Failure of kinetochore development and mitotic spindle formation in okadaic acid-induced premature mitosis in HeLa cells

1992 ◽  
Vol 201 (2) ◽  
pp. 535-540 ◽  
Author(s):  
Sibdas Ghosh ◽  
Neidhard Paweletz ◽  
Dieter Schroeter
Keyword(s):  
Okadaic Acid ◽  
Hela Cells ◽  
Mitotic Spindle ◽  
Spindle Formation

Nucleophosmin is required for chromosome congression, proper mitotic spindle formation, and kinetochore-microtubule attachment in HeLa cells

FEBS Letters ◽  
2008 ◽  
Vol 582 (27) ◽  
pp. 3839-3844 ◽  
Author(s):  
Mohammed Abdullahel Amin ◽  
Sachihiro Matsunaga ◽  
Susumu Uchiyama ◽  
Kiichi Fukui
Keyword(s):  
Hela Cells ◽  
Mitotic Spindle ◽  
Spindle Formation ◽  
Microtubule Attachment ◽  
Chromosome Congression

scholarly journals Aurora-A kinase-inactive mutants disrupt the interaction with Ajuba and cause defects in mitotic spindle formation and G2/M phase arrest in HeLa cells

BMB Reports ◽  
2014 ◽  
Vol 47 (11) ◽  
pp. 631-636 ◽  
Author(s):  
Meirong Bai ◽  
Jun Ni ◽  
Suqin Shen ◽  
Qiang Huang ◽  
Jiaxue Wu ◽  
...  
Keyword(s):  
Hela Cells ◽  
Mitotic Spindle ◽  
Aurora A Kinase ◽  
Aurora A ◽  
Spindle Formation ◽  
Phase Arrest ◽  
M Phase

scholarly journals Centriole-independent mitotic spindle assembly relies on the PCNT–CDK5RAP2 pericentriolar matrix

2020 ◽  
Vol 219 (12) ◽  
Author(s):  
Sadanori Watanabe ◽  
Franz Meitinger ◽  
Andrew K. Shiau ◽  
Karen Oegema ◽  
Arshad Desai
Keyword(s):  
Cell Lines ◽  
Cancer Cell ◽  
Hela Cells ◽  
Mitotic Spindle ◽  
Spindle Assembly ◽  
Cell Type ◽  
Matrix Assembly ◽  
Spindle Formation ◽  
Pericentriolar Material ◽  
Mitotic Spindle Assembly

Centrosomes, composed of centrioles that recruit a pericentriolar material (PCM) matrix assembled from PCNT and CDK5RAP2, catalyze mitotic spindle assembly. Here, we inhibit centriole formation and/or remove PCNT–CDK5RAP2 in RPE1 cells to address their relative contributions to spindle formation. While CDK5RAP2 and PCNT are normally dispensable for spindle formation, they become essential when centrioles are absent. Acentriolar spindle assembly is accompanied by the formation of foci containing PCNT and CDK5RAP2 via a microtubule and Polo-like kinase 1–dependent process. Foci formation and spindle assembly require PCNT-CDK5RAP2–dependent matrix assembly and the ability of CDK5RAP2 to recruit γ-tubulin complexes. Thus, the PCM matrix can self-organize independently of centrioles to generate microtubules for spindle assembly; conversely, an alternative centriole-anchored mechanism supports spindle assembly when the PCM matrix is absent. Extension to three cancer cell lines revealed similar results in HeLa cells, whereas DLD1 and U2OS cells could assemble spindles in the absence of centrioles and PCNT-CDK5RAP2, suggesting cell type variation in spindle assembly mechanisms.

EML4 and NUDC in mitotic spindle formation

Reactome ◽  
2020 ◽  
Author(s):  
Susanne Bechstedt ◽  
Andrew M. Fry ◽  
Kellie J Lucken ◽  
Laura O'Regan
Keyword(s):  
Mitotic Spindle ◽  
Spindle Formation

Regulation of Microtubule Assembly: The View From The End

2000 ◽  
Vol 6 (S2) ◽  
pp. 80-81
Author(s):  
L. Cassimeris ◽  
C. Spittle ◽  
M. Kratzer
Keyword(s):  
Chromosome Segregation ◽  
Mitotic Spindle ◽  
Dynamic Instability ◽  
Intrinsic Property ◽  
Microtubule Dynamics ◽  
Microtubule Assembly ◽  
Chromosome Movement ◽  
Spindle Formation ◽  
Associated Proteins

