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Journal articles on the topic 'Mitotic activity'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Skoufias, Dimitrios A., Rose-Laure Indorato, Françoise Lacroix, Andreas Panopoulos, and Robert L. Margolis. "Mitosis persists in the absence of Cdk1 activity when proteolysis or protein phosphatase activity is suppressed." Journal of Cell Biology 179, no. 4 (2007): 671–85. http://dx.doi.org/10.1083/jcb.200704117.

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Cellular transition to anaphase and mitotic exit has been linked to the loss of cyclin-dependent kinase 1 (Cdk1) kinase activity as a result of anaphase-promoting complex/cyclosome (APC/C)–dependent specific degradation of its cyclin B1 subunit. Cdk1 inhibition by roscovitine is known to induce premature mitotic exit, whereas inhibition of the APC/C-dependent degradation of cyclin B1 by MG132 induces mitotic arrest. In this study, we find that combining both drugs causes prolonged mitotic arrest in the absence of Cdk1 activity. Different Cdk1 and proteasome inhibitors produce similar results,

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2

Long, John J., Anne Leresche, Richard W. Kriwacki, and Joel M. Gottesfeld. "Repression of TFIIH Transcriptional Activity and TFIIH-Associated cdk7 Kinase Activity at Mitosis." Molecular and Cellular Biology 18, no. 3 (1998): 1467–76. http://dx.doi.org/10.1128/mcb.18.3.1467.

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ABSTRACT Nuclear transcription is repressed when eukaryotic cells enter mitosis. Mitotic repression of transcription of various cellular and viral gene promoters by RNA polymerase II can be reproduced in vitro either with extracts prepared from cells arrested at mitosis with the microtubule polymerization inhibitor nocodazole or with nuclear extracts prepared from asynchronous cells and the mitotic protein kinase cdc2/cyclin B. Purified cdc2/cyclin B kinase is also sufficient to inhibit transcription in reconstituted transcription reactions with biochemically purified and recombinant basal tra

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3

Al Jord, Adel, Asm Shihavuddin, Raphaël Servignat d’Aout, et al. "Calibrated mitotic oscillator drives motile ciliogenesis." Science 358, no. 6364 (2017): 803–6. http://dx.doi.org/10.1126/science.aan8311.

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Cell division and differentiation depend on massive and rapid organelle remodeling. The mitotic oscillator, centered on the cyclin-dependent kinase 1–anaphase-promoting complex/cyclosome (CDK1-APC/C) axis, spatiotemporally coordinates this reorganization in dividing cells. Here we discovered that nondividing cells could also implement this mitotic clocklike regulatory circuit to orchestrate subcellular reorganization associated with differentiation. We probed centriole amplification in differentiating mouse-brain multiciliated cells. These postmitotic progenitors fine-tuned mitotic oscillator

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4

Fabisz-Kijowska, Anna A., Katherine Lumley-Sapanski, Margaret S. Halleck, and Robert A. Schlegel. "Cellular compartmentalization of protein kinase activity during the cell cycle." Biochemistry and Cell Biology 65, no. 12 (1987): 1070–79. http://dx.doi.org/10.1139/o87-140.

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The quantities and types of protein kinases found in the cytoplasmic and nuclear or chromosomal compartments of interphase and mitotic human culture cells were compared. Using histone as substrate, the total quantity of kinases recovered from cytoplasmic and chromosomal fractions of mitotic cells was several times greater than from cytoplasmic and nuclear fractions of interphase cells. In both mitotic and interphase cells, more activity was recovered from cytoplasmic fractions than from chromosomal or nuclear fractions, respectively. When activity against various substrates was examined, mitot

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Popov, Victor I., Igor V. Kraev, Dmitri A. Ignat'ev, and Michael G. Stewart. "Suspension of Mitotic Activity in Dentate Gyrus of the Hibernating Ground Squirrel." Neural Plasticity 2011 (2011): 1–7. http://dx.doi.org/10.1155/2011/867525.

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Neurogenesis occurs in the adult mammalian hippocampus, a region of the brain important for learning and memory. Hibernation in Siberian ground squirrels provides a natural model to study mitosis as the rapid fall in body temperature in 24 h (from 35-36°C to +4–6°C) permits accumulation of mitotic cells at different stages of the cell cycle. Histological methods used to study adult neurogenesis are limited largely to fixed tissue, and the mitotic state elucidated depends on the specific phase of mitosis at the time of day. However, using an immunohistochemical study of doublecortin (DCX) and B

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Maddox, Amy Shaub, and Keith Burridge. "RhoA is required for cortical retraction and rigidity during mitotic cell rounding." Journal of Cell Biology 160, no. 2 (2003): 255–65. http://dx.doi.org/10.1083/jcb.200207130.

