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Journal articles on the topic 'Mitotic delay'

Author: Grafiati
Published: 9 March 2023
Last updated: 31 July 2025

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1

Boronat, Susanna, and Judith L. Campbell. "Mitotic Cdc6 Stabilizes Anaphase-Promoting Complex Substrates by a Partially Cdc28-Independent Mechanism, and This Stabilization Is Suppressed by Deletion of Cdc55." Molecular and Cellular Biology 27, no. 3 (2006): 1158–71. http://dx.doi.org/10.1128/mcb.01745-05.

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ABSTRACT Ectopic expression of Cdc6p results in mitotic delay, and this has been attributed to Cdc6p-mediated inhibition of Cdc28 protein kinase and failure to activate the anaphase-promoting complex (APC). Here we show that endogenous Cdc6p delays a specific subset of mitotic events and that Cdc28 inhibition is not sufficient to account for it. The depletion of Cdc6p in G2/M cells reveals that Cdc6p is rate limiting for the degradation of the APC/Cdc20 substrates Pds1p and Clb2p. Conversely, the premature expression of Cdc6p delays the degradation of APC/Cdc20 substrates. Abolishing Cdc6p/Cdc
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2

Kang, Dongmin, James Chen, Jim Wong, and Guowei Fang. "The checkpoint protein Chfr is a ligase that ubiquitinates Plk1 and inhibits Cdc2 at the G2 to M transition." Journal of Cell Biology 156, no. 2 (2002): 249–60. http://dx.doi.org/10.1083/jcb.200108016.

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The checkpoint protein Chfr delays entry into mitosis, in the presence of mitotic stress (Scolnick, D.M., and T.D. Halazonetis. 2000. Nature. 406:430–435). We show here that Chfr is a ubiquitin ligase, both in vitro and in vivo. When transfected into HEK293T cells, Myc–Chfr promotes the formation of high molecular weight ubiquitin conjugates. The ring finger domain in Chfr is required for the ligase activity; this domain auto-ubiquitinates, and mutations of conserved residues in this domain abolish the ligase activity. Using Xenopus cell-free extracts, we demonstrated that Chfr delays the entr
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3

Zachos, George, Michael D. Rainey, and David A. F. Gillespie. "Chk1-Dependent S-M Checkpoint Delay in Vertebrate Cells Is Linked to Maintenance of Viable Replication Structures." Molecular and Cellular Biology 25, no. 2 (2005): 563–74. http://dx.doi.org/10.1128/mcb.25.2.563-574.2005.

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ABSTRACT We investigated mitotic delay during replication arrest (the S-M checkpoint) in DT40 B-lymphoma cells deficient in the Chk1 or Chk2 kinase. We show here that cells lacking Chk1, but not those lacking Chk2, enter mitosis with incompletely replicated DNA when DNA synthesis is blocked, but only after an initial delay. This initial delay persists when S-M checkpoint failure is induced in Chk2−/− cells with the Chk1 inhibitor UCN-01, indicating that it does not depend on Chk1 or Chk2 activity. Surprisingly, dephosphorylation of tyrosine 15 did not accompany Cdc2 activation during premature
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4

Gong, Delquin, and James E. Ferrell. "The Roles of Cyclin A2, B1, and B2 in Early and Late Mitotic Events." Molecular Biology of the Cell 21, no. 18 (2010): 3149–61. http://dx.doi.org/10.1091/mbc.e10-05-0393.

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Here we have used siRNAs and time-lapse epifluorescence microscopy to examine the roles of various candidate mitotic cyclins in chromatin condensation in HeLa cells. Knocking down cyclin A2 resulted in a substantial (∼7 h) delay in chromatin condensation and histone H3 phosphorylation, and expressing an siRNA-resistant form of cyclin A2 partially rescued chromatin condensation. There was no detectable delay in DNA replication in the cyclin A2 knockdowns, arguing that the delay in chromatin condensation is not secondary to a delay in S-phase completion. Cyclin A2 is required for the activation
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5

Jelluma, Nannette, Tobias B. Dansen, Tale Sliedrecht, Nicholas P. Kwiatkowski, and Geert J. P. L. Kops. "Release of Mps1 from kinetochores is crucial for timely anaphase onset." Journal of Cell Biology 191, no. 2 (2010): 281–90. http://dx.doi.org/10.1083/jcb.201003038.

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Mps1 kinase activity is required for proper chromosome segregation during mitosis through its involvements in microtubule–chromosome attachment error correction and the mitotic checkpoint. Mps1 dynamically exchanges on unattached kinetochores but is largely removed from kinetochores in metaphase. Here we show that Mps1 promotes its own turnover at kinetochores and that removal of Mps1 upon chromosome biorientation is a prerequisite for mitotic checkpoint silencing. Inhibition of Mps1 activity increases its half-time of recovery at unattached kinetochores and causes accumulation of Mps1 protein
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6

Markossian, Sarine, Subbulakshmi Suresh, Aysha H. Osmani, and Stephen A. Osmani. "Nup2 requires a highly divergent partner, NupA, to fulfill functions at nuclear pore complexes and the mitotic chromatin region." Molecular Biology of the Cell 26, no. 4 (2015): 605–21. http://dx.doi.org/10.1091/mbc.e14-09-1359.

