scholarly journals Meiotic telomere clustering requires actin for its formation and cohesin for its resolution

2005 ◽  
Vol 170 (2) ◽  
pp. 213-223 ◽  
Author(s):  
Edgar Trelles-Sticken ◽  
Caroline Adelfalk ◽  
Josef Loidl ◽  
Harry Scherthan
Keyword(s):  
Chromosome Segregation ◽  
Actin Polymerization ◽  
Spindle Pole Body ◽  
Spindle Pole ◽  
Pole Body ◽  
Telomere Cluster ◽  
Cohesin Subunit ◽  
Yeast Meiosis ◽  
Bouquet Stage ◽  
Meiosis I

In diploid organisms, meiosis reduces the chromosome number by half during the formation of haploid gametes. During meiotic prophase, telomeres transiently cluster at a limited sector of the nuclear envelope (bouquet stage) near the spindle pole body (SPB). Cohesin is a multisubunit complex that contributes to chromosome segregation in meiosis I and II divisions. In yeast meiosis, deficiency for Rec8 cohesin subunit induces telomere clustering to persist, whereas telomere cluster–SPB colocalization is defective. These defects are rescued by expressing the mitotic cohesin Scc1 in rec8Δ meiosis, whereas bouquet-stage exit is independent of Cdc5 pololike kinase. An analysis of living Saccharomyces cerevisiae meiocytes revealed highly mobile telomeres from leptotene up to pachytene, with telomeres experiencing an actin- but not microtubule-dependent constraint of mobility during the bouquet stage. Our results suggest that cohesin is required for exit from actin polymerization–dependent telomere clustering and for linking the SPB to the telomere cluster in synaptic meiosis.

scholarly journals The half-bridge component Kar1 promotes centrosome separation and duplication during budding yeast meiosis

2018 ◽  
Vol 29 (15) ◽  
pp. 1798-1810
Author(s):  
Meenakshi Agarwal ◽  
Hui Jin ◽  
Melainia McClain ◽  
Jinbo Fan ◽  
Bailey A. Koch ◽  
...  
Keyword(s):  
Chromosome Segregation ◽  
Budding Yeast ◽  
Spindle Pole Body ◽  
Spindle Pole ◽  
Pole Body ◽  
Centrosome Separation ◽  
Chromatid Segregation ◽  
Yeast Meiosis ◽  
Unique Mechanism

The budding yeast centrosome, often called the spindle pole body (SPB), nucleates microtubules for chromosome segregation during cell division. An appendage, called the half bridge, attaches to one side of the SPB and regulates SPB duplication and separation. Like DNA, the SPB is duplicated only once per cell cycle. During meiosis, however, after one round of DNA replication, two rounds of SPB duplication and separation are coupled with homologue segregation in meiosis I and sister-chromatid segregation in meiosis II. How SPB duplication and separation are regulated during meiosis remains to be elucidated, and whether regulation in meiosis differs from that in mitosis is unclear. Here we show that overproduction of the half-bridge component Kar1 leads to premature SPB separation during meiosis. Furthermore, excessive Kar1 induces SPB overduplication to form supernumerary SPBs, leading to chromosome missegregation and erroneous ascospore formation. Kar1-­mediated SPB duplication bypasses the requirement of dephosphorylation of Sfi1, another half-bridge component previously identified as a licensing factor. Our results therefore reveal an unexpected role of Kar1 in licensing meiotic SPB duplication and suggest a unique mechanism of SPB regulation during budding yeast meiosis.

scholarly journals A microtubule polymerase cooperates with the kinesin-6 motor and a microtubule cross-linker to promote bipolar spindle assembly in the absence of kinesin-5 and kinesin-14 in fission yeast