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Mitotic cell rounding is the process of cell shape change in which a flat interphase cell becomes spherical at the onset of mitosis. Rearrangement of the actin cytoskeleton, de-adhesion, and an increase in cortical rigidity accompany mitotic cell rounding. The molecular mechanisms that contribute to this process have not been defined. We show that RhoA is required for cortical retraction but not de-adhesion during mitotic cell rounding. The mitotic increase in cortical rigidity also requires RhoA, suggesting that increases in cortical rigidity and cortical retraction are linked processes. Rho-

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7

Shah, Rajvee, Sanne Jensen, Lisa M. Frenz, Anthony L. Johnson, and Leland H. Johnston. "The Spo12 Protein of Saccharomyces cerevisiae: A Regulator of Mitotic Exit Whose Cell Cycle-Dependent Degradation Is Mediated by the Anaphase-Promoting Complex." Genetics 159, no. 3 (2001): 965–80. http://dx.doi.org/10.1093/genetics/159.3.965.

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Abstract The Spo12 protein plays a regulatory role in two of the most fundamental processes of biology, mitosis and meiosis, and yet its biochemical function remains elusive. In this study we concentrate on the genetic and biochemical analysis of its mitotic function. Since high-copy SPO12 is able to suppress a wide variety of mitotic exit mutants, all of which arrest with high Clb-Cdc28 activity, we speculated whether SPO12 is able to facilitate exit from mitosis when overexpressed by antagonizing mitotic kinase activity. We show, however, that Spo12 is not a potent regulator of Clb-Cdc28 act

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8

Mohl, Dane A., Michael J. Huddleston, Therese S. Collingwood, Roland S. Annan, and Raymond J. Deshaies. "Dbf2–Mob1 drives relocalization of protein phosphatase Cdc14 to the cytoplasm during exit from mitosis." Journal of Cell Biology 184, no. 4 (2009): 527–39. http://dx.doi.org/10.1083/jcb.200812022.

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Exit from mitosis is characterized by a precipitous decline in cyclin-dependent kinase (Cdk) activity, dissolution of mitotic structures, and cytokinesis. In Saccharomyces cerevisiae, mitotic exit is driven by a protein phosphatase, Cdc14, which is in part responsible for counteracting Cdk activity. Throughout interphase, Cdc14 is sequestered in the nucleolus, but successful anaphase activates the mitotic exit network (MEN), which triggers dispersal of Cdc14 throughout the cell by a mechanism that has remained unknown. In this study, we show that a MEN component, protein kinase Dbf2–Mob1, prom

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9

Li, Jie, Hiroki Shima, Hironari Nishizawa, et al. "Phosphorylation of BACH1 switches its function from transcription factor to mitotic chromosome regulator and promotes its interaction with HMMR." Biochemical Journal 475, no. 5 (2018): 981–1002. http://dx.doi.org/10.1042/bcj20170520.

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The transcription repressor BACH1 performs mutually independent dual roles in transcription regulation and chromosome alignment during mitosis by supporting polar ejection force of mitotic spindle. We now found that the mitotic spindles became oblique relative to the adhesion surface following endogenous BACH1 depletion in HeLa cells. This spindle orientation rearrangement was rescued by re-expression of BACH1 depending on its interactions with HMMR and CRM1, both of which are required for the positioning of mitotic spindle, but independently of its DNA-binding activity. A mass spectrometry an

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10

Noree, Chalongrat, and Naraporn Sirinonthanawech. "Nuclear targeted Saccharomyces cerevisiae asparagine synthetases associate with the mitotic spindle regardless of their enzymatic activity." PLOS ONE 15, no. 12 (2020): e0243742. http://dx.doi.org/10.1371/journal.pone.0243742.

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Recently, human asparagine synthetase has been found to be associated with the mitotic spindle. However, this event cannot be seen in yeast because yeast takes a different cell division process via closed mitosis (there is no nuclear envelope breakdown to allow the association between any cytosolic enzyme and mitotic spindle). To find out if yeast asparagine synthetase can also (but hiddenly) have this feature, the coding sequences of green fluorescent protein (GFP) and nuclear localization signal (NLS) were introduced downstream of ASN1 and ASN2, encoding asparagine synthetases Asn1p and Asn2

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Kalashova, Julia, Chenglu Yang, Hongmei Li, et al. "The Aurora kinase B relocation blocker LXY18 triggers mitotic catastrophe selectively in malignant cells." PLOS ONE 18, no. 10 (2023): e0293283. http://dx.doi.org/10.1371/journal.pone.0293283.

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The mitotic regulator, Aurora kinase B (AURKB), is frequently overexpressed in malignancy and is a target for therapeutic intervention. The compound, LXY18, is a potent, orally available small molecule that inhibits the proper localization of AURKB during late mitosis, without affecting its kinase activity. In this study, we demonstrate that LXY18 elicits apoptosis in cancer cells derived from various indications, but not in non-transformed cell lines. The apoptosis is p53-independent, triggered by a prolonged mitotic arrest and occurs predominantly in mitosis. Some additional cells succumb po

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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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Mitchison, T. J., J. Pineda, J. Shi, and S. Florian. "Is inflammatory micronucleation the key to a successful anti-mitotic cancer drug?" Open Biology 7, no. 11 (2017): 170182. http://dx.doi.org/10.1098/rsob.170182.