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Chromatin and nuclear pore complexes (NPCs) undergo dramatic changes during mitosis, which in vertebrates and Aspergillus nidulans involves movement of Nup2 from NPCs to the chromatin region to fulfill unknown functions. This transition is shown to require the Cdk1 mitotic kinase and be promoted prematurely by ectopic expression of the NIMA kinase. Nup2 localizes with a copurifying partner termed NupA, a highly divergent yet essential NPC protein. NupA and Nup2 locate throughout the chromatin region during prophase but during anaphase move to surround segregating DNA. NupA function is shown to
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7

Szkotnicki, Lee, John M. Crutchley, Trevin R. Zyla, Elaine S. G. Bardes, and Daniel J. Lew. "The Checkpoint Kinase Hsl1p Is Activated by Elm1p-dependent Phosphorylation." Molecular Biology of the Cell 19, no. 11 (2008): 4675–86. http://dx.doi.org/10.1091/mbc.e08-06-0663.

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Saccharomyces cerevisiae cells growing in the outdoor environment must adapt to sudden changes in temperature and other variables. Many such changes trigger stress responses that delay bud emergence until the cells can adapt. In such circumstances, the morphogenesis checkpoint delays mitosis until a bud has been formed. Mitotic delay is due to the Wee1 family mitotic inhibitor Swe1p, whose degradation is linked to bud emergence by the checkpoint kinase Hsl1p. Hsl1p is concentrated at the mother-bud neck through association with septin filaments, and it was reported that Hsl1p activation involv
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8

Muraoka-Cook, Rebecca S., Laura S. Caskey, Melissa A. Sandahl, et al. "Heregulin-Dependent Delay in Mitotic Progression Requires HER4 and BRCA1." Molecular and Cellular Biology 26, no. 17 (2006): 6412–24. http://dx.doi.org/10.1128/mcb.01950-05.

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ABSTRACT HER4 expression in human breast cancers correlates with a positive prognosis. While heregulin inhibits the growth of HER4-positive breast cancer cells, it does so by undefined mechanisms. We demonstrate that heregulin-induced HER4 activity inhibits cell proliferation and delays G2/M progression of breast cancer cells. While investigating pathways of G2/M delay, we noted that heregulin increased the expression of BRCA1 in a HER4-dependent, HER2-independent manner. Induction of BRCA1 by HER4 occurred independently of the cell cycle. Moreover, BRCA1 expression was elevated in HER4-postiv
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9

Petsalaki, Eleni, and George Zachos. "Chk2 prevents mitotic exit when the majority of kinetochores are unattached." Journal of Cell Biology 205, no. 3 (2014): 339–56. http://dx.doi.org/10.1083/jcb.201310071.

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The spindle checkpoint delays exit from mitosis in cells with spindle defects. In this paper, we show that Chk2 is required to delay anaphase onset when microtubules are completely depolymerized but not in the presence of relatively few unattached kinetochores. Mitotic exit in Chk2-deficient cells correlates with reduced levels of Mps1 protein and increased Cdk1–tyrosine 15 inhibitory phosphorylation. Chk2 localizes to kinetochores and is also required for Aurora B–serine 331 phosphorylation in nocodazole or unperturbed early prometaphase. Serine 331 phosphorylation contributed to prometaphase
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10

Chippalkatti, Rohan, Boris Egger, and Beat Suter. "Mms19 promotes spindle microtubule assembly in Drosophila neural stem cells." PLOS Genetics 16, no. 11 (2020): e1008913. http://dx.doi.org/10.1371/journal.pgen.1008913.

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Mitotic divisions depend on the timely assembly and proper orientation of the mitotic spindle. Malfunctioning of these processes can considerably delay mitosis, thereby compromising tissue growth and homeostasis, and leading to chromosomal instability. Loss of functional Mms19 drastically affects the growth and development of mitotic tissues in Drosophila larvae and we now demonstrate that Mms19 is an important factor that promotes spindle and astral microtubule (MT) growth, and MT stability and bundling. Mms19 function is needed for the coordination of mitotic events and for the rapid progres
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11

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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12

O'Regan, Laura, and Andrew M. Fry. "The Nek6 and Nek7 Protein Kinases Are Required for Robust Mitotic Spindle Formation and Cytokinesis." Molecular and Cellular Biology 29, no. 14 (2009): 3975–90. http://dx.doi.org/10.1128/mcb.01867-08.

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ABSTRACT Nek6 and Nek7 are members of the NIMA-related serine/threonine kinase family. Previous work showed that they contribute to mitotic progression downstream of another NIMA-related kinase, Nek9, although the roles of these different kinases remain to be defined. Here, we carried out a comprehensive analysis of the regulation and function of Nek6 and Nek7 in human cells. By generating specific antibodies, we show that both Nek6 and Nek7 are activated in mitosis and that interfering with their activity by either depletion or expression of reduced-activity mutants leads to mitotic arrest an
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13

Lin, Chiou-Hong, Chi-Kuo Hu, and Hsiu-Ming Shih. "Clathrin heavy chain mediates TACC3 targeting to mitotic spindles to ensure spindle stability." Journal of Cell Biology 189, no. 7 (2010): 1097–105. http://dx.doi.org/10.1083/jcb.200911120.

