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Academic literature on the topic 'Spindle bipolarity'
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Journal articles on the topic "Spindle bipolarity"
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Bird, Alexander W., and Anthony A. Hyman. "Building a spindle of the correct length in human cells requires the interaction between TPX2 and Aurora A." Journal of Cell Biology 182, no. 2 (July 28, 2008): 289–300. http://dx.doi.org/10.1083/jcb.200802005.
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To assemble mitotic spindles, cells nucleate microtubules from a variety of sources including chromosomes and centrosomes. We know little about how the regulation of microtubule nucleation contributes to spindle bipolarity and spindle size. The Aurora A kinase activator TPX2 is required for microtubule nucleation from chromosomes as well as for spindle bipolarity. We use bacterial artificial chromosome–based recombineering to introduce point mutants that block the interaction between TPX2 and Aurora A into human cells. TPX2 mutants have very short spindles but, surprisingly, are still bipolar and segregate chromosomes. Examination of microtubule nucleation during spindle assembly shows that microtubules fail to nucleate from chromosomes. Thus, chromosome nucleation is not essential for bipolarity during human cell mitosis when centrosomes are present. Rather, chromosome nucleation is involved in spindle pole separation and setting spindle length. A second Aurora A–independent function of TPX2 is required to bipolarize spindles.
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Ganem, Neil J., and Duane A. Compton. "The KinI kinesin Kif2a is required for bipolar spindle assembly through a functional relationship with MCAK." Journal of Cell Biology 166, no. 4 (August 9, 2004): 473–78. http://dx.doi.org/10.1083/jcb.200404012.
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Although the microtubule-depolymerizing KinI motor Kif2a is abundantly expressed in neuronal cells, we now show it localizes to centrosomes and spindle poles during mitosis in cultured cells. RNAi-induced knockdown of Kif2a expression inhibited cell cycle progression because cells assembled monopolar spindles. Bipolar spindle assembly was restored in cells lacking Kif2a by treatments that altered microtubule assembly (nocodazole), eliminated kinetochore–microtubule attachment (loss of Nuf2), or stabilized microtubule plus ends at kinetochores (loss of MCAK). Thus, two KinI motors, MCAK and Kif2a, play distinct roles in mitosis, and MCAK activity at kinetochores must be balanced by Kif2a activity at poles for spindle bipolarity. These treatments failed to restore bipolarity to cells lacking the activity of the kinesin Eg5. Thus, two independent pathways contribute to spindle bipolarity, with the Eg5-dependent pathway using motor force to drive spindle bipolarity and the Kif2a-dependent pathway relying on microtubule polymer dynamics to generate force for spindle bipolarity.
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Yukawa, Masashi, Tomoki Kawakami, Masaki Okazaki, Kazunori Kume, Ngang Heok Tang, and Takashi Toda. "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." Molecular Biology of the Cell 28, no. 25 (December 2017): 3647–59. http://dx.doi.org/10.1091/mbc.e17-08-0497.
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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.
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Gayek, A. Sophia, and Ryoma Ohi. "Kinetochore-microtubule stability governs the metaphase requirement for Eg5." Molecular Biology of the Cell 25, no. 13 (July 2014): 2051–60. http://dx.doi.org/10.1091/mbc.e14-03-0785.
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The mitotic spindle is a bipolar, microtubule (MT)-based cellular machine that segregates the duplicated genome into two daughter cells. The kinesin-5 Eg5 establishes the bipolar geometry of the mitotic spindle, but previous work in mammalian cells suggested that this motor is unimportant for the maintenance of spindle bipolarity. Although it is known that Kif15, a second mitotic kinesin, enforces spindle bipolarity in the absence of Eg5, how Kif15 functions in this capacity and/or whether other biochemical or physical properties of the spindle promote its bipolarity have been poorly studied. Here we report that not all human cell lines can efficiently maintain bipolarity without Eg5, despite their expressing Kif15. We show that the stability of chromosome-attached kinetochore-MTs (K-MTs) is important for bipolar spindle maintenance without Eg5. Cells that efficiently maintain bipolar spindles without Eg5 have more stable K-MTs than those that collapse without Eg5. Consistent with this observation, artificial destabilization of K-MTs promotes spindle collapse without Eg5, whereas stabilizing K-MTs improves bipolar spindle maintenance without Eg5. Our findings suggest that either rapid K-MT turnover pulls poles inward or slow K-MT turnover allows for greater resistance to inward-directed forces.