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Paclitaxel is a successful anti-cancer drug that kills cancer cells in two-dimensional culture through perturbation of mitosis, but whether it causes tumour regression by anti-mitotic actions is controversial. Drug candidates that specifically target mitosis, including inhibitors of kinesin-5, AurkA, AurkB and Plk1, disappointed in the clinic. Current explanations for this discrepancy include pharmacokinetic differences and hypothetical interphase actions of paclitaxel. Here, we discuss post-mitotic micronucleation as a special activity of taxanes that might explain their higher activity in so

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Chuang, Linda Shyue Huey, Jian Ming Khor, Soak Kuan Lai, et al. "Aurora kinase-induced phosphorylation excludes transcription factor RUNX from the chromatin to facilitate proper mitotic progression." Proceedings of the National Academy of Sciences 113, no. 23 (2016): 6490–95. http://dx.doi.org/10.1073/pnas.1523157113.

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The Runt-related transcription factors (RUNX) are master regulators of development and major players in tumorigenesis. Interestingly, unlike most transcription factors, RUNX proteins are detected on the mitotic chromatin and apparatus, suggesting that they are functionally active in mitosis. Here, we identify key sites of RUNX phosphorylation in mitosis. We show that the phosphorylation of threonine 173 (T173) residue within the Runt domain of RUNX3 disrupts RUNX DNA binding activity during mitotic entry to facilitate the recruitment of RUNX proteins to mitotic structures. Moreover, knockdown

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Ertych, Norman, Ailine Stolz, Oliver Valerius, Gerhard H. Braus, and Holger Bastians. "CHK2–BRCA1 tumor-suppressor axis restrains oncogenic Aurora-A kinase to ensure proper mitotic microtubule assembly." Proceedings of the National Academy of Sciences 113, no. 7 (2016): 1817–22. http://dx.doi.org/10.1073/pnas.1525129113.

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BRCA1 (breast cancer type 1 susceptibility protein) is a multifunctional tumor suppressor involved in DNA damage response, DNA repair, chromatin regulation, and mitotic chromosome segregation. Although the nuclear functions of BRCA1 have been investigated in detail, its role during mitosis is little understood. It is clear, however, that loss of BRCA1 in human cancer cells leads to chromosomal instability (CIN), which is defined as a perpetual gain or loss of whole chromosomes during mitosis. Moreover, our recent work has revealed that the mitotic function of BRCA1 depends on its phosphorylati

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16

Lee, Kyunghee, Alison E. Kenny, and Conly L. Rieder. "Caspase activity is not required for the mitotic checkpoint or mitotic slippage in human cells." Molecular Biology of the Cell 22, no. 14 (2011): 2470–79. http://dx.doi.org/10.1091/mbc.e11-03-0228.

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Biochemical studies suggest that caspase activity is required for a functional mitotic checkpoint (MC) and mitotic slippage. To test this directly, we followed nontransformed human telomerase immortalized human retinal pigment epithelia (RPE-1) cells through mitosis after inhibiting or depleting selected caspases. We found that inhibiting caspases individually, in combination, or in toto did not affect the duration or fidelity of mitosis in otherwise untreated cells. When satisfaction of the MC was prevented with 500 nM nocodazole or 2.5 μM dimethylenastron (an Eg5 inhibitor), 92–100% of RPE-1

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Bompard, Guillaume, Gabriel Rabeharivelo, Marie Frank, Julien Cau, Claude Delsert, and Nathalie Morin. "Subgroup II PAK-mediated phosphorylation regulates Ran activity during mitosis." Journal of Cell Biology 190, no. 5 (2010): 807–22. http://dx.doi.org/10.1083/jcb.200912056.

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Ran is an essential GTPase that controls nucleocytoplasmic transport, mitosis, and nuclear envelope formation. These functions are regulated by interaction of Ran with different partners, and by formation of a Ran-GTP gradient emanating from chromatin. Here, we identify a novel level of Ran regulation. We show that Ran is a substrate for p21-activated kinase 4 (PAK4) and that its phosphorylation on serine-135 increases during mitosis. The endogenous phosphorylated Ran and active PAK4 dynamically associate with different components of the microtubule spindle during mitotic progression. A GDP-bo

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18

Scaife, Robin M. "G2 cell cycle arrest, down-regulation of cyclin B, and induction of mitotic catastrophe by the flavoprotein inhibitor diphenyleneiodonium." Molecular Cancer Therapeutics 3, no. 10 (2004): 1229–37. http://dx.doi.org/10.1158/1535-7163.1229.3.10.