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Mitotic spindles play essential roles in chromosome congression and segregation during mitosis. Aurora A regulates spindle assembly in part via phosphorylating human TACC3 on S558, which triggers TACC3 relocalization to mitotic spindles and stabilizes microtubules (MTs). In this study, we identified clathrin heavy chain (CHC) as an adaptor protein to recruit S558-phosphorylated TACC3 onto the spindle during mitosis for MT stabilization. CHC binds phospho-S558 TACC3 via its linker domain and first CHC repeat. CHC depletion or mutation on phospho-TACC3 binding abrogates TACC3 spindle relocalizat
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14

MacKenzie, Anne, Victoria Vicory, and Soni Lacefield. "Meiotic cells escape prolonged spindle checkpoint activity through kinetochore silencing and slippage." PLOS Genetics 19, no. 4 (2023): e1010707. http://dx.doi.org/10.1371/journal.pgen.1010707.

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To prevent chromosome mis-segregation, a surveillance mechanism known as the spindle checkpoint delays the cell cycle if kinetochores are not attached to spindle microtubules, allowing the cell additional time to correct improper attachments. During spindle checkpoint activation, checkpoint proteins bind the unattached kinetochore and send a diffusible signal to inhibit the anaphase promoting complex/cyclosome (APC/C). Previous work has shown that mitotic cells with depolymerized microtubules can escape prolonged spindle checkpoint activation in a process called mitotic slippage. During slippa
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15

Silva, Victoria C., and Lynne Cassimeris. "Stathmin and microtubules regulate mitotic entry in HeLa cells by controlling activation of both Aurora kinase A and Plk1." Molecular Biology of the Cell 24, no. 24 (2013): 3819–31. http://dx.doi.org/10.1091/mbc.e13-02-0108.

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Depletion of stathmin, a microtubule (MT) destabilizer, delays mitotic entry by ∼4 h in HeLa cells. Stathmin depletion reduced the activity of CDC25 and its upstream activators, Aurora A and Plk1. Chemical inhibition of both Aurora A and Plk1 was sufficient to delay mitotic entry by 4 h, while inhibiting either kinase alone did not cause a delay. Aurora A and Plk1 are likely regulated downstream of stathmin, because the combination of stathmin knockdown and inhibition of Aurora A and Plk1 was not additive and again delayed mitotic entry by 4 h. Aurora A localization to the centrosome required
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16

Sreenivasan, Aparna, and Douglas Kellogg. "The Elm1 Kinase Functions in a Mitotic Signaling Network in Budding Yeast." Molecular and Cellular Biology 19, no. 12 (1999): 7983–94. http://dx.doi.org/10.1128/mcb.19.12.7983.

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ABSTRACT In budding yeast, the Clb2 mitotic cyclin initiates a signaling network that negatively regulates polar bud growth during mitosis. This signaling network appears to require the function of a Clb2-binding protein called Nap1, the Cdc42 GTPase, and two protein kinases called Gin4 and Cla4. In this study, we demonstrate that the Elm1 kinase also plays a role in the control of bud growth during mitosis. Cells carrying a deletion of the ELM1 gene undergo a prolonged mitotic delay, fail to negatively regulate polar bud growth during mitosis, and show defects in septin organization. In addit
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17

Colin, Didier J., Karolina O. Hain, Lindsey A. Allan, and Paul R. Clarke. "Cellular responses to a prolonged delay in mitosis are determined by a DNA damage response controlled by Bcl-2 family proteins." Open Biology 5, no. 3 (2015): 140156. http://dx.doi.org/10.1098/rsob.140156.

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Anti-cancer drugs that disrupt mitosis inhibit cell proliferation and induce apoptosis, although the mechanisms of these responses are poorly understood. Here, we characterize a mitotic stress response that determines cell fate in response to microtubule poisons. We show that mitotic arrest induced by these drugs produces a temporally controlled DNA damage response (DDR) characterized by the caspase-dependent formation of γH2AX foci in non-apoptotic cells. Following exit from a delayed mitosis, this initial response results in activation of DDR protein kinases, phosphorylation of the tumour su
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18

Carrino, J. J., and T. G. Laffler. "The effect of heat shock on the cell cycle regulation of tubulin expression in Physarum polycephalum." Journal of Cell Biology 100, no. 2 (1985): 642–47. http://dx.doi.org/10.1083/jcb.100.2.642.