2017 ◽  
Vol 28 (25) ◽  
pp. 3647-3659 ◽  
Author(s):  
Masashi Yukawa ◽  
Tomoki Kawakami ◽  
Masaki Okazaki ◽  
Kazunori Kume ◽  
Ngang Heok Tang ◽  
...  
Keyword(s):  
Fission Yeast ◽  
Chromosome Segregation ◽  
Spindle Pole Body ◽  
Spindle Assembly ◽  
Spindle Pole ◽  
Temperature Sensitive ◽  
Bipolar Spindle ◽  
Pole Body ◽  
Cross Linker ◽  
Spindle Elongation

Accurate chromosome segregation relies on the bipolar mitotic spindle. In many eukaryotes, spindle formation is driven by the plus-end–directed motor kinesin-5 that generates outward force to establish spindle bipolarity. Its inhibition leads to the emergence of monopolar spindles with mitotic arrest. Intriguingly, simultaneous inactivation of the minus-end–directed motor kinesin-14 restores spindle bipolarity in many systems. Here we show that in fission yeast, three independent pathways contribute to spindle bipolarity in the absence of kinesin-5/Cut7 and kinesin-14/Pkl1. One is kinesin-6/Klp9 that engages with spindle elongation once short bipolar spindles assemble. Klp9 also ensures the medial positioning of anaphase spindles to prevent unequal chromosome segregation. Another is the Alp7/TACC-Alp14/TOG microtubule polymerase complex. Temperature-sensitive alp7cut7pkl1 mutants are arrested with either monopolar or very short spindles. Forced targeting of Alp14 to the spindle pole body is sufficient to render alp7cut7pkl1 triply deleted cells viable and promote spindle assembly, indicating that Alp14-mediated microtubule polymerization from the nuclear face of the spindle pole body could generate outward force in place of Cut7 during early mitosis. The third pathway involves the Ase1/PRC1 microtubule cross-linker that stabilizes antiparallel microtubules. Our study, therefore, unveils multifaceted interplay among kinesin-dependent and -independent pathways leading to mitotic bipolar spindle assembly.

scholarly journals Spc24 interacts with Mps2 and is required for chromosome segregation, but is not implicated in spindle pole body duplication

2002 ◽  
Vol 43 (6) ◽  
pp. 1431-1443 ◽  
Author(s):  
Ivan Le Masson ◽  
Cosmin Saveanu ◽  
Anne Chevalier ◽  
Abdelkader Namane ◽  
Renee Gobin ◽  
...  
Keyword(s):  
Chromosome Segregation ◽  
Spindle Pole Body ◽  
Spindle Pole ◽  
Pole Body

scholarly journals Cdc14 phosphatase directs centrosome re-duplication at the meiosis I to meiosis II transition in budding yeast

2017 ◽  
Vol 2 ◽  
pp. 2 ◽  
Author(s):  
Colette Fox ◽  
Juan Zou ◽  
Juri Rappsilber ◽  
Adele L. Marston
Keyword(s):  
Cell Cycle ◽  
Dna Replication ◽  
Chromosome Segregation ◽  
Budding Yeast ◽  
Spindle Pole Body ◽  
Initial Step ◽  
Mitotic Cell ◽  
Spindle Pole ◽  
Fluorescence And Electron Microscopy ◽  
Meiosis I

