Quantification of Premature and Normal Mitosis

1996 ◽  
pp. 93-99
Author(s):  
Sun W. Tam ◽  
Robert Schlegel
Keyword(s):  
Normal Mitosis

Centrosome Structure And Function Is Altered By Experimental Manipulations With Formamide: Implications For Abnormal Cell Divisions During Cancer

1999 ◽  
Vol 5 (S2) ◽  
pp. 1286-1287
Author(s):  
Heide Schatten ◽  
Christopher N. Hueser ◽  
Amitabha Chakrabarti
Keyword(s):  
Cell Cycle ◽  
Genomic Stability ◽  
Cellular Regulation ◽  
Mitotic Apparatus ◽  
Abnormal Cell ◽  
Chemical Agents ◽  
Abnormal Mitosis ◽  
And Function ◽  
Normal Mitosis ◽  
Abnormal Cell Proliferation

The formation of abnormal mitosis associated with cancer has been intriguing for many decades. While microtubules had been the focus of previous studies, recent research has focused on centrosomes, microtubule organizing centers which organize the mitotic apparatus during cell division. During normal mitosis centrosomes form two poles but in cancer, centrosomes can form three, four, or more poles, and organize tripolar, quadripolar, and multipolar mitoses, respectively. This has severe consequences for genomic stability because chromosomes are separated unequally to three, four, or more poles. This can result in aneuploidy and gene amplifications with multiple defects in cellular regulation. It can result in malignancy that is accompanied by cell cycle imbalances and abnormal cell proliferation. While radiation and chemical agents are known to damage DNA and can lead to cell cycle abnormalities, the damage of centrosome structure leading to abnormal mitosis deserves also consideration.

The Kinetochore of Mammalian Chromosomes: Structure and Function in Normal Mitosis and Aneuploidy

Aneuploidy ◽  
1985 ◽  
pp. 243-267 ◽  
Author(s):  
B. R. Brinkley ◽  
A. Tousson ◽  
M. M. Valdivia
Keyword(s):  
Structure And Function ◽  
And Function ◽  
Normal Mitosis

scholarly journals The total length of spindle microtubules depends on the number of chromosomes present.

1985 ◽  
Vol 100 (1) ◽  
pp. 1-7 ◽  
Author(s):  
R B Nicklas ◽  
G W Gordon
Keyword(s):  
Large Fraction ◽  
Microtubule Assembly ◽  
Substantial Fraction ◽  
Left Behind ◽  
Total Length ◽  
Original Length ◽  
Melanoplus Differentialis ◽  
Spindle Microtubules ◽  
Normal Mitosis

We extracted chromosomes by micromanipulation from Melanoplus differentialis spermatocytes, producing metaphase spindles with only one or a few chromosomes instead of the usual complement of 23. Cells with various numbers of chromosomes were prepared for electron microscopy, and spindle microtubule length was measured. A constant increment of microtubule length was lost upon the removal of each chromosome; we estimate that only approximately 40% of the original length would remain in the total absence of chromosomes. Unexpectedly, kinetochore microtubules were not the only ones affected when chromosomes were removed: nonkinetochore microtubules accounted for a substantial fraction of the total length lost. No compensatory increase in microtubule length outside the spindle was found. Studies by others show that the kinetochore microtubules of extracted chromosomes are left behind in the cell and dissassemble. The resulting increase in subunit concentration would be expected from in vitro studies to drive microtubule assembly until the original total microtubule length was restored, but that did not happen in these living cells. We conclude that the assembly of a certain, large fraction of microtubule subunits into stable microtubules is dependent on the presence of chromosomes. Possible explanations include (a) limits on microtubule length that prevent any net assembly of the subunits released after chromosomes are removed or (b) a promotion of microtubule assembly by chromosomes, which therefore is reduced in their absence. Chromosome-dependent regulation of microtubule length may account for some features of normal mitosis.

scholarly journals N-terminal α-methylation of RCC1 is necessary for stable chromatin association and normal mitosis

2007 ◽  
Vol 9 (5) ◽  
pp. 596-603 ◽  
Author(s):  
Ting Chen ◽  
Tara L. Muratore ◽  
Christine E. Schaner-Tooley ◽  
Jeffrey Shabanowitz ◽  
Donald F. Hunt ◽  
...  
Keyword(s):  
Normal Mitosis

scholarly journals Spindle assembly checkpoint satisfaction occurs through end-on but not lateral kinetochore-microtubule interactions under tension

2017 ◽  
Author(s):  
Jonathan Kuhn ◽  
Sophie Dumont
Keyword(s):  
Real Time ◽  
Chromosome Segregation ◽  
Spindle Assembly Checkpoint ◽  
Spindle Assembly ◽  
Microtubule Attachment ◽  
Normal Mitosis

