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Journal articles on the topic 'Mitotic spindle checkpoint'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Encalada, Sandra E., John Willis, Rebecca Lyczak, and Bruce Bowerman. "A Spindle Checkpoint Functions during Mitosis in the Early Caenorhabditis elegans Embryo." Molecular Biology of the Cell 16, no. 3 (2005): 1056–70. http://dx.doi.org/10.1091/mbc.e04-08-0712.

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During mitosis, chromosome segregation is regulated by a spindle checkpoint mechanism. This checkpoint delays anaphase until all kinetochores are captured by microtubules from both spindle poles, chromosomes congress to the metaphase plate, and the tension between kinetochores and their attached microtubules is properly sensed. Although the spindle checkpoint can be activated in many different cell types, the role of this regulatory mechanism in rapidly dividing embryonic animal cells has remained controversial. Here, using time-lapse imaging of live embryonic cells, we show that chemical or m

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2

Rahmani, Zohra, Mary E. Gagou, Christophe Lefebvre, Doruk Emre, and Roger E. Karess. "Separating the spindle, checkpoint, and timer functions of BubR1." Journal of Cell Biology 187, no. 5 (2009): 597–605. http://dx.doi.org/10.1083/jcb.200905026.

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BubR1 performs several roles during mitosis, affecting the spindle assembly checkpoint (SAC), mitotic timing, and spindle function, but the interdependence of these functions is unclear. We have analyzed in Drosophila melanogaster the mitotic phenotypes of kinase-dead (KD) BubR1 and BubR1 lacking the N-terminal KEN box. bubR1-KD individuals have a robust SAC but abnormal spindles with thin kinetochore fibers, suggesting that the kinase activity modulates microtubule capture and/or dynamics but is relatively dispensable for SAC function. In contrast, bubR1-KEN flies have normal spindles but no

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3

Akhter, Shamima, Christopher T. Richie, Jian Min Deng, et al. "Deficiency in SNM1 Abolishes an Early Mitotic Checkpoint Induced by Spindle Stress." Molecular and Cellular Biology 24, no. 23 (2004): 10448–55. http://dx.doi.org/10.1128/mcb.24.23.10448-10455.2004.

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ABSTRACT Spindle poisons represent an important class of anticancer drugs that act by interfering with microtubule polymerization and dynamics and thereby induce mitotic checkpoints and apoptosis. Here we show that mammalian SNM1 functions in an early mitotic stress checkpoint that is distinct from the well-characterized spindle checkpoint that regulates the metaphase-to-anaphase transition. Specifically, we found that compared to wild-type cells, Snm1-deficient mouse embryonic fibroblasts exposed to spindle poisons exhibited elevated levels of micronucleus formation, decreased mitotic delay,

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4

Gorbsky, Gary J. "The mitotic spindle checkpoint." Current Biology 11, no. 24 (2001): R1001—R1004. http://dx.doi.org/10.1016/s0960-9822(01)00609-1.

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5

Fraschini, Roberta, Denis Bilotta, Giovanna Lucchini, and Simonetta Piatti. "Functional Characterization of Dma1 and Dma2, the Budding Yeast Homologues of Schizosaccharomyces pombe Dma1 and Human Chfr." Molecular Biology of the Cell 15, no. 8 (2004): 3796–810. http://dx.doi.org/10.1091/mbc.e04-02-0094.

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Proper transmission of genetic information requires correct assembly and positioning of the mitotic spindle, responsible for driving each set of sister chromatids to the two daughter cells, followed by cytokinesis. In case of altered spindle orientation, the spindle position checkpoint inhibits Tem1-dependent activation of the mitotic exit network (MEN), thus delaying mitotic exit and cytokinesis until errors are corrected. We report a functional analysis of two previously uncharacterized budding yeast proteins, Dma1 and Dma2, 58% identical to each other and homologous to human Chfr and Schizo

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6

Gadea, Bedrick B., and Joan V. Ruderman. "Aurora Kinase Inhibitor ZM447439 Blocks Chromosome-induced Spindle Assembly, the Completion of Chromosome Condensation, and the Establishment of the Spindle Integrity Checkpoint inXenopusEgg Extracts." Molecular Biology of the Cell 16, no. 3 (2005): 1305–18. http://dx.doi.org/10.1091/mbc.e04-10-0891.

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The Aurora family kinases contribute to accurate progression through several mitotic events. ZM447439 (“ZM”), the first Aurora family kinase inhibitor to be developed and characterized, was previously found to interfere with the mitotic spindle integrity checkpoint and chromosome segregation. Here, we have used extracts of Xenopus eggs, which normally proceed through the early embryonic cell cycles in the absence of functional checkpoints, to distinguish between ZM's effects on the basic cell cycle machinery and its effects on checkpoints. ZM clearly had no effect on either the kinetics or amp

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7

Farr, Katie A., and M. Andrew Hoyt. "Bub1p Kinase Activates the Saccharomyces cerevisiae Spindle Assembly Checkpoint." Molecular and Cellular Biology 18, no. 5 (1998): 2738–47. http://dx.doi.org/10.1128/mcb.18.5.2738.