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Abstract Because proliferation of eukaryotic cells requires cell cycle–regulated chromatid separation by the mitotic spindle, it is subject to regulation by mitotic checkpoints. To determine the mechanism of the antiproliferative activity of the flavoprotein-specific inhibitor diphenyleneiodonium (DPI), I have examined its effect on the cell cycle and mitosis. Similar to paclitaxel, exposure to DPI causes an accumulation of cells with a 4N DNA content. However, unlike the paclitaxel-mediated mitotic block, DPI-treated cells are arrested in the cell cycle prior to mitosis. Although DPI-treated

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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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Priego Moreno, Sara, Rebecca M. Jones, Divyasree Poovathumkadavil, Shaun Scaramuzza, and Agnieszka Gambus. "Mitotic replisome disassembly depends on TRAIP ubiquitin ligase activity." Life Science Alliance 2, no. 2 (2019): e201900390. http://dx.doi.org/10.26508/lsa.201900390.

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We have shown previously that the process of replication machinery (replisome) disassembly at the termination of DNA replication forks in the S-phase is driven through polyubiquitylation of one of the replicative helicase subunits (Mcm7) by Cul2LRR1 ubiquitin ligase. Interestingly, upon inhibition of this pathway in Caenorhabditis elegans embryos, the replisomes retained on chromatin were unloaded in the subsequent mitosis. Here, we show that this mitotic replisome disassembly pathway exists in Xenopus laevis egg extract and we determine the first elements of its regulation. The mitotic disass

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Nolan, L. A., and A. Levy. "The effects of testosterone and oestrogen on gonadectomised and intact male rat anterior pituitary mitotic and apoptotic activity." Journal of Endocrinology 188, no. 3 (2006): 387–96. http://dx.doi.org/10.1677/joe.1.06508.

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We have used a direct, non-immunochemical and highly accurate method to quantify the effects of testosterone and oestrogen on mitotic and apoptotic activity in the young, male rat anterior pituitary in vivo. Surgical gonadectomy resulted in a 3-fold increase in mitotic activity by the fourth post-operative day, which returned gradually to levels seen in intact animals over the subsequent 3–4 weeks. Both a single dose of Sustanon, a mixture of long-acting testosterone esters in arachis oil, and the same dose divided over 7 days (starting 6 days after gonadectomy), initially suppressed mitotic a

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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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Wang, Yamei, Wen-zhu Li, Alyssa E. Johnson, et al. "Dnt1 acts as a mitotic inhibitor of the spindle checkpoint protein dma1 in fission yeast." Molecular Biology of the Cell 23, no. 17 (2012): 3348–56. http://dx.doi.org/10.1091/mbc.e11-12-1020.

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The Schizosaccharomyces pombe checkpoint protein Dma1 couples mitotic progression with cytokinesis and is important in delaying mitotic exit and cytokinesis when kinetochores are not properly attached to the mitotic spindle. Dma1 is a ubiquitin ligase and potential functional relative of the human tumor suppressor Chfr. Dma1 delays mitotic exit and cytokinesis by ubiquitinating a scaffold protein (Sid4) of the septation initiation network, which, in turn, antagonizes the ability of the Polo-like kinase Plo1 to promote cell division. Here we identify Dnt1 as a Dma1-binding protein. Several line

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Lama, Bunu, Hyewon Park, Anita Saraf, et al. "PICH impacts the spindle assembly checkpoint via its DNA translocase and SUMO-interaction activities." Life Science Alliance 8, no. 4 (2025): e202403140. https://doi.org/10.26508/lsa.202403140.

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Either inhibiting or stabilizing SUMOylation in mitosis causes defects in chromosome segregation, suggesting that dynamic mitotic SUMOylation of proteins is critical to maintain integrity of the genome. Polo-like kinase 1–interacting checkpoint helicase (PICH), a mitotic chromatin remodeling enzyme, interacts with SUMOylated chromosomal proteins via threeSUMO-interactingmotifs (SIMs) to control their association with chromosomes. Using cell lines with conditional PICH depletion/PICH replacement, we revealed mitotic defects associated with compromised PICH functions toward SUMOylated chromosoma

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Morohashi, Yuichi, Zita Balklava, Matthew Ball, Helen Hughes, and Martin Lowe. "Phosphorylation and membrane dissociation of the ARF exchange factor GBF1 in mitosis." Biochemical Journal 427, no. 3 (2010): 401–12. http://dx.doi.org/10.1042/bj20091681.

