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Results: 1 to 10 of 116

Publication Record


The Plk1 Piece of the Nuclear Envelope Disassembly Puzzle.
Dawson TR, Wente SR
(2017) Dev Cell 43: 115-117
MeSH Terms: Mitosis, Nuclear Envelope, Nuclear Pore, Nuclear Pore Complex Proteins, Phosphorylation
Show Abstract · Added March 30, 2018
Reporting in this issue of Developmental Cell, Linder et al. (2017) and Martino et al. (2017) reveal in highly complementary studies that Plk1 is recruited to the nuclear pore complex upon mitotic entry, where it acts with Cdk1 to hyperphosphorylate nucleoporin interfaces to promote NPC disassembly and nuclear envelope breakdown.
Copyright © 2017 Elsevier Inc. All rights reserved.
0 Communities
1 Members
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5 MeSH Terms
Cytologic anaplasia is a prognostic factor in osteosarcoma biopsies, but mitotic rate or extent of spontaneous tumor necrosis are not: a critique of the College of American Pathologists Bone Biopsy template.
Cates JM, Dupont WD
(2017) Mod Pathol 30: 52-59
MeSH Terms: Adolescent, Adult, Anaplasia, Biopsy, Bone Neoplasms, Child, Disease-Free Survival, Female, Humans, Male, Mitosis, Necrosis, Osteosarcoma, Prognosis, Retrospective Studies, Survival Rate, Young Adult
Show Abstract · Added November 1, 2018
The current College of American Pathologists cancer template for reporting biopsies of bone tumors recommends including information that is of unproven prognostic significance for osteosarcoma, such as the presence of spontaneous tumor necrosis and mitotic rate. Conversely, the degree of cytologic anaplasia (degree of differentiation) is not reported in this template. This retrospective cohort study of 125 patients with high-grade osteosarcoma was performed to evaluate the prognostic impact of these factors in diagnostic biopsy specimens in predicting the clinical outcome and response to neoadjuvant chemotherapy. Multivariate Cox regression was performed to adjust survival analyses for well-established prognostic factors. Multivariate logistic regression was used to determine odds ratios for good chemotherapy response (≥90% tumor necrosis). Osteosarcomas with severe anaplasia were independently associated with increased overall and disease-free survival, but mitotic rate and spontaneous necrosis had no prognostic impact after controlling for other confounding factors. Mitotic rate showed a trend towards increased odds of a good histologic response, but this effect was diminished after controlling for other predictive factors. Neither spontaneous necrosis nor the degree of cytologic anaplasia observed in biopsy specimens was predictive of a good response to chemotherapy. Mitotic rate and spontaneous tumor necrosis observed in pretreatment biopsy specimens of high-grade osteosarcoma are not strong independent prognostic factors for clinical outcome or predictors of response to neoadjuvant chemotherapy. Therefore, reporting these parameters for osteosarcoma, as recommended in the College of American Pathologists Bone Biopsy template, does not appear to have clinical utility. In contrast, histologic grading schemes for osteosarcoma based on the degree of cytologic anaplasia may have independent prognostic value and should continue to be evaluated.
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MeSH Terms
Precommitment low-level Neurog3 expression defines a long-lived mitotic endocrine-biased progenitor pool that drives production of endocrine-committed cells.
Bechard ME, Bankaitis ED, Hipkens SB, Ustione A, Piston DW, Yang YP, Magnuson MA, Wright CV
(2016) Genes Dev 30: 1852-65
MeSH Terms: Animals, Basic Helix-Loop-Helix Transcription Factors, Cell Differentiation, Cell Proliferation, Endocrine Cells, Gene Expression Regulation, Developmental, Mice, Mitosis, Nerve Tissue Proteins, Pancreas, Stem Cells
Show Abstract · Added September 6, 2016
The current model for endocrine cell specification in the pancreas invokes high-level production of the transcription factor Neurogenin 3 (Neurog3) in Sox9(+) bipotent epithelial cells as the trigger for endocrine commitment, cell cycle exit, and rapid delamination toward proto-islet clusters. This model posits a transient Neurog3 expression state and short epithelial residence period. We show, however, that a Neurog3(TA.LO) cell population, defined as Neurog3 transcriptionally active and Sox9(+) and often containing nonimmunodetectable Neurog3 protein, has a relatively high mitotic index and prolonged epithelial residency. We propose that this endocrine-biased mitotic progenitor state is functionally separated from a pro-ductal pool and endows them with long-term capacity to make endocrine fate-directed progeny. A novel BAC transgenic Neurog3 reporter detected two types of mitotic behavior in Sox9(+) Neurog3(TA.LO) progenitors, associated with progenitor pool maintenance or derivation of endocrine-committed Neurog3(HI) cells, respectively. Moreover, limiting Neurog3 expression dramatically increased the proportional representation of Sox9(+) Neurog3(TA.LO) progenitors, with a doubling of its mitotic index relative to normal Neurog3 expression, suggesting that low Neurog3 expression is a defining feature of this cycling endocrine-biased state. We propose that Sox9(+) Neurog3(TA.LO) endocrine-biased progenitors feed production of Neurog3(HI) endocrine-committed cells during pancreas organogenesis.