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ABSTRACT Saccharomyces cerevisiae BUB1 encodes a protein kinase required for spindle assembly checkpoint function. In the presence of spindle damage, BUB1 is required to prevent cell cycle progression into anaphase. We have identified a dominantly actingBUB1 allele that appears to activate the spindle assembly checkpoint pathway in cells with undamaged spindles. High-level expression of BUB1-5 did not cause detectable spindle damage, yet it delayed yeast cells in mitosis at a stage following bipolar spindle assembly but prior to anaphase spindle elongation. Delayed cells possessed a G2 DNA con

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8

Rohrabaugh, Sara, Charlie Mantel, and Hal E. Broxmeyer. "Mouse Hematopoietic Stem Cells, Unlike Human and Mouse Embryonic Stem Cells, Exhibit Checkpoint-Apoptosis Coupling." Blood 110, no. 11 (2007): 3357. http://dx.doi.org/10.1182/blood.v110.11.3357.3357.

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Abstract Cell cycle checkpoints guarantee that cells move through the events of the cell cycle in the appropriate manner. The mitotic spindle checkpoint, also known as the spindle assembly checkpoint (SAC), helps to ensure the proper segregation of chromosomes into daughter cells during mitosis. Our lab recently reported on the condition of the SAC in both mouse and human embryonic stem cells (ESCs). We found that ESCs do not initiate apoptosis when the SAC is activated, which allowed these cells to tolerate a polyploid state resulting from the aberrant mitosis (Mantel et al. Blood.109: 4518–4

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9

Kapoor, Tarun M., Thomas U. Mayer, Margaret L. Coughlin, and Timothy J. Mitchison. "Probing Spindle Assembly Mechanisms with Monastrol, a Small Molecule Inhibitor of the Mitotic Kinesin, Eg5." Journal of Cell Biology 150, no. 5 (2000): 975–88. http://dx.doi.org/10.1083/jcb.150.5.975.

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Monastrol, a cell-permeable small molecule inhibitor of the mitotic kinesin, Eg5, arrests cells in mitosis with monoastral spindles. Here, we use monastrol to probe mitotic mechanisms. We find that monastrol does not inhibit progression through S and G2 phases of the cell cycle or centrosome duplication. The mitotic arrest due to monastrol is also rapidly reversible. Chromosomes in monastrol-treated cells frequently have both sister kinetochores attached to microtubules extending to the center of the monoaster (syntelic orientation). Mitotic arrest–deficient protein 2 (Mad2) localizes to a sub

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10

Wang, Xiao Min, Ye Zhai, and James E. Ferrell. "A Role for Mitogen-activated Protein Kinase in the Spindle Assembly Checkpoint in XTC Cells." Journal of Cell Biology 137, no. 2 (1997): 433–43. http://dx.doi.org/10.1083/jcb.137.2.433.

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The spindle assembly checkpoint prevents cells whose spindles are defective or chromosomes are misaligned from initiating anaphase and leaving mitosis. Studies of Xenopus egg extracts have implicated the Erk2 mitogen-activated protein kinase (MAP kinase) in this checkpoint. Other studies have suggested that MAP kinases might be important for normal mitotic progression. Here we have investigated whether MAP kinase function is required for mitotic progression or the spindle assembly checkpoint in vivo in Xenopus tadpole cells (XTC). We determined that Erk1 and/or Erk2 are present in the mitotic

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11

Gillett, Emily S., Christopher W. Espelin, and Peter K. Sorger. "Spindle checkpoint proteins and chromosome–microtubule attachment in budding yeast." Journal of Cell Biology 164, no. 4 (2004): 535–46. http://dx.doi.org/10.1083/jcb.200308100.

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Accurate chromosome segregation depends on precise regulation of mitosis by the spindle checkpoint. This checkpoint monitors the status of kinetochore–microtubule attachment and delays the metaphase to anaphase transition until all kinetochores have formed stable bipolar connections to the mitotic spindle. Components of the spindle checkpoint include the mitotic arrest defective (MAD) genes MAD1–3, and the budding uninhibited by benzimidazole (BUB) genes BUB1 and BUB3. In animal cells, all known spindle checkpoint proteins are recruited to kinetochores during normal mitoses. In contrast, we sh

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12

Luo, Jianjun, Xinjing Xu, Hana Hall, et al. "Histone H3 Exerts a Key Function in Mitotic Checkpoint Control." Molecular and Cellular Biology 30, no. 2 (2009): 537–49. http://dx.doi.org/10.1128/mcb.00980-09.

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ABSTRACT It has been firmly established that many interphase nuclear functions, including transcriptional regulation, are regulated by chromatin and histones. How mitotic progression and quality control might be influenced by histones is less well characterized. We show that histone H3 plays a crucial role in activating the spindle assembly checkpoint in response to a defect in mitosis. Prior to anaphase, all chromosomes must attach to spindles emanating from the opposite spindle pole bodies. The tension between sister chromatids generated by the poleward pulling force is an integral part of c

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13

Chow, Jeremy P. H., Wai Yi Siu, Tsz Kan Fung, et al. "DNA Damage during the Spindle-Assembly Checkpoint Degrades CDC25A, Inhibits Cyclin–CDC2 Complexes, and Reverses Cells to Interphase." Molecular Biology of the Cell 14, no. 10 (2003): 3989–4002. http://dx.doi.org/10.1091/mbc.e03-03-0168.

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Cell cycle checkpoints that monitor DNA damage and spindle assembly are essential for the maintenance of genetic integrity, and drugs that target these checkpoints are important chemotherapeutic agents. We have examined how cells respond to DNA damage while the spindle-assembly checkpoint is activated. Single cell electrophoresis and phosphorylation of histone H2AX indicated that several chemotherapeutic agents could induce DNA damage during mitotic block. DNA damage during mitotic block triggered CDC2 inactivation, histone H3 dephosphorylation, and chromosome decondensation. Cells did not pro

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14

Adames, Neil R., Jessica R. Oberle, and John A. Cooper. "The Surveillance Mechanism of the Spindle Position Checkpoint in Yeast." Journal of Cell Biology 153, no. 1 (2001): 159–68. http://dx.doi.org/10.1083/jcb.153.1.159.

