scholarly journals Perturbation of Incenp function impedes anaphase chromatid movements and chromosomal passenger protein flux at centromeres

Chromosoma ◽  
2008 ◽  
Vol 118 (1) ◽  
pp. 71-84 ◽  
Author(s):  
Leena J. Ahonen ◽  
Anu M. Kukkonen ◽  
Jeroen Pouwels ◽  
Margaret A. Bolton ◽  
Christopher D. Jingle ◽  
...  
2010 ◽  
Vol 38 (6) ◽  
pp. 1655-1659 ◽  
Author(s):  
Xavier Fant ◽  
Kumiko Samejima ◽  
Ana Carvalho ◽  
Hiromi Ogawa ◽  
Zhenjie Xu ◽  
...  

The CPC [chromosomal passenger complex; INCENP (inner centromere protein), Aurora B kinase, survivin and borealin] is implicated in many mitotic processes. In the present paper we describe how we generated DT40 conditional-knockout cell lines for incenp1 and survivin1 to better understand the role of these CPC subunits in the control of Aurora B kinase activity. These lines enabled us to reassess current knowledge of survivin function and to show that INCENP acts as a rheostat for Aurora B activity.


PLoS Genetics ◽  
2013 ◽  
Vol 9 (4) ◽  
pp. e1003448 ◽  
Author(s):  
Sreelaja Nair ◽  
Florence Marlow ◽  
Elliott Abrams ◽  
Lee Kapp ◽  
Mary C. Mullins ◽  
...  

2006 ◽  
Vol 17 (2) ◽  
pp. 779-788 ◽  
Author(s):  
Qian Chen ◽  
Hui Li ◽  
Arturo De Lozanne

Dictyostelium DdINCENP is a chromosomal passenger protein associated with centromeres, the spindle midzone, and poles during mitosis and the cleavage furrow during cytokinesis. Disruption of the single DdINCENP gene revealed important roles for this protein in mitosis and cytokinesis. DdINCENP null cells lack a robust spindle midzone and are hypersensitive to microtubule-depolymerizing drugs, suggesting that their spindles may not be stable. Furthermore DdCP224, a protein homologous to the microtubule-stabilizing protein TOGp/XMAP215, was absent from the spindle midzone of DdINCENP null cells. Overexpression of DdCP224 rescued the weak spindle midzone defect of DdINCENP null cells. Although not required for the localization of the myosin II contractile ring and subsequent formation of a cleavage furrow, DdINCENP is important for the abscission of daughter cells at the end of cytokinesis. Finally, we show that the localization of DdINCENP at the cleavage furrow is modulated by myosin II but it occurs by a mechanism different from that controlling the formation of the contractile ring.


2002 ◽  
Vol 159 (1) ◽  
pp. 45-53 ◽  
Author(s):  
Maki Murata-Hori ◽  
Yu-li Wang

To address the mechanism that coordinates cytokinesis with mitosis, we have studied the dynamics of aurora B, a chromosomal passenger protein involved in signaling cytokinesis. Photobleaching analyses indicated dynamic exchange of aurora B between a centromeric and a cytoplasmic pool before anaphase onset, and stable associations with microtubules after anaphase onset. Bleaching near centromeres upon anaphase onset affected the subsequent appearance of fluorescence along midzone microtubules, but not that near the lateral equatorial cortex, suggesting that there were centromeric-dependent and -independent pathways that transported aurora B to the equator. The former delivered centromeric aurora B along midzone microtubules, whereas the latter delivered cytoplasmic aurora B along astral microtubules. We suggest that cultured cells use midzone microtubules as the primary signaling pathway for cytokinesis, whereas embryos, with their stockpile of cytoplasmic proteins and large sizes, rely primarily on astral microtubules.


