The conserved protein kinase Ipl1 regulates microtubule binding to kinetochores in budding yeast

Biggins, Sue; Severin, Fedor F.; Bhalla, Needhi; Sassoon, Ingrid; Hyman, Anthony A.; Murray, Andrew W.

doi:10.1101/gad.13.5.532

Cited by 385 publications

(415 citation statements)

References 56 publications

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“…We introduced a GAL1-IPL1 allele into a strain with LacO sequences at TRP1 and LYS4. Overexpression of IPL1 has no obvious detrimental effect on cell growth (Biggins et al, 1999; data not shown), but we observed that ϳ50% of cells with large buds contained a condensed chromosome IV compared with ϳ20% in control cells not overexpressing IPL1. We therefore released cells from a G1 synchrony and asked if overproduction of the Ipl1 kinase could promote maintenance of chromosome IV condensation in the presence of nocodazole.…”

Section: Condensation Of Chromosome IV Can Be Restored By Overexpressmentioning

confidence: 81%

In Vivo Analysis of Chromosome Condensation inSaccharomyces cerevisiae

Vas

Andrews

Matesky

et al. 2007

MBoC

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Although chromosome condensation in the yeast Saccharomyces cerevisiae has been widely studied, visualization of this process in vivo has not been achieved. Using Lac operator sequences integrated at two loci on the right arm of chromosome IV and a Lac repressor-GFP fusion protein, we were able to visualize linear condensation of this chromosome arm during G2/M phase. As previously determined in fixed cells, condensation in yeast required the condensin complex. Not seen after fixation of cells, we found that topoisomerase II is required for linear condensation. Further analysis of perturbed mitoses unexpectedly revealed that condensation is a transient state that occurs before anaphase in budding yeast. Blocking anaphase progression by activation of the spindle assembly checkpoint caused a loss of condensation that was dependent on Mad2, followed by a delayed loss of cohesion between sister chromatids. Release of cells from spindle checkpoint arrest resulted in recondensation before anaphase onset. The loss of condensation in preanaphase-arrested cells was abrogated by overproduction of the aurora B kinase, Ipl1, whereas in ipl1-321 mutant cells condensation was prematurely lost in anaphase/telophase. In vivo analysis of chromosome condensation has therefore revealed unsuspected relationships between higher order chromatin structure and cell cycle control. INTRODUCTIONAccurate chromosome segregation during mitosis is facilitated by the resolution of chromosomes into compact structures. From the level of the nucleosome, chromatin undergoes several changes in organization (Earnshaw, 1988;Filipski et al., 1990). A scaffold of proteins form an axis along which solenoidal chromatin loops are folded into rosettes, which then coalesce to form a sausage-shaped chromonema Marsden and Laemmli, 1979; Johnson, 1979, 1980;Earnshaw and Laemmli, 1983;Earnshaw, 1988). The metaphase chromosome consists of a folded or coiled chromonema (Manton, 1950). In a more recent model of chromosome organization, chromatin is folded into fibers around the central axis, which acts as a "glue" (Kireeva et al., 2004). In both of these models, the protein scaffold is proposed to condense linearly during mitosis.The mitotic scaffold was first observed in histone-depleted mammalian chromosomes and components of this protein scaffold have been of considerable interest (Adolphs et al., 1977;Paulson and Laemmli, 1977). In higher eukaryotes, the process of condensing chromosomes before anaphase requires a protein scaffold comprised of at least condensin and topoisomerase II (Earnshaw et al., 1985;Gasser et al., 1986;Adachi et al., 1991;Saitoh et al., 1994;Gimenez-Abian et al., 1995;Hirano et al., 1997;Maeshima and Laemmli, 2003). Condensin is a five-subunit complex that was first identified in Xenopus egg extracts (Hirano, 2005). Homologues of mitotic scaffold proteins are present in all eukaryotes (reviewed in Hirano, 2005). In the budding yeast Saccharomyces cerevisiae, homologues of the condensin complex, encoded by SMC2, SMC4, YCG1, YCS4, and BRN...

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Section: Condensation Of Chromosome IV Can Be Restored By Overexpressmentioning

confidence: 81%

In Vivo Analysis of Chromosome Condensation inSaccharomyces cerevisiae

Vas

Andrews

Matesky

et al. 2007

MBoC

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“…The IPL1 gene was identi®ed originally in a screen for yeast mutants that increase in ploidy (Francisco et al, 1994). The yeast IPL1 may regulate kinetochore function via phosphorylation of Ndc10p (Biggins et al, 1999). Embryos derived from aurora mutant mothers display closely paired centrosomes and monopolar spindles (Glover et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Degradation of human Aurora2 protein kinase by the anaphase-promoting complex-ubiquitin-proteasome pathway

et al. 2000

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Human Aurora2 was originally identi®ed by its close homology to yeast IPL1 and¯y aurora, which are key regulators of chromosome segregation and a family of serine/threonine kinases. Here we demonstrate that the Aurora2 protein is degraded rapidly after G2/M phase release in mammalian cells. Aurora2 protein has a rapid turnover rate with a half-life of approximately 2 h. In eukaryotic cells, the ubiquitin-proteasome pathway is the major mechanism for the targeted degradation of unstable proteins. The treatment of mammalian cells with proteasome inhibitors blocks Aurora2 degradation. Furthermore, Aurora2 is polyubiquitinated in vivo and in vitro using anaphase-promoting complex (APC). These results demonstrate that Aurora2 protein is turned over through the APC-ubiquitin-proteasome pathway.

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“…Initial studies indicated that ipl1 and sli15 mutant cells showed frequent chromosome missegregation (Chan & Botstein 1993;Kim et al 1999). Subsequently, we and other groups discovered that sister centromeres were frequently pulled to one pole (w70%) when a bipolar spindle was established in these mutant cells (Biggins et al 1999;He et al 2001;Tanaka et al 2002).…”

Section: Roles Of the Ipl1-sli15 (Aurora B-incenp) Kinase Complex In mentioning

confidence: 99%

Chromosome bi-orientation on the mitotic spindle

Tanaka

2005

Phil. Trans. R. Soc. B

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For proper chromosome segregation, sister kinetochores must attach to microtubules extending from opposite spindle poles prior to anaphase onset. This state is called sister kinetochore bi-orientation or chromosome bi-orientation. The mechanism ensuring chromosome bi-orientation lies at the heart of chromosome segregation, but is still poorly understood. Recent evidence suggests that mal-oriented kinetochore-to-pole connections are corrected in a tension-dependent mechanism. The cohesin complex and the Ipl1/Aurora B protein kinase seem to be key regulators for this correction. In this article, I discuss how cells ensure sister kinetochore bi-orientation for all chromosomes, mainly focusing on our recent findings in budding yeast.

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The conserved protein kinase Ipl1 regulates microtubule binding to kinetochores in budding yeast

Cited by 385 publications

References 56 publications

In Vivo Analysis of Chromosome Condensation inSaccharomyces cerevisiae

In Vivo Analysis of Chromosome Condensation inSaccharomyces cerevisiae

Degradation of human Aurora2 protein kinase by the anaphase-promoting complex-ubiquitin-proteasome pathway

Chromosome bi-orientation on the mitotic spindle

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