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The spindle position checkpoint in Saccharomyces cerevisiae delays mitotic exit until the spindle has moved into the mother–bud neck, ensuring that each daughter cell inherits a nucleus. The small G protein Tem1p is critical in promoting mitotic exit and is concentrated at the spindle pole destined for the bud. The presumed nucleotide exchange factor for Tem1p, Lte1p, is concentrated in the bud. These findings suggested the hypothesis that movement of the spindle pole through the neck allows Tem1p to interact with Lte1p, promoting GTP loading of Tem1p and mitotic exit. However, we report that

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15

Hofmann, Christian, Iain M. Cheeseman, Bruce L. Goode, Kent L. McDonald, Georjana Barnes, and David G. Drubin. "Saccharomyces cerevisiae Duo1p and Dam1p, Novel Proteins Involved in Mitotic Spindle Function." Journal of Cell Biology 143, no. 4 (1998): 1029–40. http://dx.doi.org/10.1083/jcb.143.4.1029.

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In this paper, we describe the identification and characterization of two novel and essential mitotic spindle proteins, Duo1p and Dam1p. Duo1p was isolated because its overexpression caused defects in mitosis and a mitotic arrest. Duo1p was localized by immunofluorescence, by immunoelectron microscopy, and by tagging with green fluorescent protein (GFP), to intranuclear spindle microtubules and spindle pole bodies. Temperature-sensitive duo1 mutants arrest with short spindles. This arrest is dependent on the mitotic checkpoint. Dam1p was identified by two-hybrid analysis as a protein that bind

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16

Alfonso-Pérez, Tatiana, Daniel Hayward, James Holder, Ulrike Gruneberg, and Francis A. Barr. "MAD1-dependent recruitment of CDK1-CCNB1 to kinetochores promotes spindle checkpoint signaling." Journal of Cell Biology 218, no. 4 (2019): 1108–17. http://dx.doi.org/10.1083/jcb.201808015.

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Cyclin B–dependent kinase (CDK1-CCNB1) promotes entry into mitosis. Additionally, it inhibits mitotic exit by activating the spindle checkpoint. This latter role is mediated through phosphorylation of the checkpoint kinase MPS1 and other spindle checkpoint proteins. We find that CDK1-CCNB1 localizes to unattached kinetochores and like MPS1 is lost from these structures upon microtubule attachment. This suggests that CDK1-CCNB1 is an integral component and not only an upstream regulator of the spindle checkpoint pathway. Complementary proteomic and cell biological analysis demonstrate that the

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17

Lou, Yang, Jianhui Yao, Arzhang Zereshki, et al. "NEK2A Interacts with MAD1 and Possibly Functions as a Novel Integrator of the Spindle Checkpoint Signaling." Journal of Biological Chemistry 279, no. 19 (2004): 20049–57. http://dx.doi.org/10.1074/jbc.m314205200.

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Chromosome segregation in mitosis is orchestrated by protein kinase signaling cascades. A biochemical cascade named spindle checkpoint ensures the spatial and temporal order of chromosome segregation during mitosis. Here we report that spindle checkpoint protein MAD1 interacts with NEK2A, a human orthologue of theAspergillus nidulansNIMA kinase. MAD1 interacts with NEK2Ain vitroandin vivovia a leucine zipper-containing domain located at the C terminus of MAD1. Like MAD1, NEK2A is localized to HeLa cell kinetochore of mitotic cells. Elimination of NEK2A by small interfering RNA does not arrest

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18

Schnerch, Dominik, Julia Felthaus, Monika Engelhardt, and Ralph M. Waesch. "Spindle Checkpoint Insufficiency in Acute Myeloid Leukemia." Blood 110, no. 11 (2007): 873. http://dx.doi.org/10.1182/blood.v110.11.873.873.

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Abstract Chromosomal instability and aneuploidy are hallmarks of most human malignancies. Various mechanisms have been shown to give rise to numerical chromosome aberrations. Compromised function of the spindle assembly checkpoint (SAC) is generally regarded as one of the most powerful ways to drive genome instability. The SAC is a mitotic checkpoint mechanism ensuring the equal segregation of the mitotic chromosomes onto the developing daughter cells. Unfaithful mitotic surveillance by the SAC favors chromosomal misdistribution as error-prone chromosome attachment to the mitotic spindle does

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19

Hwang, Hyung-Seo, and Kiwon Song. "IBD2 Encodes a Novel Component of the Bub2p-Dependent Spindle Checkpoint in the Budding Yeast Saccharomyces cerevisiae." Genetics 161, no. 2 (2002): 595–609. http://dx.doi.org/10.1093/genetics/161.2.595.

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Abstract During mitosis, genomic integrity is maintained by the proper coordination of mitotic events through the spindle checkpoint. The bifurcated spindle checkpoint blocks cell cycle progression at metaphase by monitoring unattached kinetochores and inhibits mitotic exit in response to the incorrect orientation of the mitotic spindle. Bfa1p is a spindle checkpoint regulator of budding yeast in the Bub2p checkpoint pathway for proper mitotic exit. We have isolated a novel Bfa1p interacting protein named Ibd2p in the budding yeast Saccharomyces cerevisiae. We found that IBD2 (Inhibition of Bu

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20

Yellman, Christopher M., and Daniel J. Burke. "The Role of Cdc55 in the Spindle Checkpoint Is through Regulation of Mitotic Exit in Saccharomyces cerevisiae." Molecular Biology of the Cell 17, no. 2 (2006): 658–66. http://dx.doi.org/10.1091/mbc.e05-04-0336.