Background Gametes are generated through a specialized cell division called meiosis, in which ploidy is reduced by half because two consecutive rounds of chromosome segregation, meiosis I and meiosis II, occur without intervening DNA replication. This contrasts with the mitotic cell cycle where DNA replication and chromosome segregation alternate to maintain the same ploidy. At the end of mitosis, CDKs are inactivated. This low CDK state in late mitosis/G1 allows for critical preparatory events for DNA replication and centrosome/spindle pole body (SPB) duplication. However, their execution is inhibited until S phase, where further preparatory events are also prevented. This “licensing” ensures that both the chromosomes and the centrosomes/SPBs replicate exactly once per cell cycle, thereby maintaining constant ploidy. Crucially, between meiosis I and meiosis II, centrosomes/SPBs must be re-licensed, but DNA re-replication must be avoided. In budding yeast, the Cdc14 protein phosphatase triggers CDK down regulation to promote exit from mitosis. Cdc14 also regulates the meiosis I to meiosis II transition, though its mode of action has remained unclear. Methods Fluorescence and electron microscopy was combined with proteomics to probe SPB duplication in cells with inactive or hyperactive Cdc14. Results We demonstrate that Cdc14 ensures two successive nuclear divisions by re-licensing SPBs at the meiosis I to meiosis II transition. We show that Cdc14 is asymmetrically enriched on a single SPB during anaphase I and provide evidence that this enrichment promotes SPB re-duplication. Cells with impaired Cdc14 activity fail to promote extension of the SPB half-bridge, the initial step in morphogenesis of a new SPB. Conversely, cells with hyper-active Cdc14 duplicate SPBs, but fail to induce their separation. Conclusion Our findings implicate reversal of key CDK-dependent phosphorylations in the differential licensing of cyclical events at the meiosis I to meiosis I transition.

Assembly and dynamics of an anastral:astral spindle: the meiosis II spindle of Drosophila oocytes

1998 ◽  
Vol 111 (17) ◽  
pp. 2487-2495 ◽  
Author(s):  
S.A. Endow ◽  
D.J. Komma
Keyword(s):  
De Novo ◽  
Spindle Pole Body ◽  
Spindle Pole ◽  
The Body ◽  
Central Spindle ◽  
Spindle Poles ◽  
Pole Body ◽  
Microtubule Motor ◽  
Gamma Tubulin ◽  
Meiosis I

The meiosis II spindle of Drosophila oocytes is distinctive in structure, consisting of two tandem spindles with anastral distal poles and an aster-associated spindle pole body between the central poles. Assembly of the anastral:astral meiosis II spindle occurs by reorganization of the meiosis I spindle, without breakdown of the meiosis I spindle. The unusual disk- or ring-shaped central spindle pole body forms de novo in the center of the elongated meiosis I spindle, followed by formation of the central spindle poles. gamma-Tubulin transiently localizes to the central spindle pole body, implying that the body acts as a microtubule nucleating center for assembly of the central poles. Localization of gamma-tubulin to the meiosis II spindle is dependent on the microtubule motor protein, Nonclaret disjunctional (Ncd). Absence of Ncd results in loss of gamma-tubulin localization to the spindle and destabilization of microtubules in the central region of the spindle. Assembly of the anastral:astral meiosis II spindle probably involves rapid reassortment of microtubule plus and minus ends in the center of the meiosis I spindle - this can be accounted for by a model that also accounts for the loss of gamma-tubulin localization to the spindle and destabilization of microtubules in the absence of Ncd.

scholarly journals Relief of the Dma1-mediated checkpoint requires Dma1 autoubiquitination and dynamic localization

2018 ◽  
Vol 29 (18) ◽  
pp. 2176-2189 ◽  
Author(s):  
Christine M. Jones ◽  
Jun-Song Chen ◽  
Alyssa E. Johnson ◽  
Zachary C. Elmore ◽  
Sierra N. Cullati ◽  
...  
Keyword(s):  
Cell Division ◽  
Chromosome Segregation ◽  
Ubiquitin Ligase ◽  
Spindle Pole Body ◽  
Mitotic Checkpoint ◽  
Spindle Pole ◽  
Checkpoint Activation ◽  
Pole Body ◽  
Septation Initiation Network ◽  
Anaphase B

