Relevant bibliographies by topics / Mitotic spindle orientations

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Mitotic spindle orientations'

Author: Grafiati
Published: 25 May 2024

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Journal articles on the topic "Mitotic spindle orientations"

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Wang, S. W., F. J. Griffin, and W. H. Clark. "Cell-cell association directed mitotic spindle orientation in the early development of the marine shrimp Sicyonia ingentis." Development 124, no. 4 (February 15, 1997): 773–80. http://dx.doi.org/10.1242/dev.124.4.773.

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During early cleavages of Sicyonia ingentis embryos, mitotic spindle orientations differ between blastomeres and change in a predictable manner with each successive mitosis. From 2nd through 7th cleavages, spindles orient at a 90 degrees angle with respect to the spindle of the parent blastomere. Thus, spindle orientation is parallel to the cleavage plane that formed the blastomere. To determine if specific spindle orientations were intrinsic properties of individual blastomeres, we altered blastomere associations and asked how mitotic spindle orientation was affected in successive cleavages using laser scanning confocal microscopy. Linear embryos were constructed by dissociating 4-cell embryos and recombining the blastomeres in a linear array. The ensuing cleavage (3rd embryonic cleavage) of these linear embryos was parallel to the long axis of the embryo, resulting in four parallel pairs of blastomeres which lay in a common plane that was parallel to the substratum. The 4th cleavage produced a linear embryo with the 16 blastomeres arranged in four parallel quartets. Then, in preparation for 5th cleavage, spindles oriented at a 45 degrees angle (not parallel as in normal development) with respect to the previous cleavage plane. When 8-cell linear embryos were separated into linear half-embryos, subsequent spindle orientations were not like those observed for intact 8-cell linear embryos, but rather regressed to the orientation seen in 4-cell linear embryos. We suggest that the reorientation of mitotic spindles during early cleavage of S. ingentis is neither an intrinsic property nor age dependent, but rather is cell contact related. Further, these results in conjunction with observations of non-manipulated embryos suggest that spindle poles (centrosomes) avoid cytoplasmic regions adjacent to where there is cell-cell contact during early development.
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Juschke, C., Y. Xie, M. P. Postiglione, and J. A. Knoblich. "Analysis and modeling of mitotic spindle orientations in three dimensions." Proceedings of the National Academy of Sciences 111, no. 3 (December 31, 2013): 1014–19. http://dx.doi.org/10.1073/pnas.1314984111.

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Chan, Derek C. H., Joshua Xu, Ana Vujovic, Nicholas Wong, Victor Gordon, Laura P. M. H. de Rooij, Steven Moreira, et al. "Arhgef2 regulates mitotic spindle orientation in hematopoietic stem cells and is essential for productive hematopoiesis." Blood Advances 5, no. 16 (August 18, 2021): 3120–33. http://dx.doi.org/10.1182/bloodadvances.2020002539.

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Abstract How hematopoietic stem cells (HSCs) coordinate their divisional axis and whether this orientation is important for stem cell–driven hematopoiesis is poorly understood. Single-cell RNA sequencing data from patients with Shwachman-Diamond syndrome (SDS), an inherited bone marrow failure syndrome, show that ARHGEF2, a RhoA-specific guanine nucleotide exchange factor and determinant of mitotic spindle orientation, is specifically downregulated in SDS hematopoietic stem and progenitor cells (HSPCs). We demonstrate that transplanted Arhgef2−/− fetal liver and bone marrow cells yield impaired hematopoietic recovery and a production deficit from long-term HSCs, phenotypes that are not the result of differences in numbers of transplanted HSCs, their cell cycle status, level of apoptosis, progenitor output, or homing ability. Notably, these defects are functionally restored in vivo by overexpression of ARHGEF2 or its downstream activated RHOA GTPase. By using live imaging of dividing HSPCs, we show an increased frequency of misoriented divisions in the absence of Arhgef2. ARHGEF2 knockdown in human HSCs also impairs their ability to regenerate hematopoiesis, culminating in significantly smaller xenografts. Together, these data demonstrate a conserved role for Arhgef2 in orienting HSPC division and suggest that HSCs may divide in certain orientations to establish hematopoiesis, the loss of which could contribute to HSC dysfunction in bone marrow failure.
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Sei, Yoshitatsu, Jianying Feng, Carson C. Chow, and Stephen A. Wank. "Asymmetric cell division-dominant neutral drift model for normal intestinal stem cell homeostasis." American Journal of Physiology-Gastrointestinal and Liver Physiology 316, no. 1 (January 1, 2019): G64—G74. http://dx.doi.org/10.1152/ajpgi.00242.2018.

