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Dynamic positioning of mitotic spindles in yeast: role of microtubule motors and cortical
, 2000
"... In the budding yeast Saccharomyces cerevisiae, movement of the mitotic spindle to a predetermined cleavage plane at the bud neck is essential for partitioning chromosomes into the mother and daughter cells. Astral microtubule dynamics are critical to the mechanism that ensures nuclear migration to t ..."
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In the budding yeast Saccharomyces cerevisiae, movement of the mitotic spindle to a predetermined cleavage plane at the bud neck is essential for partitioning chromosomes into the mother and daughter cells. Astral microtubule dynamics are critical to the mechanism that ensures nuclear migration to the bud neck. The nucleus moves in the opposite direction of astral microtubule growth in the mother cell, apparently being “pushed ” by microtubule contacts at the cortex. In contrast, microtubules growing toward the neck and within the bud promote nuclear movement in the same direction of microtubule growth, thus “pulling ” the nucleus toward the bud neck. Failure of “pulling ” is evident in cells lacking Bud6p, Bni1p, Kar9p, or the kinesin homolog, Kip3p. As a consequence, there is a loss of asymmetry in spindle pole body segregation into the bud. The cytoplasmic motor protein, dynein, is not required for nuclear movement to the neck; rather, it has been postulated to contribute to spindle elongation through the neck. In the absence of KAR9, dynein-dependent spindle oscillations are evident before anaphase onset, as are postanaphase dynein-dependent pulling forces that exceed the velocity of wild-type spindle elongation threefold. In addition, dynein-mediated forces on astral microtubules are sufficient to segregate a 2N chromosome set through the neck in the absence of spindle elongation, but cytoplasmic kinesins are not. These observations support a model in which spindle polarity determinants (BUD6, BNI1, KAR9) and cytoplasmic kinesin (KIP3) provide directional cues for spindle orientation to the bud while restraining the spindle to the neck. Cytoplasmic dynein is attenuated by these spindle polarity determinants and kinesin until anaphase onset, when dynein directs spindle elongation to distal points in the mother and bud.
The spindle position checkpoint: how to deal with spindle misalignment during asymmetric cell division in budding yeast
- Biochem. Soc. Trans
, 2008
"... Abstract During asymmetric cell division, spindle positioning is critical to ensure the unequal segregation of polarity factors and generate daughter cells with different sizes or fates. In budding yeast the boundary between mother and daughter cell resides at the bud neck, where cytokinesis takes ..."
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Cited by 4 (1 self)
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Abstract During asymmetric cell division, spindle positioning is critical to ensure the unequal segregation of polarity factors and generate daughter cells with different sizes or fates. In budding yeast the boundary between mother and daughter cell resides at the bud neck, where cytokinesis takes place at the end of the cell cycle. Since budding and bud neck formation occur much earlier than bipolar spindle formation, spindle positioning is a finely regulated process. A surveillance device called the SPOC (spindle position checkpoint) oversees this process and delays mitotic exit and cytokinesis until the spindle is properly oriented along the division axis, thus ensuring genome stability. Establishment of cell polarity during asymmetric cell division Asymmetric cell division is widespread in Nature and generates unequal daughter cells with different size and/or fate. This modality of cell division is characteristic of several unicellular organisms, either prokaryotic (such as the bacterium Caulobacter crescentus) or eukaryotic (such as the budding yeast Saccharomyces cerevisiae), and is essential for embryonic development of multicellular eukaryotes. A paradigmatic example of asymmetric cell division is that of stem cells, which generate one daughter cell committed to differentiate and another stem cell that maintains its identity and self-renewing potential. This contributes to organ formation during development and to the homoeostasis of tissues during adulthood. Disrupting asymmetric cell division can lead to uncontrolled cell proliferation and, ultimately, to cancer (reviewed in [1]). In order to divide asymmetrically, cells localize polarity factors on one side of the cell, position the mitotic spindle along the polarity axis and specify the division plane with respect to these events. In this way, cell fate determinants are segregated during mitosis to only one of the two daughter cells, making them different from each other. The basic mechanisms that allow polarity establishment are conserved and initiate with the determination of a spatial cue on the cell surface that defines the point in the cell toward which the cell orientates. The axis of polarity is then propagated from this landmark throughout the
S-Phase Cyclin-Dependent Kinases Promote Sister Chromatid Cohesion in Budding Yeast
, 2011
"... Genome stability depends on faithful chromosome segregation, which relies on maintenance of chromatid cohesion during S phase. In eukaryotes, Pds1/securin is the only known inhibitor that can prevent loss of cohesion. However, pds1 yeast cells and securin-null mice are viable. We sought to identify ..."
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Genome stability depends on faithful chromosome segregation, which relies on maintenance of chromatid cohesion during S phase. In eukaryotes, Pds1/securin is the only known inhibitor that can prevent loss of cohesion. However, pds1 yeast cells and securin-null mice are viable. We sought to identify redundant mechanisms that promote cohesion within S phase in the absence of Pds1 and found that cells lacking the S-phase cyclins Clb5 and Clb6 have a cohesion defect under conditions of replication stress. Similar to the phenotype of pds1 cells, loss of cohesion in cells lacking Clb5 and Clb6 is dependent on Esp1. However, Pds1 phosphorylation by Cdk-cyclin is not required for cohesion. Moreover, cells lacking Clb5, Clb6, and Pds1 are inviable and lose cohesion during an unperturbed S phase, indicating that Pds1 and specific B-type cyclins promote cohesion independently of one another. Consistent with this, we find that Mcd1/Scc1 is less abundant on chromosomes in cells lacking Clb5 and Clb6 during replication stress. However, clb5 clb6 cells do accumulate Mcd1/Scc1 at centromeres upon mitotic arrest, suggesting that the cyclin-dependent mechanism is S phase specific. These data indicate that Clb5 and Clb6 promote cohesion which is then protected by Pds1 and that both mechanisms are required during replication stress. A temporal coupling between S phase and mitosis is essen-tial to prevent aberrant chromosome segregation that can re-
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"... Yeast Cdk1 translocates to the plus end of cytoplasmic microtubules to regulate bud cortex interactions ..."