Chromosome segregation and cell division are coupled to prevent aneuploidy and cell death. In the fission yeast Schizosaccharomyces pombe, the septation initiation network (SIN) promotes cytokinesis, but upon mitotic checkpoint activation, the SIN is actively inhibited to prevent cytokinesis from occurring before chromosomes have safely segregated. SIN inhibition during the mitotic checkpoint is mediated by the E3 ubiquitin ligase Dma1. Dma1 binds to the CK1-phosphorylated SIN scaffold protein Sid4 at the spindle pole body (SPB), and ubiquitinates it. Sid4 ubiquitination antagonizes the SPB localization of the Pololike kinase Plo1, the major SIN activator, so that SIN signaling is delayed. How this checkpoint is silenced once spindle defects are resolved has not been clear. Here we establish that Dma1 transiently leaves SPBs during anaphase B due to extensive autoubiquitination. The SIN is required for Dma1 to return to SPBs later in anaphase. Blocking Dma1 removal from SPBs by permanently tethering it to Sid4 prevents SIN activation and cytokinesis. Therefore, controlling Dma1’s SPB dynamics in anaphase is an essential step in S. pombe cell division and the silencing of the Dma1-dependent mitotic checkpoint.

scholarly journals Mps1p Regulates Meiotic Spindle Pole Body Duplication in Addition to Having Novel Roles during Sporulation

2000 ◽  
Vol 11 (10) ◽  
pp. 3525-3537 ◽  
Author(s):  
Paul D. Straight ◽  
Thomas H. Giddings ◽  
Mark Winey
Keyword(s):  
Chromosome Segregation ◽  
Spindle Assembly Checkpoint ◽  
Spindle Pole Body ◽  
Class Ii ◽  
Spindle Pole ◽  
Spore Wall ◽  
Meiotic Spindle ◽  
Restrictive Temperature ◽  
Wall Formation ◽  
Pole Body

Sporulation in yeast requires that a modified form of chromosome segregation be coupled to the development of a specialized cell type, a process akin to gametogenesis. Mps1p is a dual-specificity protein kinase essential for spindle pole body (SPB) duplication and required for the spindle assembly checkpoint in mitotically dividing cells. Four conditional mutant alleles of MPS1disrupt sporulation, producing two distinct phenotypic classes. Class I alleles of mps1 prevent SPB duplication at the restrictive temperature without affecting premeiotic DNA synthesis and recombination. Class II MPS1 alleles progress through both meiotic divisions in 30–50% of the population, but the asci are incapable of forming mature spores. Although mutations in many other genes block spore wall formation, the cells produce viable haploid progeny, whereas mps1 class II spores are unable to germinate. We have used fluorescently marked chromosomes to demonstrate that mps1 mutant cells have a dramatically increased frequency of chromosome missegregation, suggesting that loss of viability is due to a defect in spindle function. Overall, our cytological data suggest that MPS1 is required for meiotic SPB duplication, chromosome segregation, and spore wall formation.

scholarly journals The budding yeast RSC complex maintains ploidy by promoting spindle pole body insertion

2018 ◽  
Vol 217 (7) ◽  
pp. 2445-2462 ◽  
Author(s):  
Tina L. Sing ◽  
Minnie P. Hung ◽  
Shinsuke Ohnuki ◽  
Godai Suzuki ◽  
Bryan-Joseph San Luis ◽  
...  
Keyword(s):  
Chromosome Segregation ◽  
Cell Function ◽  
Spindle Pole Body ◽  
Spindle Pole ◽  
Eukaryotic Cells ◽  
Pole Body ◽  
Rapid Transition ◽  
Rsc Complex ◽  
Diagnostic Changes ◽  
Insight Into

Ploidy is tightly regulated in eukaryotic cells and is critical for cell function and survival. Cells coordinate multiple pathways to ensure replicated DNA is segregated accurately to prevent abnormal changes in chromosome number. In this study, we characterize an unanticipated role for the Saccharomyces cerevisiae “remodels the structure of chromatin” (RSC) complex in ploidy maintenance. We show that deletion of any of six nonessential RSC genes causes a rapid transition from haploid to diploid DNA content because of nondisjunction events. Diploidization is accompanied by diagnostic changes in cell morphology and is stably maintained without further ploidy increases. We find that RSC promotes chromosome segregation by facilitating spindle pole body (SPB) duplication. More specifically, RSC plays a role in distributing two SPB insertion factors, Nbp1 and Ndc1, to the new SPB. Thus, we provide insight into a role for a SWI/SNF family complex in SPB duplication and ploidy maintenance.

