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Mps1 dimerization and multisite interactions with Ndc80 complex enable responsive spindle assembly checkpoint signaling

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Journal of Molecular Cell Biology 2020年第7期12卷 486-498页

作者： Ping Gui Divine M.Sedzro Xiao Yuan Sikai Liu Mohan Hei Wei Tian Najdat Zohbi Fangwei Wang Yihan Yao Felix O.Aikhionbare Xinjiao Gao Dongmei Wang Xuebiao Yao Zhen Dou MOE Key Laboratory of Membraneless Organelle and Cellular Dynamics Hefei National Laboratory for Physical Sciences at the MicroscaleSchool of Life SciencesUniversity of Science and Technology of ChinaHefei 230027China Keck Center for Cellular Dynamics and Organoids Plasticity Morehouse School of MedicineAtlantaGA 30310USA Key Laboratory of Molecular Biophysics of the Ministry of Education College of Life Science and TechnologyHuazhong University of Science and TechnologyWuhan 430074China Life Sciences Institute and Innovation Center for Cell Signaling Network Zhejiang UniversityHangzhou 310058China

Error-free mitosis depends on accurate chromosome attachment to spindle microtubules,which is monitored by the spindle assembly checkpoint(SAC)*** an upstream factor of SAC,the precise and dynamic kinetochore localization of Mps1 kinase is critical for initiating and silencing SAC ***,the underlying molecular mechanism remains ***,we demonstrated that the multisite interactions between Mps1 and Ndc80 complex(Ndc80C)govern Mps1 kinetochore ***,we identified direct interaction between Mps1 tetratricopeptide repeat domain and *** further identified that Mps1 C-terminal fragment,which contains the protein kinase domain and C-tail,enhances Mps1 kinetochore ***,Mps1 C-terminal fragment mediates its *** of C-tail attenuates the kinetochore targeting and activity of Mps1,leading to aberrant mitosis due to compromised SAC *** together,our study highlights the importance of Mps1 dimerization and multisite interactions with Ndc80C in enabling responsive SAC signaling.

关键词： mitosis spindle assembly checkpoint kinetochore Mps1 kinase Ndc80 complex

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The spindle assembly checkpoint:perspectives in tumorigenesis and cancer therapy

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Frontiers in Biology 2011年第2期6卷 147-155页

作者： Joana BARBOSA Ana Vanessa NASCIMENTO Juliana FARIA Patrícia SILVA Hassan BOUSBAA Centro de Investigação em Ciências da Saúde(CICS) Instituto Superior de Ciências da Saúde-NorteCESPURua Central de Gandra13174585-116 Gandra PRDPortugal

Loss or gain of chromosomes,a condition known as aneuploidy,is a common feature of tumor cells and has therefore been proposed as the driving force for *** chromosomal instability can arise during mitosis as a result of mis-segregation of the duplicated sister chromatids to the two daughter *** normal cells,missegregation is usually prevented by the spindle assembly checkpoint(SAC),a sophisticated surveillance mechanism that inhibits mitotic exit until all chromosomes have successfully achieved bipolar attachment to spindle *** abrogation of SAC activity is lethal to normal as well as to tumor cells,as a consequence of massive chromosome ***,many human aneuploid tumor cells exhibit a weakened SAC activity that allows them to tolerate gains or losses of a small number of chromosomes;and interfering with this SAC residual activity may constitute a suitable strategy to kill cancer *** review focuses on the potential link between SAC and tumorigenesis,and the therapeutic strategy to target the SAC for cancer treatment.

关键词： spindle assembly checkpoint mitosis chromosome instability tumor cancer therapy

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Spatial separation of phosphatase and kinase activity within the Bub complex is required for proper mitosis

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Journal of Molecular Cell Biology 2022年第11期14卷 24-35页

作者： Lei Wang Thomas Kruse Blanca López-Méndez Yuqing Zhang Chunlin Song Lei Zhu Bing Li Jing Fang Zhimin Lu Jakob Nilsson Gang Zhang The Cancer Institute The Affiliated Hospital of Qingdao UniversityQingdao UniversityQingdao 266061China Novo Nordisk Foundation Center for Protein Research Faculty of Health and Medical SciencesUniversity of CopenhagenCopenhagen DK-2200Denmark The Department of Genetics and Cell Biology Basic Medical CollegeQingdao UniversityQingdao 266061China Institute of Translational Medicine Zhejiang University School of MedicineHangzhou 310029China