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In the myxomycete Physarum polycephalum, tubulin synthesis is subject to mitotic cycle control. Virtually all tubulin synthesis is limited to a 2-h period immediately preceding mitosis, and the peak of tubulin protein synthesis is accompanied by a parallel increase in the level of tubulin mRNA. The mechanism by which the accumulation of tubulin mRNA is turned on and off is not clear. To probe the relationship between tubulin regulation and cell cycle controls, we have used heat shocks to delay mitosis and have followed the pattern of tubulin synthesis during these delays. Two peaks of tubulin
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19

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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20

Takeda, Yutaka, Kaho Yamazaki, Kaho Hashimoto, Koki Watanabe, Takumi Chinen, and Daiju Kitagawa. "The centriole protein CEP76 negatively regulates PLK1 activity in the cytoplasm for proper mitotic progression." Journal of Cell Science 133, no. 19 (2020): jcs241281. http://dx.doi.org/10.1242/jcs.241281.

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ABSTRACTPolo-like kinase 1 (PLK1) dynamically changes its localization and plays important roles in proper mitotic progression. In particular, strict control of cytoplasmic PLK1 is needed to prevent mitotic defects. However, the regulation of cytoplasmic PLK1 is not fully understood. In this study, we show that CEP76, a centriolar protein, physically interacts with PLK1 and tightly controls the activation of cytoplasmic PLK1 during mitosis in human cells. We found that removal of centrosomes induced ectopic aggregation of PLK1, which is highly phosphorylated, in the cytoplasm during mitosis. I
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21

Mall, Moritz, Thomas Walter, Mátyás Gorjánácz, et al. "Mitotic lamin disassembly is triggered by lipid-mediated signaling." Journal of Cell Biology 198, no. 6 (2012): 981–90. http://dx.doi.org/10.1083/jcb.201205103.

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Disassembly of the nuclear lamina is a key step during open mitosis in higher eukaryotes. The activity of several kinases, including CDK1 (cyclin-dependent kinase 1) and protein kinase C (PKC), has been shown to trigger mitotic lamin disassembly, yet their precise contributions are unclear. In this study, we develop a quantitative imaging assay to study mitotic lamin B1 disassembly in living cells. We find that CDK1 and PKC act in concert to mediate phosphorylation-dependent lamin B1 disassembly during mitosis. Using ribonucleic acid interference (RNAi), we showed that diacylglycerol (DAG)-dep
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22

Brock, J. A., and K. Bloom. "A chromosome breakage assay to monitor mitotic forces in budding yeast." Journal of Cell Science 107, no. 4 (1994): 891–902. http://dx.doi.org/10.1242/jcs.107.4.891.

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During the eukaryotic cell cycle, genetic material must be accurately duplicated and faithfully segregated to each daughter cell. Segregation of chromosomes is dependent on the centromere, a region of the chromosome which interacts with mitotic spindle microtubules during cell division. Centromere function in the budding yeast, Saccharomyces cerevisiae, can be regulated by placing an inducible promotor adjacent to centromere DNA. This conditional centromere can be integrated into chromosome III to generate a conditionally functional dicentric chromosome. Activation of the dicentric chromosome
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23

Kim, Mijin, Katie Murphy, Fang Liu, et al. "Caspase-Mediated Specific Cleavage of BubR1 Is a Determinant of Mitotic Progression." Molecular and Cellular Biology 25, no. 21 (2005): 9232–48. http://dx.doi.org/10.1128/mcb.25.21.9232-9248.2005.

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ABSTRACT The fidelity of chromosomal duplication is monitored by cell cycle checkpoints operational during mitosis. One such cell cycle delay is invoked by microtubule-targeting agents such as nocodazole or paclitaxel (Taxol) and is mediated by mitotic checkpoint proteins that include BubR1. Relatively little is known about the regulation of expression and stability of BubR1 (or other checkpoint proteins) and how these factors dictate the durability of the cell cycle delay. We report here that treatment of HeLa cells with spindle-disrupting agents resulted in caspase activation and precipitate
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Prigozhina, Natalie L., C. Elizabeth Oakley, Amanda M. Lewis, Tania Nayak, Stephen A. Osmani та Berl R. Oakley. "γ-Tubulin Plays an Essential Role in the Coordination of Mitotic Events". Molecular Biology of the Cell 15, № 3 (2004): 1374–86. http://dx.doi.org/10.1091/mbc.e03-06-0405.

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Recent data from multiple organisms indicate that γ-tubulin has essential, but incompletely defined, functions in addition to nucleating microtubule assembly. To investigate these functions, we examined the phenotype of mipAD159, a cold-sensitive allele of the γ-tubulin gene of Aspergillus nidulans. Immunofluorescence microscopy of synchronized material revealed that at a restrictive temperature mipAD159 does not inhibit mitotic spindle formation. Anaphase A was inhibited in many nuclei, however, and after a slight delay in mitosis (∼6% of the cell cycle period), most nuclei reentered interpha
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25

Yunes, Sarah A., Jennifer L. S. Willoughby, Julian H. Kwan, et al. "Factor quinolinone inhibitors disrupt spindles and multiple LSF (TFCP2)-protein interactions in mitosis, including with microtubule-associated proteins." PLOS ONE 17, no. 6 (2022): e0268857. http://dx.doi.org/10.1371/journal.pone.0268857.