AbstractTo ensure accurate chromosome segregation, the spindle assembly checkpoint (SAC) prevents anaphase until all kinetochores attach to the spindle. What signals the SAC monitors remains unclear. We do not know the contributions of different microtubule attachment features, or tension from biorientation, to SAC satisfaction in normal mitosis - or how these possible cues change during attachment. Here, we quantify concurrent Mad1 intensity, reporting on SAC silencing, and real-time attachment geometry, occupancy, and tension at individual mammalian kinetochores. We show that Mad1 loss from the kinetochore occurs in switch-like events with robust kinetics, and that metaphase-like tension across sister kinetochores is established just before Mad1 loss events at the first sister. We demonstrate that CenpE-mediated lateral attachment of the second sister can persistently generate this metaphase-like tension prior to biorientation, likely stabilizing sister end-on attachment, yet cannot induce Mad1 loss from that kinetochore. Instead, Mad1 loss begins after several end-on microtubules attach. Thus, end-on attachment provides geometry-specific molecular cues, or force on specific kinetochore linkages, that other attachment geometries cannot provide.SummaryThe spindle assembly checkpoint (SAC) delays anaphase until kinetochores are properly attached to the spindle. The authors demonstrate that the SAC monitors geometry-specific molecular cues, or force on specific kinetochore linkages, that “end-on” but not “lateral” attachments generating persistent tension can provide.

scholarly journals Myosin Va plays essential roles in maintaining normal mitosis, enhancing tumor cell motility and viability

Oncotarget ◽  
2017 ◽  
Vol 8 (33) ◽  
pp. 54654-54671 ◽  
Author(s):  
Yan-Ruide Li ◽  
Ai Zhong ◽  
Han Dong ◽  
Lu-Han Ni ◽  
Fu-Qing Tan ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Cell Motility ◽  
Tumor Cell Motility ◽  
Myosin Va ◽  
Normal Mitosis

Growth Inhibition and Disruption of Mitosis by DCPA in Oat (Avena sativa) Roots

Weed Science ◽  
1984 ◽  
Vol 32 (6) ◽  
pp. 732-738 ◽  
Author(s):  
Jeffrey D. Holmsen ◽  
F. Dan Hess
Keyword(s):  
Cell Division ◽  
Root Growth ◽  
Growth Inhibition ◽  
Avena Sativa ◽  
Cell Walls ◽  
Root Growth Inhibition ◽  
Predominant Type ◽  
Division Figure ◽  
Normal Mitosis ◽  
Normal Division

One to 5.6 μM DCPA (dimethyl tetrachloroterephthalate) inhibited oat (Avena sativaL. ‘Victory’) root growth within 12 to 18 h. Treated roots were severely stunted and swollen. An analysis of cell division in roots treated with DCPA revealed a disruption of normal mitosis after prophase. Metaphase, anaphase, and telophase division figures were absent 8 to 10 h after treatment with 5.6 μM DCPA. In contrast, a 24-h treatment with 5.6 μM DCPA was necessary to eliminate prophase division figures. The number of aberrant division figures increased concomitantly with the reduction in normal division figures. The predominant type of aberrant division figure was a condensed prophase. When the aberrant division cycle was completed and cells entered interphase, the dispersed chromosomes coalesced to form large, polymorphic nuclei and, occasionally, micronuclei. Approximately 60% of the outer four tiers of cells in roots treated with 5.6 μM DCPA developed abnormal cell walls. These data suggest that DCPA causes root growth inhibition by disrupting several processes involving organized microtubules.

The S. pombe zfs1 gene is required to prevent septation if mitotic progression is inhibited

1999 ◽  
Vol 112 (18) ◽  
pp. 3103-3114 ◽  
Author(s):  
N. Beltraminelli ◽  
M. Murone ◽  
V. Simanis
Keyword(s):  
Spindle Assembly Checkpoint ◽  
Spindle Assembly ◽  
Chromosome Loss ◽  
Loss Of Function ◽  
Mitotic Progression ◽  
Septum Formation ◽  
Cell Cleavage ◽  
Multicopy Suppressors ◽  
Checkpoint Genes ◽  
Normal Mitosis

Schizosaccharomyces pombe cdc16p is required to limit the cell to forming a single division septum per cell cycle; the heat-sensitive loss-of-function mutant cdc16-116 completes mitosis, and then undergoes multiple rounds of septum formation without cell cleavage. cdc16p is a homologue of Saccharomyces cerevisiae BUB2p, and has also been implicated in the spindle assembly checkpoint function in S. pombe. To identify other proteins involved in regulating septum formation, we have screened for multicopy suppressors of the cdc16-116 mutation. In this paper, we describe one of these suppressors, zfs1. The null allele (zfs1-D1) is viable. However, at low temperatures it divides at a reduced size, while at higher temperatures, it partially suppresses heat sensitive mutants in genes signalling the onset of septum formation. Zfs1-D1 cells show an increased rate of chromosome loss during exponential growth. Moreover, if assembly of the spindle is prevented, zfs1-D1 cells do not arrest normally, but the activity of cdc2p kinase decays, and cells form a division septum without completing a normal mitosis. We conclude that zfs1 function is required to prevent septum formation and exit from mitosis if the mitotic spindle is not assembled. The suppression of cdc16-116 by zfs1 is independent of dma1 function and the spindle assembly checkpoint genes mad2 and mph1. The genetic interactions of zfs1 with genes regulating septum formation suggest that it may be a modulator of the signal transduction network controlling the onset of septum formation and exit from mitosis.

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