Kinetochore Orientation during Meiosis Is Controlled by Aurora B and the Monopolin Complex

Monje-Casas, Fernando; Prabhu, Vineet R.; Lee, Brian H.; Boselli, Monica; Amon, Angelika

doi:10.1016/j.cell.2006.12.040

Cited by 131 publications

(190 citation statements)

References 45 publications

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“…Although the molecular mechanisms that distinguish these two modes of attachment are incompletely understood, monopolar attachment is associated with cohesin binding at the core centromere (23), and the need for the monopolin complex to direct this binding has been suggested (24). Monje-Casas et al (25) reported that the mitotic expression of the normally meiosis-specific monopolin complex was sufficient to direct meiosis I-like segregation of mitotic chromosomes. Thus, one possible scenario is that a small subset of mitotic cells expresses the meiotic proteins that allow monopolar kinetochore attachment.…”

Section: Discussionmentioning

confidence: 99%

Reciprocal uniparental disomy in yeast

Andersen

Petes

2012

Proc. Natl. Acad. Sci. U.S.A.

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In the diploid cells of most organisms, including humans, each chromosome is usually distinguishable from its partner homolog by multiple single-nucleotide polymorphisms. One common type of genetic alteration observed in tumor cells is uniparental disomy (UPD), in which a pair of homologous chromosomes are derived from a single parent, resulting in loss of heterozygosity for all single-nucleotide polymorphisms while maintaining diploidy. Somatic UPD events are usually explained as reflecting two consecutive nondisjunction events. Here we report a previously undescribed mode of chromosome segregation in Saccharomyces cerevisiae in which one cell division produces daughter cells with reciprocal UPD for the same pair of chromosomes without an aneuploid intermediate. One pair of sister chromatids is segregated into one daughter cell and the other pair is segregated into the other daughter cell, mimicking a meiotic chromosome segregation pattern. We term this process “reciprocal uniparental disomy.”

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Section: Discussionmentioning

confidence: 99%

Reciprocal uniparental disomy in yeast

Andersen

Petes

2012

Proc. Natl. Acad. Sci. U.S.A.

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“…During meiosis I, sister chromatid cohesion is preserved at centromeres of monocentric chromosomes and at the long arm of holocentric chromosomes, whereas cohesion is released along chromatid arms of monocentric chromosomes and the short arm of holocentric bivalents. In monocentric organisms, Aurora B promotes preservation of cohesion at centromeres (Monje-Casas et al, 2007;Resnick et al, 2006;Yu and Koshland, 2007). By contrast, in worms, AIR-2/Aurora B functions to promote cohesion release at the short arm (Kaitna et al, 2002;Rogers et al, 2002).…”

Section: Condensin I and Chromosomal Passengersmentioning

confidence: 99%

“…8). On monocentric chromosomes, Aurora B is needed for coorientation of sister kinetochores and biorientation of kinetochores of homologs by destabilizing improper kinetochore-microtubule attachments at the centromeres (Hauf et al, 2007;Monje-Casas et al, 2007). In holocentric organisms, such as C. elegans, localized centromeres are lacking, and instead the location of crossover determines which end of the chromosome will form the short arm of the bivalent (Nabeshima et al, 2005), which in turn determines the plane of chromosome orientation (Albertson and Thomson, 1993;Wignall and Villeneuve, 2009).…”

Section: Condensin I and Chromosomal Passengersmentioning

confidence: 99%

Different roles for Aurora B in condensin targeting during mitosis and meiosis

Collette

Petty

Golenberg

et al. 2011

Journal of Cell Science

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SummaryCondensin complexes are essential for mitotic and meiotic chromosome segregation. Caenorhabditis elegans, like other metazoans, has two distinct mitotic and meiotic condensin complexes (I and II), which occupy distinct chromosomal domains and perform nonredundant functions. Despite the differences in mitotic and meiotic chromosome behavior, we uncovered several conserved aspects of condensin targeting during these processes. During both mitosis and meiosis, condensin II loads onto chromosomes in early prophase, and condensin I loads at entry into prometaphase. During both mitosis and meiosis, the localization of condensin I, but not condensin II, closely parallels the localization of the chromosomal passenger kinase Aurora B (AIR-2 in C. elegans). Interestingly, condensin I and AIR-2 also colocalize on the spindle midzone during anaphase of mitosis, and between separating chromosomes during anaphase of meiosis. Consistently, AIR-2 affects the targeting of condensin I but not condensin II. However, the role AIR-2 plays in condensin I targeting during these processes is different. In mitosis, AIR-2 activity is required for chromosomal association of condensin I. By contrast, during meiosis, AIR-2 is not required for condensin I chromosomal association, but it provides cues for correct spatial targeting of the complex.

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“…We also analyzed whether, as observed for mammalian cells (21), increased Aurora B activity leads to aneuploidy in yeast. To this end, we followed chromosome segregation using cells with chromosome 4 tagged with GFP at the centromere (CrIV-GFP) (25). In wild-type anaphase cells, two separate DNA masses of approximately equal size, each containing a fluorescent GFP dot, could be distinguished in the mother and daughter cells once the sister chromatids segregated toward opposite spindle poles (Fig.…”

Section: Overexpression Of Ipl1 and Sli15 Leads To Severe Problems Inmentioning

confidence: 99%

Increased Aurora B activity causes continuous disruption of kinetochore–microtubule attachments and spindle instability

Muñoz-Barrera

Monje-Casas

2014

Proc. Natl. Acad. Sci. U.S.A.

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Aurora B kinase regulates the proper biorientation of sister chromatids during mitosis. Lack of Aurora B kinase function results in the inability to correct erroneous kinetochore-microtubule attachments and gives rise to aneuploidy. Interestingly, increased Aurora B activity also leads to problems with chromosome segregation, and overexpression of this kinase has been observed in various types of cancer. However, little is known about the mechanisms by which an increase in Aurora B kinase activity can impair mitotic progression and cell viability. Here, using a yeast model, we demonstrate that increased Aurora B activity as a result of the overexpression of the Aurora B and inner centromere protein homologs triggers defects in chromosome segregation by promoting the continuous disruption of chromosome-microtubule attachments even when sister chromatids are correctly bioriented. This disruption leads to a constitutive activation of the spindle-assembly checkpoint, which therefore causes a lack of cytokinesis even though spindle elongation and chromosome segregation take place. Finally, we demonstrate that this increase in Aurora B activity causes premature collapse of the mitotic spindle by promoting instability of the spindle midzone.

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Kinetochore Orientation during Meiosis Is Controlled by Aurora B and the Monopolin Complex

Cited by 131 publications

References 45 publications

Reciprocal uniparental disomy in yeast

Reciprocal uniparental disomy in yeast

Different roles for Aurora B in condensin targeting during mitosis and meiosis

Increased Aurora B activity causes continuous disruption of kinetochore–microtubule attachments and spindle instability

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