚家族蛋白之间的功能关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Journal of Microbiology
Journal of Microbiology 生物-微生物学
CiteScore
5.70
自引率
3.30%
发文量
0
审稿时长
3 months
期刊介绍: Publishes papers that deal with research on microorganisms, including archaea, bacteria, yeasts, fungi, microalgae, protozoa, and simple eukaryotic microorganisms. Topics considered for publication include Microbial Systematics, Evolutionary Microbiology, Microbial Ecology, Environmental Microbiology, Microbial Genetics, Genomics, Molecular Biology, Microbial Physiology, Biochemistry, Microbial Pathogenesis, Host-Microbe Interaction, Systems Microbiology, Synthetic Microbiology, Bioinformatics and Virology. Manuscripts dealing with simple identification of microorganism(s), cloning of a known gene and its expression in a microbial host, and clinical statistics will not be considered for publication by JM.
×
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