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Cdc55, a B-type regulatory subunit of protein phosphatase 2A, has been implicated in mitotic spindle checkpoint activity and maintenance of sister chromatid cohesion during metaphase. The spindle checkpoint is composed of two independent pathways, one leading to inhibition of the metaphase-to-anaphase transition by checkpoint proteins, including Mad2, and the other to inhibition of mitotic exit by Bub2. We show that Cdc55 is a negative regulator of mitotic exit. A cdc55 mutant, like a bub2 mutant, prematurely releases Cdc14 phosphatase from the nucleolus during spindle checkpoint activation, a

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21

Musacchio, Andrea. "Spindle assembly checkpoint: the third decade." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1584 (2011): 3595–604. http://dx.doi.org/10.1098/rstb.2011.0072.

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The spindle assembly checkpoint controls cell cycle progression during mitosis, synchronizing it with the attachment of chromosomes to spindle microtubules. After the discovery of the mitotic arrest deficient ( MAD ) and budding uninhibited by benzymidazole ( BUB ) genes as crucial checkpoint components in 1991, the second decade of checkpoint studies (2001–2010) witnessed crucial advances in the elucidation of the mechanism through which the checkpoint effector, the mitotic checkpoint complex, targets the anaphase-promoting complex (APC/C) to prevent progression into anaphase. Concomitantly,

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22

Montembault, Emilie, Stéphanie Dutertre, Claude Prigent, and Régis Giet. "PRP4 is a spindle assembly checkpoint protein required for MPS1, MAD1, and MAD2 localization to the kinetochores." Journal of Cell Biology 179, no. 4 (2007): 601–9. http://dx.doi.org/10.1083/jcb.200703133.

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The spindle checkpoint delays anaphase onset until every chromosome kinetochore has been efficiently captured by the mitotic spindle microtubules. In this study, we report that the human pre–messenger RNA processing 4 (PRP4) protein kinase associates with kinetochores during mitosis. PRP4 depletion by RNA interference induces mitotic acceleration. Moreover, we frequently observe lagging chromatids during anaphase leading to aneuploidy. PRP4-depleted cells do not arrest in mitosis after nocodazole treatment, indicating a spindle assembly checkpoint (SAC) failure. Thus, we find that PRP4 is nece

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23

Wang, Y., and D. J. Burke. "Checkpoint genes required to delay cell division in response to nocodazole respond to impaired kinetochore function in the yeast Saccharomyces cerevisiae." Molecular and Cellular Biology 15, no. 12 (1995): 6838–44. http://dx.doi.org/10.1128/mcb.15.12.6838.

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Inhibition of mitosis by antimitotic drugs is thought to occur by destruction of microtubules, causing cells to arrest through the action of one or more mitotic checkpoints. We have patterned experiments in the yeast Saccharomyces cerevisiae after recent studies in mammalian cells that demonstrate the effectiveness of antimitotic drugs at concentrations that maintain spindle structure. We show that low concentrations of nocodazole delay cell division under the control of the previously identified mitotic checkpoint genes BUB1, BUB3, MAD1, and MAD2 and independently of BUB2. The same genes medi

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24

Craig, R., and C. Norbury. "The novel murine calmodulin-binding protein Sha1 disrupts mitotic spindle and replication checkpoint functions in fission yeast." Journal of Cell Science 111, no. 24 (1998): 3609–19. http://dx.doi.org/10.1242/jcs.111.24.3609.

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Entry into mitosis is normally blocked in eukaryotic cells that have not completed replicative DNA synthesis; this ‘S-M’ checkpoint control is fundamental to the maintenance of genomic integrity. Mutants of the fission yeast Schizosaccharomyces pombe defective in the S-M checkpoint fail to arrest the cell cycle when DNA replication is inhibited and hence attempt mitosis and cell division with unreplicated chromosomes, resulting in the ‘cut’ phenotype. In an attempt to identify conserved molecules involved in the S-M checkpoint we have screened a regulatable murine cDNA library in S. pombe and

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25

Zon, Wouter van, and Rob M. F. Wolthuis. "Cyclin A and Nek2A: APC/C–Cdc20 substrates invisible to the mitotic spindle checkpoint." Biochemical Society Transactions 38, no. 1 (2010): 72–77. http://dx.doi.org/10.1042/bst0380072.

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Active cyclin B1–Cdk1 (cyclin-dependent kinase 1) keeps cells in mitosis, allowing time for spindle microtubules to capture the chromosomes and for incorrect chromosome-spindle attachments to be repaired. Meanwhile, securin, an inhibitor of separase, secures cohesion between sister chromatids, preventing anaphase onset. The spindle checkpoint is a signalling pathway emerging from improperly attached chromosomes that inhibits Cdc20, the mitotic activator of the APC/C (anaphase-promoting complex/cyclosome) ubiquitin ligase. Blocking Cdc20 stabilizes cyclin B1 and securin to delay mitotic exit an

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Orr, Bernardo, Hassan Bousbaa, and Claudio E. Sunkel. "Mad2-independent Spindle Assembly Checkpoint Activation and Controlled Metaphase–Anaphase Transition inDrosophilaS2 Cells." Molecular Biology of the Cell 18, no. 3 (2007): 850–63. http://dx.doi.org/10.1091/mbc.e06-07-0587.