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Yeast Cdk1 translocates to the plus end of cytoplasmic microtubules to regulate bud cortex interactions
Actin-mediated Delivery of Astral Microtubules Instructs Kar9p Asymmetric Loading to the Bud-Ward Spindle Pole
, 2010
"... In Saccharomyces cerevisiae, Kar9p, one player in spindle alignment, guides the bud-ward spindle pole by linking astral microtubule plus ends to Myo2p-based transport along actin cables generated by the formins Bni1p and Bnr1p and the polarity determinant Bud6p. Initially, Kar9p labels both poles bu ..."
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In Saccharomyces cerevisiae, Kar9p, one player in spindle alignment, guides the bud-ward spindle pole by linking astral microtubule plus ends to Myo2p-based transport along actin cables generated by the formins Bni1p and Bnr1p and the polarity determinant Bud6p. Initially, Kar9p labels both poles but progressively singles out the bud-ward pole. Here, we show that this polarization requires cell polarity determinants, actin cables, and microtubules. Indeed, in a bud6 bni1 mutant or upon direct depolymerization of actin cables Kar9p symmetry increased. Furthermore, symmetry was selec-tively induced by myo2 alleles, preventing Kar9p binding to the Myo2p cargo domain. Kar9p polarity was rebuilt after transient disruption of microtubules, dependent on cell polarity and actin cables. Symmetry breaking also occurred after transient depolymerization of actin cables, with Kar9p increasing at the spindle pole engaging in repeated cycles of Kar9p-mediated transport. Kar9p returning to the spindle pole on shrinking astral microtubules may contribute toward this bias. Thus, Myo2p transport along actin cables may support a feedback loop by which delivery of astral microtubule plus ends sustains Kar9p polarized recruitment to the bud-ward spindle pole. Our findings also explain the link between Kar9p polarity and the choice setting aside the old spindle pole for daughter-bound fate.
Reverse Genetic Analysis of the Yeast RSC Chromatin Remodeler Reveals a Role for RSC3
"... The yeast ‘‘remodels the structure of chromatin’ ’ (RSC) complex is a multi-subunit ‘‘switching deficient/sucrose non-fermenting’ ’ type ATP-dependent nucleosome remodeler, with human counterparts that are well-established tumor suppressors. Using temperature-inducible degron fusions of all the esse ..."
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The yeast ‘‘remodels the structure of chromatin’ ’ (RSC) complex is a multi-subunit ‘‘switching deficient/sucrose non-fermenting’ ’ type ATP-dependent nucleosome remodeler, with human counterparts that are well-established tumor suppressors. Using temperature-inducible degron fusions of all the essential RSC subunits, we set out to map RSC requirement as a function of the mitotic cell cycle. We found that RSC executes essential functions during G1, G2, and mitosis. Remarkably, we observed a doubling of chromosome complements when degron alleles of the RSC subunit SFH1, the yeast hSNF5 tumor suppressor ortholog, and RSC3 were combined. The requirement for simultaneous deregulation of SFH1 and RSC3 to induce these ploidy shifts was eliminated by knockout of the S-phase cyclin CLB5 and by transient depletion of replication origin licensing factor Cdc6p. Further, combination of the degron alleles of SFH1 and RSC3, with deletion alleles of each of the nine Cdc28/Cdk1-associated cyclins, revealed a strong and specific genetic interaction between the S-phase cyclin genes CLB5 and RSC3, indicating a role for Rsc3p in proper S-phase regulation. Taken together, our results implicate RSC in regulation of the G1/S-phase transition and establish a hitherto unanticipated role for RSC-mediated chromatin remodeling in ploidy maintenance. Citation: Campsteijn C, Wijnands-Collin AMJ, Logie C (2007) Reverse genetic analysis of the yeast RSC chromatin remodeler reveals a role for RSC3 and SNF5 homolog 1 in ploidy maintenance. PLoS Genet 3(6): e92. doi:10.1371/journal.pgen.0030092
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"... Cell-cycle progression in all eukaryotes is coupled to the oscillatory activation of cyclin-dependent kinases (CDKs). These are serine/threonine protein kinase complexes containing a core catalytic subunit activated by stage-specific ..."
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Cell-cycle progression in all eukaryotes is coupled to the oscillatory activation of cyclin-dependent kinases (CDKs). These are serine/threonine protein kinase complexes containing a core catalytic subunit activated by stage-specific
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"... Spatial coordination between chromosomal segregation and the division plane in an asymmetrically dividing cell is achieved by coupling mitotic spindle orientation to the cell polarity axis. The yeast S. cerevisiae adheres to this general principle: the yeast ..."
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Spatial coordination between chromosomal segregation and the division plane in an asymmetrically dividing cell is achieved by coupling mitotic spindle orientation to the cell polarity axis. The yeast S. cerevisiae adheres to this general principle: the yeast