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Secretory protein trafficking is arrested and the Golgi apparatus fragmented when mammalian cells enter mitosis. These changes are thought to facilitate cell-cycle progression and Golgi inheritance, and are brought about through the actions of mitotically active protein kinases. To better understand how the Golgi apparatus undergoes mitotic fragmentation we have sought to identify novel Golgi targets for mitotic kinases. We report in the present paper the identification of the ARF (ADP-ribosylation factor) exchange factor GBF1 (Golgi-specific brefeldin A-resistant guanine nucleotide-exchange f

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White, R. J., T. M. Gottlieb, C. S. Downes, and S. P. Jackson. "Mitotic regulation of a TATA-binding-protein-containing complex." Molecular and Cellular Biology 15, no. 4 (1995): 1983–92. http://dx.doi.org/10.1128/mcb.15.4.1983.

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The mitotic state is associated with a generalized repression of transcription. We show that mitotic repression of RNA polymerase III transcription can be reproduced by using extracts of synchronized HeLa cells. We have used this system to investigate the molecular basis of transcriptional repression during mitosis. We find a specific decrease in the activity of the TATA-binding-protein (TBP)-containing complex TFIIIB. TBP itself is hyperphosphorylated at mitosis, but this does not appear to account for the loss of TFIIIB activity. Instead, one or more TBP-associated components appear to be re

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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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Jaspersen, Sue L., Julia F. Charles, Rachel L. Tinker-Kulberg, and David O. Morgan. "A Late Mitotic Regulatory Network Controlling Cyclin Destruction in Saccharomyces cerevisiae." Molecular Biology of the Cell 9, no. 10 (1998): 2803–17. http://dx.doi.org/10.1091/mbc.9.10.2803.

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Exit from mitosis requires the inactivation of mitotic cyclin-dependent kinase–cyclin complexes, primarily by ubiquitin-dependent cyclin proteolysis. Cyclin destruction is regulated by a ubiquitin ligase known as the anaphase-promoting complex (APC). In the budding yeast Saccharomyces cerevisiae, members of a large class of late mitotic mutants, including cdc15,cdc5, cdc14, dbf2, andtem1, arrest in anaphase with a phenotype similar to that of cells expressing nondegradable forms of mitotic cyclins. We addressed the possibility that the products of these genes are components of a regulatory net

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Andreassen, P. R., and R. L. Margolis. "Microtubule dependency of p34cdc2 inactivation and mitotic exit in mammalian cells." Journal of Cell Biology 127, no. 3 (1994): 789–802. http://dx.doi.org/10.1083/jcb.127.3.789.

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The protein kinase inhibitor 2-aminopurine induces checkpoint override and mitotic exit in BHK cells which have been arrested in mitosis by inhibitors of microtubule function (Andreassen, P. R., and R. L. Margolis. 1991. J. Cell Sci. 100:299-310). Mitotic exit is monitored by loss of MPM-2 antigen, by the reformation of nuclei, and by the extinction of p34cdc2-dependent H1 kinase activity. 2-AP-induced inactivation of p34cdc2 and mitotic exit depend on the assembly state of microtubules. During mitotic arrest generated by the microtubule assembly inhibitor nocodazole, the rate of mitotic exit

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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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Moreira, Joana, Patrícia M. A. Silva, Eliseba Castro, et al. "BP-M345 as a Basis for the Discovery of New Diarylpentanoids with Promising Antimitotic Activity." International Journal of Molecular Sciences 25, no. 3 (2024): 1691. http://dx.doi.org/10.3390/ijms25031691.

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Recently, the diarylpentanoid BP-M345 (5) has been identified as a potent in vitro growth inhibitor of cancer cells, with a GI50 value between 0.17 and 0.45 µM, showing low toxicity in non-tumor cells. BP-M345 (5) promotes mitotic arrest by interfering with mitotic spindle assembly, leading to apoptotic cell death. Following on from our previous work, we designed and synthesized a library of BP-M345 (5) analogs and evaluated the cell growth inhibitory activity of three human cancer cell lines within this library in order to perform structure–activity relationship (SAR) studies and to obtain co

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Sudakin, Valery, Gordon K. T. Chan, and Tim J. Yen. "Checkpoint inhibition of the APC/C in HeLa cells is mediated by a complex of BUBR1, BUB3, CDC20, and MAD2." Journal of Cell Biology 154, no. 5 (2001): 925–36. http://dx.doi.org/10.1083/jcb.200102093.

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The mitotic checkpoint prevents cells with unaligned chromosomes from prematurely exiting mitosis by inhibiting the anaphase-promoting complex/cyclosome (APC/C) from targeting key proteins for ubiquitin-mediated proteolysis. We have examined the mechanism by which the checkpoint inhibits the APC/C by purifying an APC/C inhibitory factor from HeLa cells. We call this factor the mitotic checkpoint complex (MCC) as it consists of hBUBR1, hBUB3, CDC20, and MAD2 checkpoint proteins in near equal stoichiometry. MCC inhibitory activity is 3,000-fold greater than that of recombinant MAD2, which has al

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Gandhi, Shashi, Raizy Mitterhoff, Rachel Rapoport, et al. "Mitotic H3K9ac is controlled by phase-specific activity of HDAC2, HDAC3, and SIRT1." Life Science Alliance 5, no. 10 (2022): e202201433. http://dx.doi.org/10.26508/lsa.202201433.