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The spindle assembly checkpoint is essential to maintain genomic stability during cell division. We analyzed the role of the putative Drosophila Mad2 homologue in the spindle assembly checkpoint and mitotic progression. Depletion of Mad2 by RNAi from S2 cells shows that it is essential to prevent mitotic exit after spindle damage, demonstrating its conserved role. Mad2-depleted cells also show accelerated transit through prometaphase and premature sister chromatid separation, fail to form metaphases, and exit mitosis soon after nuclear envelope breakdown with extensive chromatin bridges that r

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27

Brito, Daniela A., Zhenye Yang, and Conly L. Rieder. "Microtubules do not promote mitotic slippage when the spindle assembly checkpoint cannot be satisfied." Journal of Cell Biology 182, no. 4 (2008): 623–29. http://dx.doi.org/10.1083/jcb.200805072.

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When the spindle assembly checkpoint (SAC) cannot be satisfied, cells exit mitosis via mitotic slippage. In microtubule (MT) poisons, slippage requires cyclin B proteolysis, and it appears to be accelerated in drug concentrations that allow some MT assembly. To determine if MTs accelerate slippage, we followed mitosis in human RPE-1 cells exposed to various spindle poisons. At 37°C, the duration of mitosis in nocodazole, colcemid, or vinblastine concentrations that inhibit MT assembly varied from 20 to 30 h, revealing that different MT poisons differentially depress the cyclin B destruction ra

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Hardwick, Kevin G., Rong Li, Cathy Mistrot, et al. "Lesions in Many Different Spindle Components Activate the Spindle Checkpoint in the Budding Yeast Saccharomyces cerevisiae." Genetics 152, no. 2 (1999): 509–18. http://dx.doi.org/10.1093/genetics/152.2.509.

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Abstract The spindle checkpoint arrests cells in mitosis in response to defects in the assembly of the mitotic spindle or errors in chromosome alignment. We determined which spindle defects the checkpoint can detect by examining the interaction of mutations that compromise the checkpoint (mad1, mad2, and mad3) with those that damage various structural components of the spindle. Defects in microtubule polymerization, spindle pole body duplication, microtubule motors, and kinetochore components all activate the MAD-dependent checkpoint. In contrast, the cell cycle arrest caused by mutations that

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Wang, Mengqiao, and Ruth N. Collins. "A lysine deacetylase Hos3 is targeted to the bud neck and involved in the spindle position checkpoint." Molecular Biology of the Cell 25, no. 18 (2014): 2720–34. http://dx.doi.org/10.1091/mbc.e13-10-0619.

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An increasing number of cellular activities can be regulated by reversible lysine acetylation. Targeting the enzymes responsible for such posttranslational modifications is instrumental in defining their substrates and functions in vivo. Here we show that a Saccharomyces cerevisiae lysine deacetylase, Hos3, is asymmetrically targeted to the daughter side of the bud neck and to the daughter spindle pole body (SPB). The morphogenesis checkpoint member Hsl7 recruits Hos3 to the neck region. Cells with a defect in spindle orientation trigger Hos3 to load onto both SPBs. When associated symmetrical

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Weiss, E., and M. Winey. "The Saccharomyces cerevisiae spindle pole body duplication gene MPS1 is part of a mitotic checkpoint." Journal of Cell Biology 132, no. 1 (1996): 111–23. http://dx.doi.org/10.1083/jcb.132.1.111.

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M-phase checkpoints inhibit cell division when mitotic spindle function is perturbed. Here we show that the Saccharomyces cerevisiae MPS1 gene product, an essential protein kinase required for spindle pole body (SPB) duplication (Winey et al., 1991; Lauze et al., 1995), is also required for M-phase check-point function. In cdc31-2 and mps2-1 mutants, conditional failure of SPB duplication results in cell cycle arrest with high p34CDC28 kinase activity that depends on the presence of the wild-type MAD1 checkpoint gene, consistent with checkpoint arrest of mitosis. In contrast, mps1 mutant cells

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Nelson, Scott A., and John A. Cooper. "A Novel Pathway that Coordinates Mitotic Exit with Spindle Position." Molecular Biology of the Cell 18, no. 9 (2007): 3440–50. http://dx.doi.org/10.1091/mbc.e07-03-0242.

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In budding yeast, the spindle position checkpoint (SPC) delays mitotic exit until the mitotic spindle moves into the neck between the mother and bud. This checkpoint works by inhibiting the mitotic exit network (MEN), a signaling cascade initiated and controlled by Tem1, a small GTPase. Tem1 is regulated by a putative guanine exchange factor, Lte1, but the function and regulation of Lte1 remains poorly understood. Here, we identify novel components of the checkpoint that operate upstream of Lte1. We present genetic evidence in agreement with existing biochemical evidence for the molecular mech

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Orjalo, Arturo V., Alexei Arnaoutov, Zhouxin Shen, et al. "The Nup107-160 Nucleoporin Complex Is Required for Correct Bipolar Spindle Assembly." Molecular Biology of the Cell 17, no. 9 (2006): 3806–18. http://dx.doi.org/10.1091/mbc.e05-11-1061.