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Factor quinolinone inhibitors (FQIs), a first-in-class set of small molecule inhibitors targeted to the transcription factor LSF (TFCP2), exhibit promising cancer chemotherapeutic properties. FQI1, the initial lead compound identified, unexpectedly induced a concentration-dependent delay in mitotic progression. Here, we show that FQI1 can rapidly and reversibly lead to mitotic arrest, even when added directly to mitotic cells, implying that FQI1-mediated mitotic defects are not transcriptionally based. Furthermore, treatment with FQIs resulted in a striking, concentration-dependent diminishmen
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Chen, Yu-Zen, Vitaly Zimyanin, and Stefanie Redemann. "Loss of the mitochondrial protein SPD-3 elevates PLK-1 levels and dysregulates mitotic events." Life Science Alliance 6, no. 11 (2023): e202302011. http://dx.doi.org/10.26508/lsa.202302011.

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In metazoans, Polo-like kinase (PLK1) controls several mitotic events including nuclear envelope breakdown, centrosome maturation, spindle assembly and progression through mitosis. Here we show that a mutation in the mitochondria-localized protein SPD-3 affects mitotic events by inducing elevated levels of PLK-1 in earlyCaenorhabditis elegansembryos. SPD-3 mutant embryos contain abnormally positioned mitotic chromosomes, show a delay in anaphase onset and asymmetrically disassemble the nuclear lamina. We found that more PLK-1 accumulated on centrosomes, nuclear envelope, nucleoplasm, and chrom
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27

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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van de Weerdt, Barbara C. M., Marcel A. T. M. van Vugt, Catherine Lindon, et al. "Uncoupling Anaphase-Promoting Complex/Cyclosome Activity from Spindle Assembly Checkpoint Control by Deregulating Polo-Like Kinase 1." Molecular and Cellular Biology 25, no. 5 (2005): 2031–44. http://dx.doi.org/10.1128/mcb.25.5.2031-2044.2005.

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ABSTRACT Polo-like kinase 1 (Plk1) plays a role in numerous events in mitosis, but how the multiple functions of Plk1 are separated is poorly understood. We studied regulation of Plk1 through two putative phosphorylation residues, Ser-137 and Thr-210. Using phospho-specific antibodies, we found that Thr-210 phosphorylation precedes Ser-137 phosphorylation in vivo, the latter occurring specifically in late mitosis. We show that expression of two activating mutants of these residues, S137D and T210D, results in distinct mitotic phenotypes. Whereas expression of both phospho-mimicking mutants as
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den Elzen, Nicole, and Jonathon Pines. "Cyclin a Is Destroyed in Prometaphase and Can Delay Chromosome Alignment and Anaphase." Journal of Cell Biology 153, no. 1 (2001): 121–36. http://dx.doi.org/10.1083/jcb.153.1.121.

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Mitosis is controlled by the specific and timely degradation of key regulatory proteins, notably the mitotic cyclins that bind and activate the cyclin-dependent kinases (Cdks). In animal cells, cyclin A is always degraded before cyclin B, but the exact timing and the mechanism underlying this are not known. Here we use live cell imaging to show that cyclin A begins to be degraded just after nuclear envelope breakdown. This degradation requires the 26S proteasome, but is not affected by the spindle checkpoint. Neither deletion of its destruction box nor disrupting Cdk binding prevents cyclin A
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Shirnekhi, Hazheen K., Erin P. Kelley, Jennifer G. DeLuca, and Jacob A. Herman. "Spindle assembly checkpoint signaling and sister chromatid cohesion are disrupted by HPV E6-mediated transformation." Molecular Biology of the Cell 28, no. 15 (2017): 2035–41. http://dx.doi.org/10.1091/mbc.e16-12-0853.

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Aneuploidy, a condition that results from unequal partitioning of chromosomes during mitosis, is a hallmark of many cancers, including those caused by human papillomaviruses (HPVs). E6 and E7 are the primary transforming proteins in HPV that drive tumor progression. In this study, we stably expressed E6 and E7 in noncancerous RPE1 cells and analyzed the specific mitotic defects that contribute to aneuploidy in each cell line. We find that E6 expression results in multiple chromosomes associated with one or both spindle poles, causing a significant mitotic delay. In most cells, the misaligned c
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Tanudji, Marcel, John Shoemaker, Lawrence L'Italien, Loren Russell, Gregory Chin, and Xiao Min Schebye. "Gene Silencing of CENP-E by Small Interfering RNA in HeLa Cells Leads to Missegregation of Chromosomes after a Mitotic Delay." Molecular Biology of the Cell 15, no. 8 (2004): 3771–81. http://dx.doi.org/10.1091/mbc.e03-07-0482.