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Histone acetylation levels are reduced during mitosis. To study the mitotic regulation of H3K9ac, we used an array of inhibitors targeting specific histone deacetylases. We evaluated the involvement of the targeted enzymes in regulating H3K9ac during all mitotic stages by immunofluorescence and immunoblots. We identified HDAC2, HDAC3, and SIRT1 as modulators of H3K9ac mitotic levels. HDAC2 inhibition increased H3K9ac levels in prophase, whereas HDAC3 or SIRT1 inhibition increased H3K9ac levels in metaphase. Next, we performed ChIP-seq on mitotic-arrested cells following targeted inhibition of

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Park, J., and C. A. Cartwright. "Src activity increases and Yes activity decreases during mitosis of human colon carcinoma cells." Molecular and Cellular Biology 15, no. 5 (1995): 2374–82. http://dx.doi.org/10.1128/mcb.15.5.2374.

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Src and Yes protein-tyrosine kinase activities are elevated in malignant and premalignant tumors of the colon. To determine whether Src activity is elevated throughout the human colon carcinoma cell cycle as it is in polyomavirus middle T antigen- or F527 Src-transformed cells, and whether Yes activity, which is lower than that of Src in the carcinoma cells, is regulated differently, we measured their activities in cycling cells. We observed that the activities of both kinases were higher throughout all phases of the HT-29 colon carcinoma cell cycle than in corresponding phases of the fibrobla

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Feldman, Michal, Zlata Vershinin, Inna Goliand, Natalie Elia, and Dan Levy. "The methyltransferase SETD6 regulates Mitotic progression through PLK1 methylation." Proceedings of the National Academy of Sciences 116, no. 4 (2019): 1235–40. http://dx.doi.org/10.1073/pnas.1804407116.

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Lysine methylation, catalyzed by protein lysine methyltransferases (PKMTs), is a key player in regulating intracellular signaling pathways. However, the role of PKMTs and the methylation of nonhistone proteins during the cell cycle are largely unexplored. In a recent proteomic screen, we identified that the PKMT SETD6 methylates PLK1—a key regulator of mitosis and highly expressed in tumor cells. In this study, we provide evidence that SETD6 is involved in cell cycle regulation. SETD6-deficient cells were observed to progress faster through the different mitotic steps toward the cytokinesis st

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Govindaraghavan, Meera, Alisha A. Lad, and Stephen A. Osmani. "The NIMA Kinase Is Required To Execute Stage-Specific Mitotic Functions after Initiation of Mitosis." Eukaryotic Cell 13, no. 1 (2013): 99–109. http://dx.doi.org/10.1128/ec.00231-13.

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ABSTRACTThe G2-M transition inAspergillus nidulansrequires the NIMA kinase, the founding member of the Nek kinase family. Inactivation of NIMA results in a late G2arrest, while overexpression of NIMA is sufficient to promote mitotic events independently of cell cycle phase. Endogenously tagged NIMA-GFP has dynamic mitotic localizations appearing first at the spindle pole body and then at nuclear pore complexes before transitioning to within nuclei and the mitotic spindle and back at the spindle pole bodies at mitotic exit, suggesting that it functions sequentially at these locations. Since NIM

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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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Chan, G. K. T., S. A. Jablonski, V. Sudakin, J. C. Hittle, and T. J. Yen. "Human Bubr1 Is a Mitotic Checkpoint Kinase That Monitors Cenp-E Functions at Kinetochores and Binds the Cyclosome/APC." Journal of Cell Biology 146, no. 5 (1999): 941–54. http://dx.doi.org/10.1083/jcb.146.5.941.

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Human cells express two kinases that are related to the yeast mitotic checkpoint kinase BUB1. hBUB1 and hBUBR1 bind to kinetochores where they are postulated to be components of the mitotic checkpoint that monitors kinetochore activities to determine if chromosomes have achieved alignment at the spindle equator (Jablonski, S.A., G.K.T. Chan, C.A. Cooke, W.C. Earnshaw, and T.J. Yen. 1998. Chromosoma. 107:386–396). In support of this, hBUB1 and the homologous mouse BUB1 have been shown to be important for the mitotic checkpoint (Cahill, D.P., C. Lengauer, J. Yu, G.J. Riggins, J.K. Willson, S.D.

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Hartl, P., J. Gottesfeld, and D. J. Forbes. "Mitotic repression of transcription in vitro." Journal of Cell Biology 120, no. 3 (1993): 613–24. http://dx.doi.org/10.1083/jcb.120.3.613.