scholarly journals Inactivation of Mitotic Kinase Triggers Translocation of MEN Components to Mother-Daughter Neck in Yeast

2003 ◽  
Vol 14 (11) ◽  
pp. 4734-4743 ◽  
Author(s):  
Hong Hwa Lim ◽  
Foong May Yeong ◽  
Uttam Surana
Keyword(s):  
Chromosome Segregation ◽  
Spindle Pole Body ◽  
Spindle Pole ◽  
Mitotic Exit ◽  
Mitotic Kinase ◽  
Division Site ◽  
Pole Body ◽  
Spindle Pole Bodies ◽  
Mitotic Exit Network ◽  
Mutant Cells

Chromosome segregation, mitotic exit, and cytokinesis are executed in this order during mitosis. Although a scheme coordinating sister chromatid separation and initiation of mitotic exit has been proposed, the mechanism that temporally links the onset of cytokinesis to mitotic exit is not known. Exit from mitosis is regulated by the mitotic exit network (MEN), which includes a GTPase (Tem1) and various kinases (Cdc15, Cdc5, Dbf2, and Dbf20). Here, we show that Dbf2 and Dbf20 functions are necessary for the execution of cytokinesis. Relocalization of these proteins from spindle pole bodies to mother daughter neck seems to be necessary for this role because cdc15-2 mutant cells, though capable of exiting mitosis at semipermissive temperature, are unable to localize Dbf2 (and Dbf20) to the “neck” and fail to undergo cytokinesis. These cells can assemble and constrict the actomyosin ring normally but are incapable of forming a septum, suggesting that MEN components are critical for the initiation of septum formation. Interestingly, the spindle pole body to neck translocation of Dbf2 and Dbf20 is triggered by the inactivation of mitotic kinase. The requirement of kinase inactivation for translocation of MEN components to the division site thus provides a mechanism that renders mitotic exit a prerequisite for cytokinesis.

scholarly journals Spindle pole body components are reorganized during fission yeast meiosis

2012 ◽  
Vol 23 (10) ◽  
pp. 1799-1811 ◽  
Author(s):  
Midori Ohta ◽  
Masamitsu Sato ◽  
Masayuki Yamamoto
Keyword(s):  
Fission Yeast ◽  
Meiotic Prophase ◽  
Spindle Pole Body ◽  
Mitotic Cell ◽  
Spindle Pole ◽  
Nuclear Movement ◽  
Pole Body ◽  
Proper Number ◽  
Body Components ◽  
Yeast Meiosis

During meiosis, the centrosome/spindle pole body (SPB) must be regulated in a manner distinct from that of mitosis to achieve a specialized cell division that will produce gametes. In this paper, we demonstrate that several SPB components are localized to SPBs in a meiosis-specific manner in the fission yeast Schizosaccharomyces pombe. SPB components, such as Cut12, Pcp1, and Spo15, which stay on the SPB during the mitotic cell cycle, disassociate from the SPB during meiotic prophase and then return to the SPB immediately before the onset of meiosis I. Interestingly, the polo kinase Plo1, which normally localizes to the SPB during mitosis, is excluded from them in meiotic prophase, when meiosis-specific, horse-tail nuclear movement occurs. We found that exclusion of Plo1 during this period was essential to properly remodel SPBs, because artificial targeting of Plo1 to SPBs resulted in an overduplication of SPBs. We also found that the centrin Cdc31 was required for meiotic SPB remodeling. Thus Plo1 and a centrin play central roles in the meiotic SPB remodeling, which is essential for generating the proper number of meiotic SPBs and, thereby provide unique characteristics to meiotic divisions.

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