© 2016 Bechard et al.; Published by Cold Spring Harbor Laboratory Press.
2 Communities
4 Members
0 Resources
11 MeSH Terms
Focal adhesions control cleavage furrow shape and spindle tilt during mitosis.
Taneja N, Fenix AM, Rathbun L, Millis BA, Tyska MJ, Hehnly H, Burnette DT
(2016) Sci Rep 6: 29846
MeSH Terms: Animals, Cell Differentiation, Cell Shape, Centrosome, Dogs, Focal Adhesion Protein-Tyrosine Kinases, Focal Adhesions, HeLa Cells, Humans, Madin Darby Canine Kidney Cells, Mitosis, Spindle Apparatus, Vinculin
Show Abstract · Added April 7, 2017
The geometry of the cleavage furrow during mitosis is often asymmetric in vivo and plays a critical role in stem cell differentiation and the relative positioning of daughter cells during development. Early observations of adhesive cell lines revealed asymmetry in the shape of the cleavage furrow, where the bottom (i.e., substrate attached side) of the cleavage furrow ingressed less than the top (i.e., unattached side). This data suggested substrate attachment could be regulating furrow ingression. Here we report a population of mitotic focal adhesions (FAs) controls the symmetry of the cleavage furrow. In single HeLa cells, stronger adhesion to the substrate directed less ingression from the bottom of the cell through a pathway including paxillin, focal adhesion kinase (FAK) and vinculin. Cell-cell contacts also direct ingression of the cleavage furrow in coordination with FAs in epithelial cells-MDCK-within monolayers and polarized cysts. In addition, mitotic FAs established 3D orientation of the mitotic spindle and the relative positioning of mother and daughter centrosomes. Therefore, our data reveals mitotic FAs as a key link between mitotic cell shape and spindle orientation, and may have important implications in our understanding stem cell homeostasis and tumorigenesis.
1 Communities
2 Members
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13 MeSH Terms
Resistance is not futile: Surviving Eg5 inhibition.
Dumas ME, Sturgill EG, Ohi R
(2016) Cell Cycle 15: 2845-2847
MeSH Terms: Kinesin, Microtubules, Mitosis, Spindle Apparatus
Added April 18, 2017
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4 MeSH Terms
Early Detection of Treatment-Induced Mitotic Arrest Using Temporal Diffusion Magnetic Resonance Spectroscopy.
Jiang X, Li H, Zhao P, Xie J, Khabele D, Xu J, Gore JC
(2016) Neoplasia 18: 387-97
MeSH Terms: Albumins, Animals, Antineoplastic Agents, Phytogenic, Apoptosis, Biomarkers, Tumor, Cell Line, Tumor, Cell Size, Female, Flow Cytometry, Humans, Magnetic Resonance Spectroscopy, Mice, Mice, Nude, Mitosis, Mitotic Index, Paclitaxel, Xenograft Model Antitumor Assays
Show Abstract · Added November 1, 2016
PURPOSE - A novel quantitative magnetic resonance imaging (MRI) method, namely, temporal diffusion spectroscopy (TDS), was used to detect the response of tumor cells (notably, mitotic arrest) to a specific antimitotic treatment (Nab-paclitaxel) in culture and human ovarian xenografts and evaluated as an early imaging biomarker of tumor responsiveness.
