Cell division: control of the chromosomal passenger complex in time and space

Horst, Armando van der; Lens, Susanne M.A.

doi:10.1007/s00412-013-0437-6

Cited by 115 publications

(124 citation statements)

References 186 publications

(312 reference statements)

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“…Immunohistological findings showing that survivin expression was higher in cortical than in medullary human thymocytes were consistent with flow cytometry findings showing that survivin expression was upregulated in DP but downregulated in SP mouse thymocytes [32,94]. The aforementioned results are in keeping with evidence that survivin is crucial for mitotic progression [95].…”

Section: Expression Of Cell Cycle and Apoptosis Regulators In Thymussupporting

confidence: 84%

Expression of cell cycle and apoptosis regulators in thymus and thymic epithelial tumors

et al. 2015

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The human thymus supports the production of self-tolerant T cells with competent and regulatory functions. Various cellular components of the thymic microenvironment such as thymic epithelial cells (TEC) and dendritic cells play essential roles in thymic T cell differentiation. The multiple cellular events occurring during thymic T cell and TEC differentiation involve proteins regulating cell cycle and apoptosis. Dysregulation of the cell cycle and apoptosis networks is involved in the pathogenesis of thymic epithelial tumors (TET) which are divided into two broad categories, thymomas and thymic carcinomas. The present review focuses on the usefulness of the analysis of the expression patterns of major cell cycle and apoptosis regulators in order to gain insight in the histophysiology of thymus and the histopathology, the clinical behavior and the biology of TET.

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Section: Expression Of Cell Cycle and Apoptosis Regulators In Thymussupporting

confidence: 84%

Expression of cell cycle and apoptosis regulators in thymus and thymic epithelial tumors

et al. 2015

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“…5 AURORA B along with 3 other proteins, SURVIVIN, BOREALIN and INCENP form the chromosome passenger complex (CPC). 4,15 Our results so far have shown that MAD2 ablation results in the reduced phosphorylation of histone H3. In order to identify the role of MAD2 in the regulation of mitotic localization of AURORA B, we silenced MAD2 in different cell lines and studied AURORA B localization using immunofluorescence analysis.…”

Section: Mad2 Regulates Aurora B Localization During Mitosismentioning

confidence: 89%

Regulation of AURORA B function by mitotic checkpoint protein MAD2

2016

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Cell cycle checkpoint signaling stringently regulates chromosome segregation during cell division. MAD2 is one of the key components of the spindle and mitotic checkpoint complex that regulates the fidelity of cell division along with MAD1, CDC20, BUBR1, BUB3 and MAD3. MAD2 ablation leads to erroneous attachment of kinetochore-spindle fibers and defective chromosome separation. A potential role for MAD2 in the regulation of events beyond the spindle and mitotic checkpoints is not clear. Together with active spindle assembly checkpoint signaling, AURORA B kinase activity is essential for chromosome condensation as cells enter mitosis. AURORA B phosphorylates histone H3 at serine 10 and serine 28 to facilitate the formation of condensed metaphase chromosomes. In the absence of functional AURORA B cells escape mitosis despite the presence of misaligned chromosomes. In this study we report that silencing of MAD2 results in a drastic reduction of metaphase-specific histone H3 phosphorylation at serine 10 and serine 28. We demonstrate that this is due to mislocalization of AURORA B in the absence of MAD2. Conversely, overexpression of MAD2 concentrated the localization of AURORA B at the metaphase plate and caused hyper-phosphorylation of histone H3. We find that MAD1 plays a minor role in influencing the MAD2-dependent regulation of AURORA B suggesting that the effects of MAD2 on AURORA B are independent of the spindle checkpoint complex. Our findings reveal that, in addition to its role in checkpoint signaling, MAD2 ensures chromosome stability through the regulation of AURORA B.

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“…The mechanism by which the CPC is recruited to the centromere consists of various feedback loops among the CPC components, phosphorylation of histones H3 and H2A, and multiple mitotic kinases, including Haspin, Aurora B, Plk1, Bub1, and CDK1. Recent reviews discuss this topic in detail (Carmena et al 2012;van der Horst and Lens 2014;Krenn and Musacchio 2015;Kitagawa and Lee 2015).…”

Section: Regulation Of Outer Kinetochore Dynamicsmentioning

confidence: 99%

Kinetochore assembly and function through the cell cycle

Nagpal

Fukagawa

2016

Chromosoma

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The kinetochore is an essential structure for the chromosome segregation machinery in eukaryotes; it serves as a bridge between the spindle microtubules and chromosomes. The kinetochore consists of multiple interconnecting components on the centromere; therefore, understanding its formation, molecular function, and regulation has remained an ongoing challenge. Recent studies have provided new insights into centromere identity, kinetochore assembly, and function. In this review, we discuss recent advances in our understanding of the function and regulation of key kinetochore components. We highlight the reciprocal localization dependencies of the different sub-complexes of the kinetochore and describe their regulation during the cell cycle.

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Cell division: control of the chromosomal passenger complex in time and space

Cited by 115 publications

References 186 publications

Expression of cell cycle and apoptosis regulators in thymus and thymic epithelial tumors

Expression of cell cycle and apoptosis regulators in thymus and thymic epithelial tumors

Regulation of AURORA B function by mitotic checkpoint protein MAD2

Kinetochore assembly and function through the cell cycle

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