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A normal consequence of mitosis in eukaryotes is the repression of transcription. Using Xenopus egg extracts shifted to a mitotic state by the addition of purified cyclin, we have for the first time been able to reproduce a mitotic repression of transcription in vitro. Active RNA polymerase III transcription is observed in interphase extracts, but strongly repressed in extracts converted to mitosis. With the topoisomerase II inhibitor VM-26, we demonstrate that this mitotic repression of RNA polymerase III transcription does not require normal chromatin condensation. Similarly; in vitro mitoti

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Rudner, Adam D., and Andrew W. Murray. "Phosphorylation by Cdc28 Activates the Cdc20-Dependent Activity of the Anaphase-Promoting Complex." Journal of Cell Biology 149, no. 7 (2000): 1377–90. http://dx.doi.org/10.1083/jcb.149.7.1377.

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Budding yeast initiates anaphase by activating the Cdc20-dependent anaphase-promoting complex (APC). The mitotic activity of Cdc28 (Cdk1) is required to activate this form of the APC, and mutants that are impaired in mitotic Cdc28 function have difficulty leaving mitosis. This defect can be explained by a defect in APC phosphorylation, which depends on mitotic Cdc28 activity in vivo and can be catalyzed by purified Cdc28 in vitro. Mutating putative Cdc28 phosphorylation sites in three components of the APC, Cdc16, Cdc23, and Cdc27, makes the APC resistant to phosphorylation both in vivo and in

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Tran, Suzanne, Alice Thomas, Mehdi Touat, et al. "PATH-16. THRESHOLDS OF MITOTIC ACTIVITY AND POST-SURGERY RESIDUAL VOLUME ARE INDEPENDENT PROGNOSTIC FACTORS IN ASTROCYTOMA IDH-MUTANT." Neuro-Oncology 24, Supplement_7 (2022): vii153. http://dx.doi.org/10.1093/neuonc/noac209.589.

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Abstract BACKGROUND The distinction between grade 2 and 3 is instrumental to choose between observational follow-up and adjuvant treatment in resected astrocytoma IDH-mutant. However, criteria for discriminating grade 2 and 3 tumors have not been updated since the WHO 2007 classification. There is no consensus on the method of evaluation of the mitotic activity or a mitosis cut-off for grading. The objectives were to evaluate the maximal mitotic activity on a series of resected astrocytoma IDH-mutant and assess its prognostic impact on survival. METHODS Maximal mitotic activity on consecutive

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Vorlaufer, Elisabeth, and Jan-Michael Peters. "Regulation of the Cyclin B Degradation System by an Inhibitor of Mitotic Proteolysis." Molecular Biology of the Cell 9, no. 7 (1998): 1817–31. http://dx.doi.org/10.1091/mbc.9.7.1817.

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The initiation of anaphase and exit from mitosis depend on the anaphase-promoting complex (APC), which mediates the ubiquitin-dependent proteolysis of anaphase-inhibiting proteins and mitotic cyclins. We have analyzed whether protein phosphatases are required for mitotic APC activation. In Xenopus egg extracts APC activation occurs normally in the presence of protein phosphatase 1 inhibitors, suggesting that the anaphase defects caused by protein phosphatase 1 mutation in several organisms are not due to a failure to activate the APC. Contrary to this, the initiation of mitotic cyclin B proteo

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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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Onischenko, Evgeny A., Natalia V. Gubanova, Elena V. Kiseleva, and Einar Hallberg. "Cdk1 and Okadaic Acid-sensitive Phosphatases Control Assembly of Nuclear Pore Complexes in Drosophila Embryos." Molecular Biology of the Cell 16, no. 11 (2005): 5152–62. http://dx.doi.org/10.1091/mbc.e05-07-0642.

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Disassembly and reassembly of the nuclear pore complexes (NPCs) is one of the major events during open mitosis in higher eukaryotes. However, how this process is controlled by the mitotic machinery is not clear. To investigate this we developed a novel in vivo model system based on syncytial Drosophila embryos. We microinjected different mitotic effectors into the embryonic cytoplasm and monitored the dynamics of disassembly/reassembly of NPCs in live embryos using fluorescently labeled wheat germ agglutinin (WGA) or in fixed embryos using electron microscopy and immunostaining techniques. We

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Damizia, Michela, Ludovica Altieri, Vincenzo Costanzo, and Patrizia Lavia. "Distinct Mitotic Functions of Nucleolar and Spindle-Associated Protein 1 (NuSAP1) Are Controlled by Two Consensus SUMOylation Sites." Cells 12, no. 21 (2023): 2545. http://dx.doi.org/10.3390/cells12212545.