METHODS - TDS measures a series of apparent diffusion coefficients (ADCs) of tissue water over a range of effective diffusion times, which may correspond to diffusion distances ranging from subcellular to cellular levels (~3-20 μm). By fitting the measured ADC data to a tissue model, parameters reflecting structural properties such as restriction size in solid tumors can be extracted. Two types of human ovarian cell lines (OVCAR-8 as a responder to Nab-paclitaxel and NCI/ADR-RES as a resistant type) were treated with either vehicle (PBS) or Nab-paclitaxel, and treatment responses of both in vitro and in vivo cases were investigated using TDS.
RESULTS - Acute cell size increases induced by Nab-paclitaxel in responding tumors were confirmed by flow cytometry and light microscopy in cell culture. Nab-paclitaxel-induced mitotic arrest in treated tumors/cells was quantified histologically by measuring the mitotic index in vivo using a mitosis-specific marker (anti-phosphohistone H3). Changes in the fitted restriction size, one of the parameters obtained from TDS, were able to detect and quantify increases in tumor cell sizes. All the MR results had a high degree of consistency with other flow, microscopy, and histological data. Moreover, with an appropriate analysis, the Nab-paclitaxel-responsive tumors in vivo could be easily distinguished from all the other vehicle-treated and Nab-paclitaxel-resistant tumors.
CONCLUSION - TDS detects increases in cell sizes associated with antimitotic-therapy-induced mitotic arrest in solid tumors in vivo which occur before changes in tissue cellularity or conventional diffusion MRI metrics. By quantifying changes in cell size, TDS has the potential to improve the specificity of MRI methods in the evaluation of therapeutic response and enable a mechanistic understanding of therapy-induced changes in tumors.
Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.
0 Communities
2 Members
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17 MeSH Terms
Loss of CENP-F results in distinct microtubule-related defects without chromosomal abnormalities.
Pfaltzgraff ER, Roth GM, Miller PM, Gintzig AG, Ohi R, Bader DM
(2016) Mol Biol Cell 27: 1990-9
MeSH Terms: Animals, Cell Cycle, Centromere, Chromosomal Proteins, Non-Histone, Chromosome Aberrations, Chromosome Segregation, Fibroblasts, Interphase, Kinetochores, Mice, Mice, Knockout, Microfilament Proteins, Microtubules, Mitosis, Protein Binding
Show Abstract · Added March 29, 2017
Microtubule (MT)-binding centromere protein F (CENP-F) was previously shown to play a role exclusively in chromosome segregation during cellular division. Many cell models of CENP-F depletion show a lag in the cell cycle and aneuploidy. Here, using our novel genetic deletion model, we show that CENP-F also regulates a broader range of cellular functions outside of cell division. We characterized CENP-F(+/+) and CENP-F(-/-) mouse embryonic fibroblasts (MEFs) and found drastic differences in multiple cellular functions during interphase, including cell migration, focal adhesion dynamics, and primary cilia formation. We discovered that CENP-F(-/-) MEFs have severely diminished MT dynamics, which underlies the phenotypes we describe. These data, combined with recent biochemical research demonstrating the strong binding of CENP-F to the MT network, support the conclusion that CENP-F is a powerful regulator of MT dynamics during interphase and affects heterogeneous cell functions.
© 2016 Pfaltzgraff et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).
1 Communities
2 Members
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15 MeSH Terms
Wnt/Wingless Pathway Activation Is Promoted by a Critical Threshold of Axin Maintained by the Tumor Suppressor APC and the ADP-Ribose Polymerase Tankyrase.
Wang Z, Tacchelly-Benites O, Yang E, Thorne CA, Nojima H, Lee E, Ahmed Y
(2016) Genetics 203: 269-81
MeSH Terms: Adenomatous Polyposis Coli Protein, Animals, Axin Protein, Drosophila, Genotype, Mitosis, Protein Interaction Domains and Motifs, Protein Stability, Tankyrases, Wnt Proteins, Wnt Signaling Pathway, Xenopus
Show Abstract · Added February 13, 2017
Wnt/β-catenin signal transduction directs metazoan development and is deregulated in numerous human congenital disorders and cancers. In the absence of Wnt stimulation, a multiprotein "destruction complex," assembled by the scaffold protein Axin, targets the key transcriptional activator β-catenin for proteolysis. Axin is maintained at very low levels that limit destruction complex activity, a property that is currently being exploited in the development of novel therapeutics for Wnt-driven cancers. Here, we use an in vivo approach in Drosophila to determine how tightly basal Axin levels must be controlled for Wnt/Wingless pathway activation, and how Axin stability is regulated. We find that for nearly all Wingless-driven developmental processes, a three- to fourfold increase in Axin is insufficient to inhibit signaling, setting a lower-limit for the threshold level of Axin in the majority of in vivo contexts. Further, we find that both the tumor suppressor adenomatous polyposis coli (APC) and the ADP-ribose polymerase Tankyrase (Tnks) have evolutionarily conserved roles in maintaining basal Axin levels below this in vivo threshold, and we define separable domains in Axin that are important for APC- or Tnks-dependent destabilization. Together, these findings reveal that both APC and Tnks maintain basal Axin levels below a critical in vivo threshold to promote robust pathway activation following Wnt stimulation.