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The Nup107-160 complex is a critical subunit of the nuclear pore. This complex localizes to kinetochores in mitotic mammalian cells, where its function is unknown. To examine Nup107-160 complex recruitment to kinetochores, we stained human cells with antisera to four complex components. Each antibody stained not only kinetochores but also prometaphase spindle poles and proximal spindle fibers, mirroring the dual prometaphase localization of the spindle checkpoint proteins Mad1, Mad2, Bub3, and Cdc20. Indeed, expanded crescents of the Nup107-160 complex encircled unattached kinetochores, simila

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Lee, Kyunghee, Alison E. Kenny, and Conly L. Rieder. "P38 Mitogen-activated Protein Kinase Activity Is Required during Mitosis for Timely Satisfaction of the Mitotic Checkpoint But Not for the Fidelity of Chromosome Segregation." Molecular Biology of the Cell 21, no. 13 (2010): 2150–60. http://dx.doi.org/10.1091/mbc.e10-02-0125.

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Although p38 activity is reported to be required as cells enter mitosis for proper spindle assembly and checkpoint function, its role during the division process remains controversial in lieu of direct data. We therefore conducted live cell studies to determine the effect on mitosis of inhibiting or depleting p38. We found that in the absence of p38 activity the duration of mitosis is prolonged by ∼40% in nontransformed human RPE-1, ∼80% in PtK2 (rat kangaroo), and ∼25% in mouse cells, and this prolongation leads to an elevated mitotic index. However, under this condition chromatid segregation

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34

Hardwick, K. G., and A. W. Murray. "Mad1p, a phosphoprotein component of the spindle assembly checkpoint in budding yeast." Journal of Cell Biology 131, no. 3 (1995): 709–20. http://dx.doi.org/10.1083/jcb.131.3.709.

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The spindle assembly checkpoint prevents cells from initiating anaphase until the spindle has been fully assembled. We previously isolated mitotic arrest deficient (mad) mutants that inactivate this checkpoint and thus increase the sensitivity of cells to benomyl, a drug that interferes with mitotic spindle assembly by depolymerizing microtubules. We have cloned the MAD1 gene and show that when it is disrupted yeast cells have the same phenotype as the previously isolated mad1 mutants: they fail to delay the metaphase to anaphase transition in response to microtubule depolymerization. MAD1 is

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35

De Souza, Colin P., Shahr B. Hashmi, Tania Nayak, Berl Oakley, and Stephen A. Osmani. "Mlp1 Acts as a Mitotic Scaffold to Spatially Regulate Spindle Assembly Checkpoint Proteins in Aspergillus nidulans." Molecular Biology of the Cell 20, no. 8 (2009): 2146–59. http://dx.doi.org/10.1091/mbc.e08-08-0878.

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During open mitosis several nuclear pore complex (NPC) proteins have mitotic specific localizations and functions. We find that the Aspergillus nidulans Mlp1 NPC protein has previously unrealized mitotic roles involving spatial regulation of spindle assembly checkpoint (SAC) proteins. In interphase, An-Mlp1 tethers the An-Mad1 and An-Mad2 SAC proteins to NPCs. During a normal mitosis, An-Mlp1, An-Mad1, and An-Mad2 localize similarly on, and around, kinetochores until telophase when they transiently localize near the spindle but not at kinetochores. During SAC activation, An-Mlp1 remains associ

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Heasley, Lydia R., Steven M. Markus, and Jennifer G. DeLuca. "“Wait anaphase” signals are not confined to the mitotic spindle." Molecular Biology of the Cell 28, no. 9 (2017): 1186–94. http://dx.doi.org/10.1091/mbc.e17-01-0036.

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The spindle assembly checkpoint ensures the faithful inheritance of chromosomes by arresting mitotic progression in the presence of kinetochores that are not attached to spindle microtubules. This is achieved through inhibition of the anaphase-promoting complex/cyclosome by a kinetochore-derived “wait anaphase” signal known as the mitotic checkpoint complex. It remains unclear whether the localization and activity of these inhibitory complexes are restricted to the mitotic spindle compartment or are diffusible throughout the cytoplasm. Here we report that “wait anaphase” signals are indeed abl

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Garber, Peter M., and Jasper Rine. "Overlapping Roles of the Spindle Assembly and DNA Damage Checkpoints in the Cell-Cycle Response to Altered Chromosomes in Saccharomyces cerevisiae." Genetics 161, no. 2 (2002): 521–34. http://dx.doi.org/10.1093/genetics/161.2.521.

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Abstract The MAD2-dependent spindle checkpoint blocks anaphase until all chromosomes have achieved successful bipolar attachment to the mitotic spindle. The DNA damage and DNA replication checkpoints block anaphase in response to DNA lesions that may include single-stranded DNA and stalled replication forks. Many of the same conditions that activate the DNA damage and DNA replication checkpoints also activated the spindle checkpoint. The mad2Δ mutation partially relieved the arrest responses of cells to mutations affecting the replication proteins Mcm3p and Pol1p. Thus a previously unrecognize

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Vader, Gerben, Carin W. A. Cruijsen, Tanja van Harn, Martijn J. M. Vromans, René H. Medema, and Susanne M. A. Lens. "The Chromosomal Passenger Complex Controls Spindle Checkpoint Function Independent from Its Role in Correcting Microtubule–Kinetochore Interactions." Molecular Biology of the Cell 18, no. 11 (2007): 4553–64. http://dx.doi.org/10.1091/mbc.e07-04-0328.