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Wolff, Ian D., Michael V. Tran, Timothy J. Mullen, Anne M. Villeneuve, and Sarah M. Wignall. "Assembly of Caenorhabditis elegans acentrosomal spindles occurs without evident microtubule-organizing centers and requires microtubule sorting by KLP-18/kinesin-12 and MESP-1." Molecular Biology of the Cell 27, no. 20 (October 15, 2016): 3122–31. http://dx.doi.org/10.1091/mbc.e16-05-0291.
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Although centrosomes contribute to spindle formation in most cell types, oocytes of many species are acentrosomal and must organize spindles in their absence. Here we investigate this process in Caenorhabditis elegans, detailing how acentrosomal spindles form and revealing mechanisms required to establish bipolarity. Using high-resolution imaging, we find that in meiosis I, microtubules initially form a “cage-like” structure inside the disassembling nuclear envelope. This structure reorganizes so that minus ends are sorted to the periphery of the array, forming multiple nascent poles that then coalesce until bipolarity is achieved. In meiosis II, microtubules nucleate in the vicinity of chromosomes but then undergo similar sorting and pole formation events. We further show that KLP-18/kinesin-12 and MESP-1, previously shown to be required for spindle bipolarity, likely contribute to bipolarity by sorting microtubules. After their depletion, minus ends are not sorted outward at the early stages of spindle assembly and instead converge. These proteins colocalize on microtubules, are interdependent for localization, and can interact, suggesting that they work together. We propose that KLP-18/kinesin-12 and MESP-1 form a complex that functions to sort microtubules of mixed polarity into a configuration in which minus ends are away from the chromosomes, enabling formation of nascent poles.
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Prigozhina, Natalie L., Richard A. Walker, C. Elizabeth Oakley, and Berl R. Oakley. "γ-Tubulin and the C-Terminal Motor Domain Kinesin-like Protein, KLPA, Function in the Establishment of Spindle Bipolarity inAspergillus nidulans." Molecular Biology of the Cell 12, no. 10 (October 2001): 3161–74. http://dx.doi.org/10.1091/mbc.12.10.3161.
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Previous research has found that a γ-tubulin mutation inSchizosaccharomyces pombe is synthetically lethal with a deletion of the C-terminal motor domain kinesin-like protein genepkl1, but the lethality of the double mutant prevents a phenotypic analysis of the synthetic interaction. We have investigated interactions between klpA1, a deletion of an Aspergillus nidulans homolog of pkl1, and mutations in the mipA, γ-tubulin gene. We find that klpA1 dramatically increases the cold sensitivity and slightly reduces the growth rate at all temperatures, of threemipA alleles. In synchronized cells we find thatklpA1 causes a substantial but transient inhibition of the establishment of spindle bipolarity. At a restrictive temperature,mipAD123 causes a slight, transient inhibition of spindle bipolarity and a more significant inhibition of anaphase A. In the mipAD123/klpA1 strain, formation of bipolar spindles is more strongly inhibited than in theklpA1 single mutant and many spindles apparently never become bipolar. These results indicate, surprisingly, that γ-tubulin and the klpA kinesin have overlapping roles in the establishment of spindle bipolarity. We propose a model to account for these data.
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Godinho, Susana A. "The principles of spindle bipolarity." Nature Reviews Molecular Cell Biology 20, no. 6 (April 24, 2019): 325. http://dx.doi.org/10.1038/s41580-019-0135-1.
