The chromosomal passenger complex: guiding Aurora-B through mitosis

Abstract

During mitosis, the chromosomal passenger complex (CPC) orchestrates highly different processes, such as chromosome alignment, histone modification, and cytokinesis. Proper and timely localization of this complex is the key to precise control over the enzymatic core of the CPC, the Aurora-B kinase. We discuss the molecular mechanisms by which the CPC members direct the dynamic localization of the complex throughout cell division. Also, we summarize posttranslational modifications that occur on the CPC and discuss their roles in regulating localization and function of this mitotic complex.

N-(4-Hydroxyphenyl)retinamide induced differentiation with repression of telomerase and cell cycle to increase interferon-γ sensitivity for apoptosis in human glioblastoma cells

“…Previous studies attributed this down regulation of survivin to upregulation of caspase-3 mediated apoptotic cascade [38,39]. Recent studies indicate a more refined role for survivin, which is postulated to be one of the three non-enzymatic subunits required for the enzymatic function of Aurora-B kinase [40]. Aurora-B kinase constitutes the enzymatic heart of the chromosomal passenger complex, which is responsible for chromosome alignment, segregation, and cytokinesis during mitosis.…”

A Link between Aurora Kinase and Clp1/Cdc14 Regulation Uncovered by the Identification of a Fission Yeast Borealin-Like Protein

“…Similar to their orthologues in other organisms (Vagnarelli and Earnshaw, 2004;Vader et al, 2006;Ruchaud et al, 2007), the S. pombe proteins Ark1, Pic1, and Bir1 function within a chromosomal passenger complex that regulates critical mitotic events such as chromosome segregation and spindle elongation (Morishita et al, 2001;Petersen et al, 2001; Leverson Rajagopalan and Balasubramanian, 2002;Huang et al, 2005;Widlund et al, 2006). However, whether these three proteins operate alone in this complex has remained unclear, for a Borealin homologue has not been previously described in S. pombe.…”

“…However, it has proven difficult to identify Borealin homologues in yeasts. Though some have speculated that yeast Borealin homologues might not exist because of fusion of the Borealin and Survivin subunits into a single yeast Survivin homologue (Vader et al, 2006), recent evidence suggests that there are in fact yeast Borealin homologues (Nakajima et al, 2009). Nonetheless, a Borealin homologue in the fission yeast, Schizosaccharomyces pombe, has not been characterized.…”

“…As its name implies, this complex travels on chromosomes to various sites during cell division such that it can execute specific tasks at distinct locations and times (Earnshaw and Bernat, 1991). These functions include, but are not limited to, chromosome condensation, stabilization of the mitotic spindle, correction of improper kinetochore-microtubule attachments, and regulation of cytokinesis (for reviews, see Vagnarelli and Earnshaw, 2004;Vader et al, 2006;Ruchaud et al, 2007).The four CPC subunits are highly interdependent for proper localization, activity, and stability (Ruchaud et al, 2007). Consistent with such interdependency, these subunits are widely conserved among eukaryotes (Ruchaud et al, 2007).…”

AURKB and MAPK involvement in the regulation of the early stages of mouse zygote development

“…During cytokinesis it is important that the cleavage furrow is positioned correctly between the two daughter nuclei after chromosome segregation. Several studies have revealed that AURKB controlled the cleavage furrow-specific Vimentin phosphorylation as well as other proteins involved in cytokinesis, such as Myosin II regulatory light chain and glial fibrillary astrocytic protein (GFAP) [19,20]. In the current study, loss of function of AURKB by RNAi caused improper positioning of the cleavage furrows followed by unequal cell division in some of the early embryos; it would also compromise the spindle checkpoint because its activity is required for checkpoint protein recruitment [19], which might provide a good explanation for why down-regulation of AURKB generated multinuclear phenotype and asymmetric division.…”