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The normal intestinal epithelium is continuously regenerated at a rapid rate from actively cycling Lgr5-expressing intestinal stem cells (ISCs) that reside at the crypt base. Recent mathematical modeling based on several lineage-tracing studies in mice shows that the symmetric cell division-dominant neutral drift model fits well with the observed in vivo growth of ISC clones and suggests that symmetric divisions are central to ISC homeostasis. However, other studies suggest a critical role for asymmetric cell division in the maintenance of ISC homeostasis in vivo. Here, we show that the stochastic branching and Moran process models with both a symmetric and asymmetric division mode not only simulate the stochastic growth of the ISC clone in silico but also closely fit the in vivo stem cell dynamics observed in lineage-tracing studies. In addition, the proposed model with highest probability for asymmetric division is more consistent with in vivo observations reported here and by others. Our in vivo studies of mitotic spindle orientations and lineage-traced progeny pairs indicate that asymmetric cell division is a dominant mode used by ISCs under normal homeostasis. Therefore, we propose the asymmetric cell division-dominant neutral drift model for normal ISC homeostasis. NEW & NOTEWORTHY The prevailing mathematical model suggests that intestinal stem cells (ISCs) divide symmetrically. The present study provides evidence that asymmetric cell division is the major contributor to ISC maintenance and thus proposes an asymmetric cell division-dominant neutral drift model. Consistent with this model, in vivo studies of mitotic spindle orientation and lineage-traced progeny pairs indicate that asymmetric cell division is the dominant mode used by ISCs under normal homeostasis.
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Copp, A. J., F. A. Brook, and H. J. Roberts. "A cell-type-specific abnormality of cell proliferation in mutant (curly tail) mouse embryos developing spinal neural tube defects." Development 104, no. 2 (October 1, 1988): 285–95. http://dx.doi.org/10.1242/dev.104.2.285.

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The mouse mutant curly tail (ct) provides a model system for studies of neurulation mechanisms. 60% of ct/ct embryos develop spinal neural tube defects (NTD) as a result of delayed neurulation at the posterior neuropore whereas the remaining 40% of embryos develop normally. In order to investigate the role of cell proliferation during mouse neurulation, cell cycle parameters were studied in curly tail embryos developing spinal NTD and in their normally developing litter-mates. Measurements were made of mitotic index, median length of S-phase and percent reduction of labelling index during a [3H]thymidine pulse-chase experiment. These independent measures of cell proliferation rate indicate a reduced rate of proliferation of gut endoderm and notochord cells in the neuropore region of embryos developing spinal NTD compared with normally developing controls. The incidence of cell death and the relative frequency of mitotic spindle orientations does not differ consistently between normal and abnormal embryos. These results suggest a mechanism of spinal NTD pathogenesis in curly tail embryos based on failure of normal cell proliferation in gut endoderm and notochord.
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Li, Jie, Hiroki Shima, Hironari Nishizawa, Masatoshi Ikeda, Andrey Brydun, Mitsuyo Matsumoto, Hiroki Kato, et al. "Phosphorylation of BACH1 switches its function from transcription factor to mitotic chromosome regulator and promotes its interaction with HMMR." Biochemical Journal 475, no. 5 (March 15, 2018): 981–1002. http://dx.doi.org/10.1042/bcj20170520.