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Centromeric protein-E (CENP-E) is a kinesin-like motor protein required for chromosome congression at prometaphase. Functional perturbation of CENP-E by various methods results in a consistent phenotype, i.e., unaligned chromosomes during mitosis. One unresolved question from previous studies is whether cells complete mitosis or sustain mitotic arrest in the presence of unaligned chromosomes. Using RNA interference and video-microscopy, we analyzed the dynamic process of mitotic progression of HeLa(H2B)-GFP cells lacking CENP-E. Our results demonstrate that these cells initiated anaphase after
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32

Shiozaki, K., M. Shiozaki, and P. Russell. "Mcs4 mitotic catastrophe suppressor regulates the fission yeast cell cycle through the Wik1-Wis1-Spc1 kinase cascade." Molecular Biology of the Cell 8, no. 3 (1997): 409–19. http://dx.doi.org/10.1091/mbc.8.3.409.

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Spc1 in Schizosaccharomyces pombe is a member of the stress-activated protein kinase family, an evolutionary conserved subfamily of mitogen-activated protein kinases (MAPKs). Spc1 is activated by a MAPK kinase homologue, Wis1, and negatively regulated by Pyp1 and Pyp2 tyrosine phosphatases. Mutations in the spc1+ and wis1+ genes cause a G2 cell cycle delay that is exacerbated during stress. Herein, we describe two upstream regulators of the Wis1-Spc1 cascade. wik1+ (Wis1 kinase) was identified from its homology to budding yeast SSK2, which encodes a MAPKK kinase that regulates the HOG1 osmosen
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Krauss, Sharon Wald, Jeffrey R. Spence, Shirin Bahmanyar, et al. "Downregulation of Protein 4.1R, a Mature Centriole Protein, Disrupts Centrosomes, Alters Cell Cycle Progression, and Perturbs Mitotic Spindles and Anaphase." Molecular and Cellular Biology 28, no. 7 (2008): 2283–94. http://dx.doi.org/10.1128/mcb.02021-07.

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ABSTRACT Centrosomes nucleate and organize interphase microtubules and are instrumental in mitotic bipolar spindle assembly, ensuring orderly cell cycle progression with accurate chromosome segregation. We report that the multifunctional structural protein 4.1R localizes at centrosomes to distal/subdistal regions of mature centrioles in a cell cycle-dependent pattern. Significantly, 4.1R-specific depletion mediated by RNA interference perturbs subdistal appendage proteins ninein and outer dense fiber 2/cenexin at mature centrosomes and concomitantly reduces interphase microtubule anchoring and
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34

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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35

Kim, Seul, Kyoungho Jun, Ye-Hyun Kim, and Jae Sung Kim. "Abstract 1638: Regulation of spindle pole integrity by the MASTL-ENSA-aurora a pathway during mitosis." Cancer Research 84, no. 6_Supplement (2024): 1638. http://dx.doi.org/10.1158/1538-7445.am2024-1638.

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Abstract The preservation of spindle pole integrity is crucial for proper spindle assembly and chromosome segregation in mitosis, yet the precise mechanisms governing spindle pole integrity remain elusive. During mitosis, phosphorylated Ensa (p-ENSA) localizes to spindle poles, and the inhibition of ENSA leads to a range of mitotic defects, including misaligned chromosomes, multipolar spindles, asymmetric bipolar spindles, and centrosome aberrations, resulting in a delayed mitotic progression. Remarkably, the mitotic delay induced by ENSA inhibition is alleviated upon depletion of PP2A-B55α, b
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36

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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37

Schnerch, Dominik, Julia Felthaus, Monika Engelhardt, and Ralph M. Waesch. "Spindle Checkpoint Insufficiency and Unscheduled APC-Dependent Proteolysis in Acute Myeloid Leukemia." Blood 108, no. 11 (2006): 2082. http://dx.doi.org/10.1182/blood.v108.11.2082.2082.

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Abstract Genetic instability including aneuploidy is frequent in most cancers. The spindle assembly checkpoint (SAC) is a mitotic surveillance mechanism responsible for accurate chromosome segregation. Unattached chromosomes or lack of spindle tension are sensed by the SAC. The activated SAC inhibits the ubiquitin-ligase anaphase-promoting complex (APC), which prevents the proteolysis of cell cycle regulators in order to delay progression through mitosis and allow cells to recover from defective mitotic spindle attachment. Spindle checkpoint malfunction proved to favor the generation of aneupl
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38

Rischitor, Patricia E., Sven Konzack, and Reinhard Fischer. "The Kip3-Like Kinesin KipB Moves along Microtubules and Determines Spindle Position during Synchronized Mitoses in Aspergillus nidulans Hyphae." Eukaryotic Cell 3, no. 3 (2004): 632–45. http://dx.doi.org/10.1128/ec.3.3.632-645.2004.

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ABSTRACT Kinesins are motor proteins which are classified into 11 different families. We identified 11 kinesin-like proteins in the genome of the filamentous fungus Aspergillus nidulans. Relatedness analyses based on the motor domains grouped them into nine families. In this paper, we characterize KipB as a member of the Kip3 family of microtubule depolymerases. The closest homologues of KipB are Saccharomyces cerevisiae Kip3 and Schizosaccharomyces pombe Klp5 and Klp6, but sequence similarities outside the motor domain are very low. A disruption of kipB demonstrated that it is not essential f
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39

Kadauke, Stephan, Amy E. Campbell, Aaron J. Stonestrom, Deepti P. Jain, Ross C. Hardison, and Gerd A. Blobel. "GATA1 and the BET Family Protein Brd3 Form a Mitotic Bookmarking Complex." Blood 120, no. 21 (2012): 282. http://dx.doi.org/10.1182/blood.v120.21.282.282.