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Cassimeris, Lynne, and Justin Morabito. "TOGp, the Human Homolog of XMAP215/Dis1, Is Required for Centrosome Integrity, Spindle Pole Organization, and Bipolar Spindle Assembly." Molecular Biology of the Cell 15, no. 4 (April 2004): 1580–90. http://dx.doi.org/10.1091/mbc.e03-07-0544.
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The XMAP215/Dis1 MAP family is thought to regulate microtubule plus-end assembly in part by antagonizing the catastrophe-promoting function of kin I kinesins, yet XMAP215/Dis1 proteins localize to centrosomes. We probed the mitotic function of TOGp (human homolog of XMAP215/Dis1) using siRNA. Cells lacking TOGp assembled multipolar spindles, confirming results of Gergely et al. (2003. Genes Dev. 17, 336–341). Eg5 motor activity was necessary to maintain the multipolar morphology. Depletion of TOGp decreased microtubule length and density in the spindle by ∼20%. Depletion of MCAK, a kin I kinesin, increased MT lengths and density by ∼20%, but did not disrupt spindle morphology. Mitotic cells lacking both TOGp and MCAK formed bipolar and monopolar spindles, indicating that TOGp and MCAK contribute to spindle bipolarity, without major effects on MT stability. TOGp localized to centrosomes in the absence of MTs and depletion of TOGp resulted in centrosome fragmentation. TOGp depletion also disrupted MT minus-end focus at the spindle poles, detected by localizations of NuMA and the p150 component of dynactin. The major functions of TOGp during mitosis are to focus MT minus ends at spindle poles, maintain centrosome integrity, and contribute to spindle bipolarity.
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Zhang, Xin, Stephanie C. Ems-McClung, and Claire E. Walczak. "Aurora A Phosphorylates MCAK to Control Ran-dependent Spindle Bipolarity." Molecular Biology of the Cell 19, no. 7 (July 2008): 2752–65. http://dx.doi.org/10.1091/mbc.e08-02-0198.
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During mitosis, mitotic centromere-associated kinesin (MCAK) localizes to chromatin/kinetochores, a cytoplasmic pool, and spindle poles. Its localization and activity in the chromatin region are regulated by Aurora B kinase; however, how the cytoplasmic- and pole-localized MCAK are regulated is currently not clear. In this study, we used Xenopus egg extracts to form spindles in the absence of chromatin and centrosomes and found that MCAK localization and activity are tightly regulated by Aurora A. This regulation is important to focus microtubules at aster centers and to facilitate the transition from asters to bipolar spindles. In particular, we found that MCAK colocalized with NuMA and XMAP215 at the center of Ran asters where its activity is regulated by Aurora A-dependent phosphorylation of S196, which contributes to proper pole focusing. In addition, we found that MCAK localization at spindle poles was regulated through another Aurora A phosphorylation site (S719), which positively enhances bipolar spindle formation. This is the first study that clearly defines a role for MCAK at the spindle poles as well as identifies another key Aurora A substrate that contributes to spindle bipolarity.
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Connolly, Amy A., Kenji Sugioka, Chien-Hui Chuang, Joshua B. Lowry, and Bruce Bowerman. "KLP-7 acts through the Ndc80 complex to limit pole number in C. elegans oocyte meiotic spindle assembly." Journal of Cell Biology 210, no. 6 (September 14, 2015): 917–32. http://dx.doi.org/10.1083/jcb.201412010.
Full textAbstract:
During oocyte meiotic cell division in many animals, bipolar spindles assemble in the absence of centrosomes, but the mechanisms that restrict pole assembly to a bipolar state are unknown. We show that KLP-7, the single mitotic centromere–associated kinesin (MCAK)/kinesin-13 in Caenorhabditis elegans, is required for bipolar oocyte meiotic spindle assembly. In klp-7(−) mutants, extra microtubules accumulated, extra functional spindle poles assembled, and chromosomes frequently segregated as three distinct masses during meiosis I anaphase. Moreover, reducing KLP-7 function in monopolar klp-18(−) mutants often restored spindle bipolarity and chromosome segregation. MCAKs act at kinetochores to correct improper kinetochore–microtubule (k–MT) attachments, and depletion of the Ndc-80 kinetochore complex, which binds microtubules to mediate kinetochore attachment, restored bipolarity in klp-7(−) mutant oocytes. We propose a model in which KLP-7/MCAK regulates k–MT attachment and spindle tension to promote the coalescence of early spindle pole foci that produces a bipolar structure during the acentrosomal process of oocyte meiotic spindle assembly.