The mitotic spindle is responsible for chromosome movement during mitosis. It is composed of a dynamic array of microtubules and associated proteins whose assembly and constant turnover are required for both spindle formation and chromosome movement. Because microtubule assembly and turnover are necessary for chromosome segregation, we are studying how cells regulate microtubule dynamics. Microtubules are polarized polymers composed of tubulin subunits; they assemble by a process of dynamic instability where individual microtubules exist in persistent phases of elongation or rapid shortening with abrupt transitions between these two states. The switch from elongation to shortening is termed catastrophe, and the switch from shortening to elongation, rescue. Although dynamic instability is an intrinsic property of the tubulin subunits, cells use associated proteins to both speed elongation (∼ 10 fold) and regulate transitions.The only protein isolated to date capable of promoting fast polymerization consistent with rates in vivo is XMAP215, a 215 kD protein from Xenopus eggs.

The role ofSaccharomyces cerevisiae Cdc40p in DNA replication and mitotic spindle formation and/or maintenance

1995 ◽  
Vol 247 (2) ◽  
pp. 123-136 ◽  
Author(s):  
Nora Vaisman ◽  
Andrey Tsouladze ◽  
Kenneth Robzyk ◽  
Sigal Ben-Yehuda ◽  
Martin Kupiec ◽  
...  
Keyword(s):  
Dna Replication ◽  
Mitotic Spindle ◽  
Spindle Formation

scholarly journals Role of Polo-like kinase 1 in the regulation of the action of p31comet in the disassembly of mitotic checkpoint complexes

2019 ◽  
pp. 201902970 ◽  
Author(s):  
Sharon Kaisari ◽  
Pnina Shomer ◽  
Tamar Ziv ◽  
Danielle Sitry-Shevah ◽  
Shirly Miniowitz-Shemtov ◽  
...  
Keyword(s):  
Ubiquitin Ligase ◽  
Hela Cells ◽  
Mitotic Spindle ◽  
Joint Action ◽  
Mitotic Checkpoint ◽  
Anaphase Promoting Complex ◽  
Futile Cycle ◽  
Mitotic Checkpoint Complex ◽  
Bi 2536

The Mad2-binding protein p31comet has important roles in the inactivation of the mitotic checkpoint system, which delays anaphase until chromosomes attach correctly to the mitotic spindle. The activation of the checkpoint promotes the assembly of a Mitotic Checkpoint Complex (MCC), which inhibits the action of the ubiquitin ligase APC/C (Anaphase-Promoting Complex/Cyclosome) to degrade inhibitors of anaphase initiation. The inactivation of the mitotic checkpoint requires the disassembly of MCC. p31comet promotes the disassembly of mitotic checkpoint complexes by liberating their Mad2 component in a joint action with the ATPase TRIP13. Here, we investigated the regulation of p31comet action. The release of Mad2 from checkpoint complexes in extracts from nocodazole-arrested HeLa cells was inhibited by Polo-like kinase 1 (Plk1), as suggested by the effects of selective inhibitors of Plk1. Purified Plk1 bound to p31comet and phosphorylated it, resulting in the suppression of its activity (with TRIP13) to disassemble checkpoint complexes. Plk1 phosphorylated p31comet on S102, as suggested by the prevention of the phosphorylation of this residue in checkpoint extracts by the selective Plk1 inhibitor BI-2536 and by the phosphorylation of S102 with purified Plk1. An S102A mutant of p31comet had a greatly decreased sensitivity to inhibition by Plk1 of its action to disassemble mitotic checkpoint complexes. We propose that the phosphorylation of p31comet by Plk1 prevents a futile cycle of MCC assembly and disassembly during the active mitotic checkpoint.

scholarly journals Challenges In Modeling Chromosome-driven Mitotic Spindle Formation

2009 ◽  
Vol 96 (3) ◽  
pp. 505a
Author(s):  
Stuart Schaffner ◽  
Jorge V. Jose
Keyword(s):  
Mitotic Spindle ◽  
Spindle Formation
Sign in / Sign up

Export Citation Format

Share Document