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Abstract Abstract 282 Erythroid-specific transcription patterns are maintained throughout cell division. During mitosis, transcription is silenced globally. This raises the question whether mechanisms are in place that ensure the spatially and temporally correct reassembly of transcriptional regulators and thus maintain lineage fidelity. We recently found that, in contrast to most nuclear regulators, the master hematopoietic regulator GATA1 remains associated at a subset of its targets within mitotic chromosomes in erythroid cells (Kadauke et al., Cell 2012). GATA1 appears to function by creat
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40

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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41

Maekawa, Hiromi, Claire Priest, Johannes Lechner, Gislene Pereira, and Elmar Schiebel. "The yeast centrosome translates the positional information of the anaphase spindle into a cell cycle signal." Journal of Cell Biology 179, no. 3 (2007): 423–36. http://dx.doi.org/10.1083/jcb.200705197.

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The spindle orientation checkpoint (SPOC) of budding yeast delays mitotic exit when cytoplasmic microtubules (MTs) are defective, causing the spindle to become misaligned. Delay is achieved by maintaining the activity of the Bfa1–Bub2 guanosine triphosphatase–activating protein complex, an inhibitor of mitotic exit. In this study, we show that the spindle pole body (SPB) component Spc72, a transforming acidic coiled coil–like molecule that interacts with the γ-tubulin complex, recruits Kin4 kinase to both SPBs when cytoplasmic MTs are defective. This allows Kin4 to phosphorylate the SPB-associ
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42

Kishi, Kazuhiro, Marcel A. T. M. van Vugt, Ken-ichi Okamoto, Yasunori Hayashi, and Michael B. Yaffe. "Functional Dynamics of Polo-Like Kinase 1 at the Centrosome." Molecular and Cellular Biology 29, no. 11 (2009): 3134–50. http://dx.doi.org/10.1128/mcb.01663-08.

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ABSTRACT Polo-like kinase 1 (Plk1) functions as a key regulator of mitotic events by phosphorylating substrate proteins on centrosomes, kinetochores, the mitotic spindle, and the midbody. Through mechanisms that are incompletely understood, Plk1 is released from and relocalizes to different mitotic structures as cells proceed through mitosis. We used fluorescence recovery after photobleaching to examine the kinetics of this process in more detail. We observed that Plk1 displayed a range of different recovery rates that differ at each mitotic substructure and depend on both the Polo-box domain
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43

Martineau, S. N., P. R. Andreassen, and R. L. Margolis. "Delay of HeLa cell cleavage into interphase using dihydrocytochalasin B: retention of a postmitotic spindle and telophase disc correlates with synchronous cleavage recovery." Journal of Cell Biology 131, no. 1 (1995): 191–205. http://dx.doi.org/10.1083/jcb.131.1.191.

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The molecular signals that determine the position and timing of the cleavage furrow during mammalian cell cytokinesis are presently unknown. We have studied in detail the effect of dihydrocytochalasin B (DCB), a drug that interferes with actin assembly, on specific late mitotic events in synchronous HeLa cells. When cleavage furrow formation is blocked at 10 microM DCB, cells return to interphase by the criteria of reformation of nuclei with lamin borders, degradation of the cyclin B component of p34cdc2 kinase, and loss of mitosis specific MPM-2 antigens. However, the machinery for cell cleav
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44

Maldonado-Codina, G., S. Llamazares, and D. M. Glover. "Heat shock results in cell cycle delay and synchronisation of mitotic domains in cellularised Drosophila melanogaster embryos." Journal of Cell Science 105, no. 3 (1993): 711–20. http://dx.doi.org/10.1242/jcs.105.3.711.

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Cells of Drosophila embryos that are subjected to a 37 degrees C temperature shock whilst undergoing the S-phase of cell cycle 14 arrest with their microtubules in an interphase-like state, and with nuclei showing unusual chromatin condensation. They do not recover from this state within a 30 minute period even though extensive gastrulation movements can occur. Cells of embryos heat shocked in G2-phase are delayed in interphase with high levels of cyclins A and B. Within ten minutes recovery from heat shock, cells enter mitosis throughout the embryo. The degradation of the mitotic cyclins A an
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45

Dewey, Evan B., and Christopher A. Johnston. "Diverse mitotic functions of the cytoskeletal cross-linking protein Shortstop suggest a role in Dynein/Dynactin activity." Molecular Biology of the Cell 28, no. 19 (2017): 2555–68. http://dx.doi.org/10.1091/mbc.e17-04-0219.