Dissertations / Theses on the topic "Spindle bipolarity"
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Costa, Mariana Fernandes Alves. "Molecular remodelling of the spindle architecture during metaphase arrest in oocytes." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31255.
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Oocytes of most species assemble and maintain a functional bipolar spindle in the absence of centrosomes. Strikingly, after bipolar spindle formation, oocytes arrest in metaphase for several hours before fertilisation. How the dynamic spindle maintains its bipolarity during this long arrest is poorly understood. I hypothesise that the bipolar spindle is stably maintained by changes in the distribution of microtubule-associated proteins (MAPs) on the spindle during the long oocyte arrest. To test this, I generated transgenic flies expressing GFP-tagged microtubule-associated proteins (MAPs), and found that 13 out of 24 proteins change localisation between early and late oocytes. I refer to these changes in MAP localisation after establishment of bipolarity as 'spindle maturation'. In order to identify the molecular mechanisms triggering MAP relocalisation, I manipulated the kinase activity of the cell cycle regulator Cdk1 by over-expressing non-degradable cyclin A or B, the major activators of Cdk1. Their expression prevented re-localisation of distinct sets of MAPs, and disrupted spindle bipolarity and accurate chromosome segregation in oocytes. Kinesin-6 Pavarotti/MKlp1 localised strongly to the spindle equator in late oocytes, whilst nearly always absent from this region in early oocytes. The localisation of Pavarotti to the spindle equator in late oocytes was reduced when cyclin B is over-expressed in oocytes, suggesting a role for Cdk1/cyclin B complex in regulating Pavarotti localisation. Indeed, a Pavarotti/Mklp1 mutant non-phosphorylatable by Cdk1 prematurely localised to the meiotic spindle and disrupted spindle bipolarity. Moreover, removal of Pavarotti from the metaphase-I spindle by RNAi induced spindle defects in oocytes. Therefore, it is likely that the microtubule cross-linking activity of Pavarotti enhances the stability of the metaphase-I spindle during the long arrest. Consistent with this, I found that the microtubule density in the spindle equator is higher in late oocytes. Altogether, I propose that remodelling the molecular architecture of the spindle during the long oocyte arrest is important to stabilise the bipolar spindle without centrosomes.
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Breuer, Manuel. "The role of HURP in acentriolar spindle assembly." Paris 6, 2010. http://www.theses.fr/2010PA066013.
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Les fuseaux acentriolaires se forment grâce à la nucléation de microtubules à partir des MTOCs. Les mécanismes qui aboutissent à l’assemblage de la région centrale du fuseau, essentielle pour la mise en place de la bipolarité, sont très peu connus. HURP (Hepatoma UpRegulated Protein) s’accumule de préférence sur les microtubules dans cette région. HURP est également une cible de RanGTP. Par ailleurs, l’accumulation est dépendante du moteur Eg5, un facteur essentiel à la mise en place de la bipolarité. Les femelles invalidées pour HURP sont stériles. Une analyse détailleé in vivo montre que HURP est requis pour l’établissement et le maintien de la bipolarité. Des mesures de croissance et de densité des microtubules par microscopie de type spinning disk démontrent un rôle crucial de HURP dans l’assemblage des microtubules à proximité des chromosomes. Je propose un modèle où HURP, stabilisateur de microtubules dans la région enrichie en MTs interpolaires, assure un échafaudage permettant la formation d’un fuseau robuste et la congression des chromosomes