New mutations in the core Schizosaccharomyces pombe spindle pole body scaffold Ppc89 reveal separable functions in regulating cell division.

IF 2.1 3区 生物学 Q3 GENETICS & HEREDITY
Sarah M Hanna, Bita Tavafoghi, Jun-Song Chen, Isaac Howard, Liping Ren, Alaina H Willet, Kathleen L Gould
{"title":"New mutations in the core Schizosaccharomyces pombe spindle pole body scaffold Ppc89 reveal separable functions in regulating cell division.","authors":"Sarah M Hanna, Bita Tavafoghi, Jun-Song Chen, Isaac Howard, Liping Ren, Alaina H Willet, Kathleen L Gould","doi":"10.1093/g3journal/jkae249","DOIUrl":null,"url":null,"abstract":"<p><p>Centrosomes and spindle pole bodies (SPB) are important for mitotic spindle formation and also serve as signaling platforms. In the fission yeast Schizosaccharomyces pombe, genetic ablation and high-resolution imaging indicate that the ɑ-helical Ppc89 is central to SPB structure and function. Here, we developed and characterized conditional and truncation mutants of ppc89. Alleles with mutations in two predicted ɑ-helices near the C-terminus were specifically defective in anchoring Sid4, the scaffold for the septation initiation network (SIN), and proteins dependent on Sid4 (Cdc11, Dma1, Mto1 and Mto2). Artificial tethering of Sid4 to the SPB fully rescued these ppc89 mutants. Another ppc89 allele had mutations located throughout the coding region. While this mutant was also defective in Sid4 anchoring, it displayed additional defects including fragmented SPBs and forming and constricting a second cytokinetic ring in one daughter cell. These defects were shared with a ppc89 allele truncated of the most C-terminal predicted ɑ-helices that is still able to recruit Sid4 and the SIN. We conclude that Ppc89 not only tethers the SIN to the SPB but is also necessary for the integrity of the SPB and faithful coordination of cytokinesis with mitosis.</p>","PeriodicalId":12468,"journal":{"name":"G3: Genes|Genomes|Genetics","volume":null,"pages":null},"PeriodicalIF":2.1000,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"G3: Genes|Genomes|Genetics","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1093/g3journal/jkae249","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
引用次数: 0

Abstract

Centrosomes and spindle pole bodies (SPB) are important for mitotic spindle formation and also serve as signaling platforms. In the fission yeast Schizosaccharomyces pombe, genetic ablation and high-resolution imaging indicate that the ɑ-helical Ppc89 is central to SPB structure and function. Here, we developed and characterized conditional and truncation mutants of ppc89. Alleles with mutations in two predicted ɑ-helices near the C-terminus were specifically defective in anchoring Sid4, the scaffold for the septation initiation network (SIN), and proteins dependent on Sid4 (Cdc11, Dma1, Mto1 and Mto2). Artificial tethering of Sid4 to the SPB fully rescued these ppc89 mutants. Another ppc89 allele had mutations located throughout the coding region. While this mutant was also defective in Sid4 anchoring, it displayed additional defects including fragmented SPBs and forming and constricting a second cytokinetic ring in one daughter cell. These defects were shared with a ppc89 allele truncated of the most C-terminal predicted ɑ-helices that is still able to recruit Sid4 and the SIN. We conclude that Ppc89 not only tethers the SIN to the SPB but is also necessary for the integrity of the SPB and faithful coordination of cytokinesis with mitosis.

Ppc89 的核心 Schizosaccharomyces pombe 纺锤极体支架的新突变揭示了其在调控细胞分裂中的可分离功能。
中心体和纺锤极体(SPB)对有丝分裂纺锤体的形成非常重要,同时也是信号平台。在裂殖酵母 Schizosaccharomyces pombe 中,基因消融和高分辨率成像表明,ɑ-螺旋形 Ppc89 是 SPB 结构和功能的核心。在这里,我们开发并鉴定了ppc89的条件突变体和截断突变体。C端附近的两个预测ɑ螺旋发生突变的等位基因在锚定Sid4(隔膜起始网络(SIN)的支架)和依赖于Sid4的蛋白(Cdc11、Dma1、Mto1和Mto2)方面存在特异性缺陷。将Sid4人工拴系到SPB上可完全拯救这些ppc89突变体。另一个ppc89等位基因在整个编码区都有突变。虽然该突变体也存在 Sid4 锚定缺陷,但它还表现出其他缺陷,包括 SPB 断裂以及在一个子细胞中形成并收缩第二个细胞运动环。ppc89等位基因被截去了最长的C-末端ɑ-螺旋,但仍能招募Sid4和SIN。我们的结论是,Ppc89 不仅能将 SIN 与 SPB 连接起来,而且对于 SPB 的完整性以及细胞分裂与有丝分裂的忠实协调也是必要的。
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
G3: Genes|Genomes|Genetics
G3: Genes|Genomes|Genetics GENETICS & HEREDITY-
CiteScore
5.10
自引率
3.80%
发文量
305
审稿时长
3-8 weeks
期刊介绍: G3: Genes, Genomes, Genetics provides a forum for the publication of high‐quality foundational research, particularly research that generates useful genetic and genomic information such as genome maps, single gene studies, genome‐wide association and QTL studies, as well as genome reports, mutant screens, and advances in methods and technology. The Editorial Board of G3 believes that rapid dissemination of these data is the necessary foundation for analysis that leads to mechanistic insights. G3, published by the Genetics Society of America, meets the critical and growing need of the genetics community for rapid review and publication of important results in all areas of genetics. G3 offers the opportunity to publish the puzzling finding or to present unpublished results that may not have been submitted for review and publication due to a perceived lack of a potential high-impact finding. G3 has earned the DOAJ Seal, which is a mark of certification for open access journals, awarded by DOAJ to journals that achieve a high level of openness, adhere to Best Practice and high publishing standards.
×
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