1999 ◽  
Vol 10 (2) ◽  
pp. 297-311 ◽  
Author(s):  
Matthew S. Savoian ◽  
William C. Earnshaw ◽  
Alexey Khodjakov ◽  
Conly L. Rieder

PtK1 cells containing two independent mitotic spindles can cleave between neighboring centrosomes, in the absence of an intervening spindle, as well as at the spindle equators. We used same-cell video, immunofluorescence, and electron microscopy to compare the structure and composition of normal equatorial furrows with that of ectopic furrows formed between spindles. As in controls, ectopic furrows contained midbodies composed of microtubule bundles and an electron-opaque matrix. Despite the absence of an intervening spindle and chromosomes, the midbodies associated with ectopic furrows also contained the microtubule-bundling protein CHO1 and the chromosomal passenger protein INCENP. However, CENP-E, another passenger protein, was not found in ectopic furrows but was always present in controls. We also examined cells in which the ectopic furrow initiated but relaxed. Although relaxing furrows contained overlapping microtubules from opposing centrosomes, they lacked microtubule bundles as well as INCENP and CHO1. Together these data suggest that the mechanism defining the site of furrow formation during mitosis in vertebrates does not depend on the presence of underlying microtubule bundles and chromosomes or on the stable association of INCENP or CHO1. The data also suggest that the completion of cytokinesis requires the presence of microtubule bundles and specific proteins (e.g., INCENP, CHO1, etc.) that do not include CENP-E.


2005 ◽  
Vol 25 (20) ◽  
pp. 9000-9015 ◽  
Author(s):  
Han-Kuei Huang ◽  
Julie M. Bailis ◽  
Joel D. Leverson ◽  
Eliana B. Gómez ◽  
Susan L. Forsburg ◽  
...  

ABSTRACT Fission yeast Bir1p/Cut17p/Pbh1p, the homolog of human Survivin, is a conserved chromosomal passenger protein that is required for cell division and cytokinesis. To study how Bir1p promotes accurate segregation of chromosomes, we generated and analyzed a temperature-sensitive allele, bir1-46, and carried out genetic screens to find genes that interact with bir1 + . We identified Psf2p, a component of the GINS complex required for DNA replication initiation, as a high-copy-number suppressor of the bir1-46 growth defect. Loss of Psf2p function by depletion or deletion or by use of a temperature-sensitive allele, psf2-209, resulted in chromosome missegregation that was associated with mislocalization of Bir1p. We also found that the human homolog of Psf2p, PSF2, was required for proper chromosome segregation. In addition, we observed that high-copy-number expression of Pic1p, the fission yeast homolog of INCENP (inner centromere protein), suppressed bir1-46. Pic1p exhibited a localization pattern typical of chromosomal passenger proteins. Deletion of pic1 + caused chromosome missegregation phenotypes similar to those of bir1-46. Our data suggest that Bir1p and Pic1p act as part of a conserved chromosomal passenger complex and that Psf2p/GINS indirectly affects the localization and function of this complex in chromosome segregation, perhaps through an S-phase role in centromere replication.


2006 ◽  
Vol 17 (3) ◽  
pp. 1065-1074 ◽  
Author(s):  
Per O. Widlund ◽  
John S. Lyssand ◽  
Scott Anderson ◽  
Sherry Niessen ◽  
John R. Yates ◽  
...  

The Saccharomyces cerevisiae inhibitor of apoptosis (IAP) repeat protein Bir1 localizes as a chromosomal passenger. A deletion analysis of Bir1 identified two regions important for function. The C-terminal region is essential for growth, binds Sli15, and is necessary and sufficient for the localization of Bir1 as a chromosomal passenger. The middle region is not essential but is required to localize the inner kinetochore protein Ndc10 to the spindle during anaphase and to the midzone at telophase. In contrast, precise deletion of the highly conserved IAP repeats conferred no phenotype and did not alter the cell cycle delay caused by loss of cohesin. Bir1 is phosphorylated in a cell cycle-dependent manner. Mutation of all nine CDK consensus sites in the middle region of Bir1 significantly decreased the level of phosphorylation and blocked localization of Ndc10 to the spindle at anaphase. Moreover, immunoprecipitation of Ndc10 with Bir1 was dependent on phosphorylation. The loss of Ndc10 from the anaphase spindle prevented elongation of the spindle beyond 7 μm. We conclude that phosphorylation of the middle region of Bir1 is required to bring Ndc10 to the spindle at anaphase, which is required for full spindle elongation.


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