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The chromosomal passenger complex (CPC) is a critical regulator of chromosome segregation during mitosis by correcting nonbipolar microtubule-kinetochore interactions. By severing these interactions, the CPC is thought to create unattached kinetochores that are subsequently sensed by the spindle assembly checkpoint (SAC) to prevent premature mitotic exit. We now show that spindle checkpoint function of the CPC and its role in eliminating nonbipolar attachments can be uncoupled. Replacing the chromosomal passenger protein INCENP with a mutant allele that lacks its coiled-coil domain results in

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Saitoh, Shigeaki, Kojiro Ishii, Yasuyo Kobayashi, and Kohta Takahashi. "Spindle Checkpoint Signaling Requires the Mis6 Kinetochore Subcomplex, Which Interacts with Mad2 and Mitotic Spindles." Molecular Biology of the Cell 16, no. 8 (2005): 3666–77. http://dx.doi.org/10.1091/mbc.e05-01-0014.

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The spindle checkpoint coordinates cell cycle progression and chromosome segregation by inhibiting anaphase promoting complex/cyclosome until all kinetochores interact with the spindle properly. During early mitosis, the spindle checkpoint proteins, such as Mad2 and Bub1, accumulate at kinetochores that do not associate with the spindle. Here, we assess the requirement of various kinetochore components for the accumulation of Mad2 and Bub1 on the kinetochore in fission yeast and show that the necessity of the Mis6-complex and the Nuf2-complex is an evolutionarily conserved feature in the loadi

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Brandeis, Michael. "Slip slidin’ away of mitosis with CRL2Zyg11." Journal of Cell Biology 215, no. 2 (2016): 143–45. http://dx.doi.org/10.1083/jcb.201609086.

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The spindle assembly checkpoint arrests mitotic cells by preventing degradation of cyclin B1 by the anaphase-promoting complex/cyclosome, but some cells evade this checkpoint and slip out of mitosis. Balachandran et al. (2016. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201601083) show that the E3 ligase CRL2ZYG11 degrades cyclin B1, allowing mitotic slippage.

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Tao, Weikang, Victoria J. South, Ronald E. Diehl, et al. "An Inhibitor of the Kinesin Spindle Protein Activates the Intrinsic Apoptotic Pathway Independently of p53 and De Novo Protein Synthesis." Molecular and Cellular Biology 27, no. 2 (2006): 689–98. http://dx.doi.org/10.1128/mcb.01505-06.

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ABSTRACT The kinesin spindle protein (KSP), a microtubule motor protein, is essential for the formation of bipolar spindles during mitosis. Inhibition of KSP activates the spindle checkpoint and causes apoptosis. It was shown that prolonged inhibition of KSP activates Bax and caspase-3, which requires a competent spindle checkpoint and couples with mitotic slippage. Here we investigated how Bax is activated by KSP inhibition and the roles of Bax and p53 in KSP inhibitor-induced apoptosis. We demonstrate that small interfering RNA-mediated knockdown of Bax greatly attenuates KSP inhibitor-induc

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Tavormina, P. A., Y. Wang, and D. J. Burke. "Differential requirements for DNA replication in the activation of mitotic checkpoints in Saccharomyces cerevisiae." Molecular and Cellular Biology 17, no. 6 (1997): 3315–22. http://dx.doi.org/10.1128/mcb.17.6.3315.

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Checkpoints prevent inaccurate chromosome segregation by inhibiting cell division when errors in mitotic processes are encountered. We used a temperature-sensitive mutation, dbf4, to examine the requirement for DNA replication in establishing mitotic checkpoint arrest. We used gamma-irradiation to induce DNA damage and hydroxyurea to limit deoxyribonucleotides in cells deprived of DBF4 function to investigate the requirement for DNA replication in DNA-responsive checkpoints. In the absence of DNA replication, mitosis was not inhibited by these treatments, which normally activate the DNA damage

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Ditchfield, Claire, Victoria L. Johnson, Anthony Tighe, et al. "Aurora B couples chromosome alignment with anaphase by targeting BubR1, Mad2, and Cenp-E to kinetochores." Journal of Cell Biology 161, no. 2 (2003): 267–80. http://dx.doi.org/10.1083/jcb.200208091.

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The Aurora/Ipl1 family of protein kinases plays multiple roles in mitosis and cytokinesis. Here, we describe ZM447439, a novel selective Aurora kinase inhibitor. Cells treated with ZM447439 progress through interphase, enter mitosis normally, and assemble bipolar spindles. However, chromosome alignment, segregation, and cytokinesis all fail. Despite the presence of maloriented chromosomes, ZM447439-treated cells exit mitosis with normal kinetics, indicating that the spindle checkpoint is compromised. Indeed, ZM447439 prevents mitotic arrest after exposure to paclitaxel. RNA interference experi

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Thomas, Jennifer T., and Laimonis A. Laimins. "Human Papillomavirus Oncoproteins E6 and E7 Independently Abrogate the Mitotic Spindle Checkpoint." Journal of Virology 72, no. 2 (1998): 1131–37. http://dx.doi.org/10.1128/jvi.72.2.1131-1137.1998.

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ABSTRACT The E6 and E7 genes of the high-risk human papillomavirus (HPV) types encode oncoproteins, and both act by interfering with the activity of cellular tumor suppressor proteins. E7 proteins act by associating with members of the retinoblastoma family, while E6 increases the turnover of p53. p53 has been implicated as a regulator of both the G1/S cell cycle checkpoint and the mitotic spindle checkpoint. When fibroblasts from p53 knockout mice are treated with the spindle inhibitor nocodazole, a rereplication of DNA occurs without transit through mitosis. We investigated whether E6 or E7

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Serpico, Angela Flavia, and Domenico Grieco. "Recent advances in understanding the role of Cdk1 in the Spindle Assembly Checkpoint." F1000Research 9 (January 28, 2020): 57. http://dx.doi.org/10.12688/f1000research.21185.1.