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Proper assembly and orientation of the bipolar mitotic spindle is critical to the fidelity of cell division. Mitotic precision fundamentally contributes to cell fate specification, tissue development and homeostasis, and chromosome distribution within daughter cells. Defects in these events are thought to contribute to several human diseases. The underlying mechanisms that function in spindle morphogenesis and positioning remain incompletely defined, however. Here we describe diverse roles for the actin-microtubule cross-linker Shortstop (Shot) in mitotic spindle function in Drosophila. Shot l
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46

Ramírez-Valle, Francisco, Michelle L. Badura, Steve Braunstein, Manisha Narasimhan, and Robert J. Schneider. "Mitotic Raptor Promotes mTORC1 Activity, G2/M Cell Cycle Progression, and Internal Ribosome Entry Site-Mediated mRNA Translation." Molecular and Cellular Biology 30, no. 13 (2010): 3151–64. http://dx.doi.org/10.1128/mcb.00322-09.

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ABSTRACT The mTOR signaling complex integrates signals from growth factors and nutrient availability to control cell growth and proliferation, in part through effects on the protein-synthetic machinery. Protein synthesis rates fluctuate throughout the cell cycle but diminish significantly during the G2/M transition. The fate of the mTOR complex and its role in coordinating cell growth and proliferation signals with protein synthesis during mitosis remain unknown. Here we demonstrate that the mTOR complex 1 (mTORC1) pathway, which stimulates protein synthesis, is actually hyperactive during mit
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47

Lindqvist, Arne, Helena Källström, Andreas Lundgren, Emad Barsoum, and Christina Karlsson Rosenthal. "Cdc25B cooperates with Cdc25A to induce mitosis but has a unique role in activating cyclin B1–Cdk1 at the centrosome." Journal of Cell Biology 171, no. 1 (2005): 35–45. http://dx.doi.org/10.1083/jcb.200503066.

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Cdc25 phosphatases are essential for the activation of mitotic cyclin–Cdks, but the precise roles of the three mammalian isoforms (A, B, and C) are unclear. Using RNA interference to reduce the expression of each Cdc25 isoform in HeLa and HEK293 cells, we observed that Cdc25A and -B are both needed for mitotic entry, whereas Cdc25C alone cannot induce mitosis. We found that the G2 delay caused by small interfering RNA to Cdc25A or -B was accompanied by reduced activities of both cyclin B1–Cdk1 and cyclin A–Cdk2 complexes and a delayed accumulation of cyclin B1 protein. Further, three-dimension
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48

Jin, P., Y. Gu, and D. O. Morgan. "Role of inhibitory CDC2 phosphorylation in radiation-induced G2 arrest in human cells." Journal of Cell Biology 134, no. 4 (1996): 963–70. http://dx.doi.org/10.1083/jcb.134.4.963.

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The activity of the mitosis-promoting kinase CDC2-cyclin B is normally suppressed in S phase and G2 by inhibitory phosphorylation at Thr14 and Tyr15. This work explores the possibility that these phosphorylations are responsible for the G2 arrest that occurs in human cells after DNA damage. HeLa cell lines were established in which CDC2AF, a mutant that cannot be phosphorylated at Thr14 and Tyr15, was expressed from a tetracycline-repressible promoter. Expression of CDC2AF did not induce mitotic events in cells arrested at the beginning of S phase with DNA synthesis inhibitors, but induced low
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49

Carroll, Christopher W., Roger Altman, David Schieltz, John R. Yates, and Douglas Kellogg. "The Septins Are Required for the Mitosis-specific Activation of the Gin4 Kinase." Journal of Cell Biology 143, no. 3 (1998): 709–17. http://dx.doi.org/10.1083/jcb.143.3.709.

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In budding yeast, a protein kinase called Gin4 is specifically activated during mitosis and functions in a pathway initiated by the Clb2 cyclin to control bud growth. We have used genetics and biochemistry to identify additional proteins that function with Gin4 in this pathway, and both of these approaches have identified members of the septin family. Loss of septin function produces a phenotype that is very similar to the phenotype caused by loss of Gin4 function, and the septins are required early in mitosis to activate Gin4 kinase activity. Furthermore, septin mutants display a prolonged mi
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50

Krause, Sue A., Marie-Louise Loupart, Sharron Vass, Stefan Schoenfelder, Steve Harrison, and Margarete M. S. Heck. "Loss of Cell Cycle Checkpoint Control in Drosophila Rfc4 Mutants." Molecular and Cellular Biology 21, no. 15 (2001): 5156–68. http://dx.doi.org/10.1128/mcb.21.15.5156-5168.2001.

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ABSTRACT Two alleles of the Drosophila melanogaster Rfc4(DmRfc4) gene, which encodes subunit 4 of the replication factor C (RFC) complex, cause striking defects in mitotic chromosome cohesion and condensation. These mutations produce larval phenotypes consistent with a role in DNA replication but also result in mitotic chromosomal defects appearing either as premature chromosome condensation-like or precocious sister chromatid separation figures. Though the DmRFC4 protein localizes to all replicating nuclei, it is dispersed from chromatin in mitosis. Thus the mitotic defects appear not to be t
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