The Bub1 and BubR1 kinetochore proteins support proper chromosome segregation and mitotic checkpoint activity. Bub1 and BubR1 are paralogs with Bub1 being a kinase, while BubR1 localizes the PP2A-B56 protein phosphatase to kinetochores in humans. Whether this spatial separation of kinase and phosphatase activity is important is unclear as some organisms integrate both activities into one Bub protein. Here, we engineer human Bub1 and BubR1 proteins integrating kinase and phosphatase activities into one protein and show that these do not support normal mitotic progression. A Bub1–PP2A-B56 complex can support chromosome alignment but results in impairment of the checkpoint due to dephosphorylation of the Mad1 binding site in Bub1. Furthermore, a chimeric BubR1 protein containing the Bub1 kinase domain induces delocalized H2ApT120 phosphorylation, resulting in the reduction of centromeric hSgo2 and chromosome segregation errors. Collectively, these results argue that the spatial separation of kinase and phosphatase activities within the Bub complex is required for balancing its functions in the checkpoint and chromosome alignment.

关键词： mitosis spindle assembly checkpoint kinetochores Bub1 BubR1 PP2A/B56

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Comparative analysis of chromosome segregation in human, yeasts and trypanosome

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Frontiers in Biology 2014年第6期9卷 472-480页

作者： Xianxian HAN Ziyin LI Department of Microbiology and Moleeular Genetics University of Texas Medical School Houston TX 77030 USA

Chromosome segregation is a tightly regulated process through which duplicated genetic materials are equally partitioned into daughter cells. During the past decades, tremendous efforts have been made to understand the molecular mechanism of chromosome segregation using animals and yeasts as model systems. Recently, new insights into chromosome segregation have gradually emerged using trypanosome, an early branching parasitic protozoan, as a model organism. To uncover the unique aspects of chromosome segregation in trypanosome, which potentially could serve as new drug targets for anti-trypanosome chemotherapy, it is necessary to perform a comparative analysis of the chromosome segregation machinery between trypanosome and its human host. Here, we briefly review the current knowledge about chromosome segregation in human and Trypanosoma brucei, with a focus on the regulation of cohesin and securin degradation triggered by the activation of the anaphase promoting complex/cyclosome （APC/C）. We also include yeasts in our comparative analysis since some of the original discoveries were made using budding and fission yeasts as the model organisms and, therefore, these could provide hints about the evolution of the machinery. We highlight both common and unique features in these model systems and also provide perspectives for future research in trypanosome.

关键词： cohesin separase securin anaphase promoting complex spindle assembly checkpoint T^panosoma brucei

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Identification and Characterization of Two Putative SAC Genes Involved in Fungal Development and Benzimidazole Resistance in Gibberella zeae

Identification and Characterization of Two Putative SAC Gene...

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中国植物病理学会2012年学术年会

作者： ZHANG Lei-Gang YU Xin-Yan JIA Xiao-Jing WANG Jian-Xin CHEN Chang-Jun ZHOU Ming-Guo~* (College of Plant Protection,Nanjing Agricultural University,Nanjing,China)

Resistance to carbendazim and other benzimidazole fungicides in Gibberella zeae is conferred by point mutations in theβ-tubulin gene,a gene that plays an important role in spindle assembly. The spindle assembly checkpoint is a cellular surveillance system that ensures the fidelity of chromosome segregation,which is critical for maintaining genomic *** this study,we isolated and characterized two predicted checkpoint protein-encoding genes(Mad2 and Bub1 ) in *** and designated them as FgMad2 and FgBub1,*** sequenced the two genes in two parental strains(one was sensitive to carbendazim while the other was highly resistant) and found no mutation,indicating that the resistance did not result from mutation of the two checkpoint *** FgMad2 deletion mutants grew slowlier and produced fewer conidia,both hyphae and conidia ***,the deletion of FgBub1 had no effect on fungal development other than a 47.7%～48.2%reduction in conidia ***2 deletion mutants exhibited a severe decrease(from 89.6%-90.4%) in perithecia production and pathogenicity along with a 39.5%～47.2%down-regulation of deoxynivalenol synthesis, whereas FgBub1 deletion mutants exhibited only a slight reduction in perithecia production but their pathogenicity was decreased by 51.1%～54.8%;these results suggested that asexual development,sexual development,and pathogenicity depend more on FgMad2 than on ***,the decrease in the pathogenicity of FgBub1 deletion mutants was accompanied by a two-fold increase in deoxynivalenol *** sensitivity of FgMad2 and FgBub1 deletion mutants to benzimidazole fungicides were both enhanced,especially for mutants original from MBC-high-resistant strain ***,parental strains and theirβ orβ -tubulin deletion mutants displayed high Mad2 expression when treated with MBC,which was not observed for Bub1,suggesting that FgMad2 responsed to spindle damage resulted from *** can

关键词： Gibberella zeae spindle assembly checkpoint Mad2 Bub1 benzimidazole resistance

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