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The goal of mitosis is to form two daughter cells each containing one copy of each mother cell chromosome, replicated in the previous S phase. To achieve this, sister chromatids held together back-to-back at their primary constriction, the centromere, have to interact with microtubules of the mitotic spindle so that each chromatid takes connections with microtubules emanating from opposite spindle poles (we will refer to this condition as bipolar attachment). Only once all replicated chromosomes have reached bipolar attachments can sister chromatids lose cohesion with each other, at the onset

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Cowley, Dale O., Ginger W. Muse, and Terry Van Dyke. "A Dominant Interfering Bub1 Mutant Is Insufficient To Induce or Alter Thymic Tumorigenesis In Vivo, Even in a Sensitized Genetic Background." Molecular and Cellular Biology 25, no. 17 (2005): 7796–802. http://dx.doi.org/10.1128/mcb.25.17.7796-7802.2005.

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ABSTRACT Aneuploidy is a common feature of human tumors, often correlating with poor prognosis. The mitotic spindle checkpoint is thought to play a major role in aneuploidy suppression. To investigate the role of the spindle checkpoint in tumor suppression in vivo, we developed transgenic mice in which thymocytes express a dominant interfering fragment of Bub1, a kinase regulator of the spindle checkpoint. We report that, despite high-level expression of dominant-negative Bub1 (Bub1DN), a protein known to inhibit spindle checkpoint activity in cultured cells, thymocytes show no evidence of spi

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Sharp-Baker, Hilary, and Rey-Huei Chen. "Spindle Checkpoint Protein Bub1 Is Required for Kinetochore Localization of Mad1, Mad2, Bub3, and Cenp-E, Independently of Its Kinase Activity." Journal of Cell Biology 153, no. 6 (2001): 1239–50. http://dx.doi.org/10.1083/jcb.153.6.1239.

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The spindle checkpoint inhibits the metaphase to anaphase transition until all the chromosomes are properly attached to the mitotic spindle. We have isolated a Xenopus homologue of the spindle checkpoint component Bub1, and investigated its role in the spindle checkpoint in Xenopus egg extracts. Antibodies raised against Bub1 recognize a 150-kD phosphoprotein at both interphase and mitosis, but the molecular mass is reduced to 140 upon dephosphorylation in vitro. Bub1 is essential for the establishment and maintenance of the checkpoint and is localized to kinetochores, similar to the spindle c

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Siller, Karsten H., Madeline Serr, Ruth Steward, Tom S. Hays, and Chris Q. Doe. "Live Imaging of Drosophila Brain Neuroblasts Reveals a Role for Lis1/Dynactin in Spindle Assembly and Mitotic Checkpoint Control." Molecular Biology of the Cell 16, no. 11 (2005): 5127–40. http://dx.doi.org/10.1091/mbc.e05-04-0338.

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Lis1 is required for nuclear migration in fungi, cell cycle progression in mammals, and the formation of a folded cerebral cortex in humans. Lis1 binds dynactin and the dynein motor complex, but the role of Lis1 in many dynein/dynactin-dependent processes is not clearly understood. Here we generate and/or characterize mutants for Drosophila Lis1 and a dynactin subunit, Glued, to investigate the role of Lis1/dynactin in mitotic checkpoint function. In addition, we develop an improved time-lapse video microscopy technique that allows live imaging of GFP-Lis1, GFP-Rod checkpoint protein, green fl

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Isokane, Mayumi, Thomas Walter, Robert Mahen, et al. "ARHGEF17 is an essential spindle assembly checkpoint factor that targets Mps1 to kinetochores." Journal of Cell Biology 212, no. 6 (2016): 647–59. http://dx.doi.org/10.1083/jcb.201408089.

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To prevent genome instability, mitotic exit is delayed until all chromosomes are properly attached to the mitotic spindle by the spindle assembly checkpoint (SAC). In this study, we characterized the function of ARHGEF17, identified in a genome-wide RNA interference screen for human mitosis genes. Through a series of quantitative imaging, biochemical, and biophysical experiments, we showed that ARHGEF17 is essential for SAC activity, because it is the major targeting factor that controls localization of the checkpoint kinase Mps1 to the kinetochore. This mitotic function is mediated by direct

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Hixon, Mary L., Ana I. Flores, Mark W. Wagner, and Antonio Gualberto. "Ectopic Expression of cdc2/cdc28 Kinase Subunit Homo sapiens 1 Uncouples Cyclin B Metabolism from the Mitotic Spindle Cell Cycle Checkpoint." Molecular and Cellular Biology 18, no. 11 (1998): 6224–37. http://dx.doi.org/10.1128/mcb.18.11.6224.

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ABSTRACT Primary human fibroblasts arrest growth in response to the inhibition of mitosis by mitotic spindle-depolymerizing drugs. We show that the mechanism of mitotic arrest is transient and implicates a decrease in the expression of cdc2/cdc28 kinase subunit Homo sapiens 1 (CKsHs1) and a delay in the metabolism of cyclin B. Primary human fibroblasts infected with a retroviral vector that drives the expression of a mutant p53 protein failed to downregulate CKsHs1 expression, degraded cyclin B despite the absence of chromosomal segregation, and underwent DNA endoreduplication. In addition, ec

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