Copyright © 2016 by the Genetics Society of America.
0 Communities
1 Members
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12 MeSH Terms
Temporal Regulation of Lipin Activity Diverged to Account for Differences in Mitotic Programs.
Makarova M, Gu Y, Chen JS, Beckley JR, Gould KL, Oliferenko S
(2016) Curr Biol 26: 237-243
MeSH Terms: Cell Nucleus, Cell Nucleus Division, Chromosome Segregation, Mitosis, Organic Chemicals, Schizosaccharomyces
Show Abstract · Added February 4, 2016
Eukaryotes remodel the nucleus during mitosis using a variety of mechanisms that differ in the timing and the extent of nuclear envelope (NE) breakdown. Here, we probe the principles enabling this functional diversity by exploiting the natural divergence in NE management strategies between the related fission yeasts Schizosaccharomyces pombe and Schizosaccharomyces japonicus [1-3]. We show that inactivation of Ned1, the phosphatidic acid phosphatase of the lipin family, by CDK phosphorylation is both necessary and sufficient to promote NE expansion required for "closed" mitosis in S. pombe. In contrast, Ned1 is not regulated during division in S. japonicus, thus limiting membrane availability and necessitating NE breakage. Interspecies gene swaps result in phenotypically normal divisions with the S. japonicus lipin acquiring an S. pombe-like mitotic phosphorylation pattern. Our results provide experimental evidence for the mitotic regulation of phosphatidic acid flux and suggest that the regulatory networks governing lipin activity diverged in evolution to give rise to strikingly dissimilar mitotic programs.
Copyright © 2016 The Authors. Published by Elsevier Ltd.. All rights reserved.
0 Communities
1 Members
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6 MeSH Terms
ER trapping reveals Golgi enzymes continually revisit the ER through a recycling pathway that controls Golgi organization.
Sengupta P, Satpute-Krishnan P, Seo AY, Burnette DT, Patterson GH, Lippincott-Schwartz J
(2015) Proc Natl Acad Sci U S A 112: E6752-61
MeSH Terms: Animals, COS Cells, Cercopithecus aethiops, Endoplasmic Reticulum, Golgi Apparatus, HeLa Cells, Humans, Mitosis, Phospholipases A2, Calcium-Independent, Sirolimus, Tacrolimus Binding Protein 1A, Tacrolimus Binding Proteins, rab GTP-Binding Proteins
Show Abstract · Added August 25, 2017
Whether Golgi enzymes remain localized within the Golgi or constitutively cycle through the endoplasmic reticulum (ER) is unclear, yet is important for understanding Golgi dependence on the ER. Here, we demonstrate that the previously reported inefficient ER trapping of Golgi enzymes in a rapamycin-based assay results from an artifact involving an endogenous ER-localized 13-kD FK506 binding protein (FKBP13) competing with the FKBP12-tagged Golgi enzyme for binding to an FKBP-rapamycin binding domain (FRB)-tagged ER trap. When we express an FKBP12-tagged ER trap and FRB-tagged Golgi enzymes, conditions precluding such competition, the Golgi enzymes completely redistribute to the ER upon rapamycin treatment. A photoactivatable FRB-Golgi enzyme, highlighted only in the Golgi, likewise redistributes to the ER. These data establish Golgi enzymes constitutively cycle through the ER. Using our trapping scheme, we identify roles of rab6a and calcium-independent phospholipase A2 (iPLA2) in Golgi enzyme recycling, and show that retrograde transport of Golgi membrane underlies Golgi dispersal during microtubule depolymerization and mitosis.
0 Communities
1 Members
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13 MeSH Terms