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Nucleolar and Spindle-Associated Protein 1 (NuSAP1) is an important mitotic regulator, implicated in control of mitotic microtubule stability and chromosome segregation. NuSAP1 regulates these processes by interacting with several protein partners. Its abundance, activity and interactions are therefore tightly regulated during mitosis. Protein conjugation with SUMO (Small Ubiquitin-like MOdifier peptide) is a reversible post-translational modification that modulates rapid changes in the structure, interaction(s) and localization of proteins. NuSAP1 was previously found to interact with RANBP2,

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Kawahara, H., R. Philipova, H. Yokosawa, R. Patel, K. Tanaka, and M. Whitaker. "Inhibiting proteasome activity causes overreplication of DNA and blocks entry into mitosis in sea urchin embryos." Journal of Cell Science 113, no. 15 (2000): 2659–70. http://dx.doi.org/10.1242/jcs.113.15.2659.

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The proteasome has been shown to be involved in exit from mitosis by bringing about destruction of mitotic cyclins. Here, we present evidence that the proteasome is also required for proper completion of S phase and for entry into mitosis in the sea urchin embryonic cleavage cycle. A series of structurally related peptide-aldehydes prevent nuclear envelope breakdown in their order of inhibitory efficacies against the proteasome. Their efficacies in blocking exit from S phase and exit from mitosis correlate well, indicating that the proteasome is involved at both these steps. Mitotic histone HI

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Egorshina, Aleksandra Yu, Alexey V. Zamaraev, Vitaliy O. Kaminskyy, Tatiana V. Radygina, Boris Zhivotovsky, and Gelina S. Kopeina. "Necroptosis as a Novel Facet of Mitotic Catastrophe." International Journal of Molecular Sciences 23, no. 7 (2022): 3733. http://dx.doi.org/10.3390/ijms23073733.

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Mitotic catastrophe is a defensive mechanism that promotes elimination of cells with aberrant mitosis by triggering the cell-death pathways and/or cellular senescence. Nowadays, it is known that apoptosis, autophagic cell death, and necrosis could be consequences of mitotic catastrophe. Here, we demonstrate the ability of a DNA-damaging agent, doxorubicin, at 600 nM concentration to stimulate mitotic catastrophe. We observe that the inhibition of caspase activity leads to accumulation of cells with mitotic catastrophe hallmarks in which RIP1-dependent necroptotic cell death is triggered. The s

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Chu, Chi-Shuen, Pang-Hung Hsu, Pei-Wen Lo, et al. "Protein Kinase A-mediated Serine 35 Phosphorylation Dissociates Histone H1.4 from Mitotic Chromosome." Journal of Biological Chemistry 286, no. 41 (2011): 35843–51. http://dx.doi.org/10.1074/jbc.m111.228064.

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Global histone H1 phosphorylation correlates with cell cycle progression. However, the function of site-specific H1 variant phosphorylation remains unclear. Our mass spectrometry analysis revealed a novel N-terminal phosphorylation of the major H1 variant H1.4 at serine 35 (H1.4S35ph), which accumulates at mitosis immediately after H3 phosphorylation at serine 10. Protein kinase A (PKA) was found to be a kinase for H1.4S35. Importantly, Ser-35-phosphorylated H1.4 dissociates from mitotic chromatin. Moreover, H1.4S35A substitution mutant cannot efficiently rescue the mitotic defect following H1

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Yuan, Jin-Hui, Yang Feng, Rebecca H. Fisher, Sharon Maloid, Dan L. Longo, and Douglas K. Ferris. "Polo-Like Kinase 1 Inactivation Following Mitotic DNA Damaging Treatments Is Independent of Ataxia Telangiectasia Mutated Kinase." Molecular Cancer Research 2, no. 7 (2004): 417–26. http://dx.doi.org/10.1158/1541-7786.417.2.7.

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Abstract Polo-like kinase 1 (Plk1) is an important regulator of several events during mitosis. Recent reports show that Plk1 is involved in both G2 and mitotic DNA damage checkpoints. Ataxia telangiectasia mutated kinase (ATM) is an important enzyme involved in G2 phase cell cycle arrest following interphase DNA damage, and inhibition of Plk1 by DNA damage during G2 occurs in an ATM-/ATM-Rad3–related kinase (ATR)–dependent fashion. However, it is unclear how Plk1 is regulated in response to M phase DNA damage. We found that treatment of mitotic cells with DNA damaging agents inhibits Plk1 acti

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Turner, Roberta L., Peter Groitl, Thomas Dobner, and David A. Ornelles. "Adenovirus Replaces Mitotic Checkpoint Controls." Journal of Virology 89, no. 9 (2015): 5083–96. http://dx.doi.org/10.1128/jvi.00213-15.

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ABSTRACTInfection with adenovirus triggers the cellular DNA damage response, elements of which include cell death and cell cycle arrest. Early adenoviral proteins, including the E1B-55K and E4orf3 proteins, inhibit signaling in response to DNA damage. A fraction of cells infected with an adenovirus mutant unable to express the E1B-55K and E4orf3 genes appeared to arrest in a mitotic-like state. Cells infected early in G1of the cell cycle were predisposed to arrest in this state at late times of infection. This arrested state, which displays hallmarks of mitotic catastrophe, was prevented by ex

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