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The transcription repressor BACH1 performs mutually independent dual roles in transcription regulation and chromosome alignment during mitosis by supporting polar ejection force of mitotic spindle. We now found that the mitotic spindles became oblique relative to the adhesion surface following endogenous BACH1 depletion in HeLa cells. This spindle orientation rearrangement was rescued by re-expression of BACH1 depending on its interactions with HMMR and CRM1, both of which are required for the positioning of mitotic spindle, but independently of its DNA-binding activity. A mass spectrometry analysis of BACH1 complexes in interphase and M phase revealed that BACH1 lost during mitosis interactions with proteins involved in chromatin and gene expression but retained interactions with HMMR and its known partners including CHICA. By analyzing BACH1 modification using stable isotope labeling with amino acids in cell culture, mitosis-specific phosphorylations of BACH1 were observed, and mutations of these residues abolished the activity of BACH1 to restore mitotic spindle orientation in knockdown cells and to interact with HMMR. Detailed histological analysis of Bach1-deficient mice revealed lengthening of the epithelial fold structures of the intestine. These observations suggest that BACH1 performs stabilization of mitotic spindle orientation together with HMMR and CRM1 in mitosis, and that the cell cycle-specific phosphorylation switches the transcriptional and mitotic functions of BACH1.
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Kapoor, Tarun M., Thomas U. Mayer, Margaret L. Coughlin, and Timothy J. Mitchison. "Probing Spindle Assembly Mechanisms with Monastrol, a Small Molecule Inhibitor of the Mitotic Kinesin, Eg5." Journal of Cell Biology 150, no. 5 (September 4, 2000): 975–88. http://dx.doi.org/10.1083/jcb.150.5.975.

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Monastrol, a cell-permeable small molecule inhibitor of the mitotic kinesin, Eg5, arrests cells in mitosis with monoastral spindles. Here, we use monastrol to probe mitotic mechanisms. We find that monastrol does not inhibit progression through S and G2 phases of the cell cycle or centrosome duplication. The mitotic arrest due to monastrol is also rapidly reversible. Chromosomes in monastrol-treated cells frequently have both sister kinetochores attached to microtubules extending to the center of the monoaster (syntelic orientation). Mitotic arrest–deficient protein 2 (Mad2) localizes to a subset of kinetochores, suggesting the activation of the spindle assembly checkpoint in these cells. Mad2 localizes to some kinetochores that have attached microtubules in monastrol-treated cells, indicating that kinetochore microtubule attachment alone may not satisfy the spindle assembly checkpoint. Monastrol also inhibits bipolar spindle formation in Xenopus egg extracts. However, it does not prevent the targeting of Eg5 to the monoastral spindles that form. Imaging bipolar spindles disassembling in the presence of monastrol allowed direct observations of outward directed forces in the spindle, orthogonal to the pole-to-pole axis. Monastrol is thus a useful tool to study mitotic processes, detection and correction of chromosome malorientation, and contributions of Eg5 to spindle assembly and maintenance.
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Woodard, Geoffrey E., Ning-Na Huang, Hyeseon Cho, Toru Miki, Gregory G. Tall, and John H. Kehrl. "Ric-8A and Giα Recruit LGN, NuMA, and Dynein to the Cell Cortex To Help Orient the Mitotic Spindle." Molecular and Cellular Biology 30, no. 14 (May 17, 2010): 3519–30. http://dx.doi.org/10.1128/mcb.00394-10.

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ABSTRACT In model organisms, resistance to inhibitors of cholinesterase 8 (Ric-8), a G protein α (Gα) subunit guanine nucleotide exchange factor (GEF), functions to orient mitotic spindles during asymmetric cell divisions; however, whether Ric-8A has any role in mammalian cell division is unknown. We show here that Ric-8A and Gαi function to orient the metaphase mitotic spindle of mammalian adherent cells. During mitosis, Ric-8A localized at the cell cortex, spindle poles, centromeres, central spindle, and midbody. Pertussis toxin proved to be a useful tool in these studies since it blocked the binding of Ric-8A to Gαi, thus preventing its GEF activity for Gαi. Linking Ric-8A signaling to mammalian cell division, treatment of cells with pertussis toxin, reduction of Ric-8A expression, or decreased Gαi expression similarly affected metaphase cells. Each treatment impaired the localization of LGN (GSPM2), NuMA (microtubule binding nuclear mitotic apparatus protein), and dynein at the metaphase cell cortex and disturbed integrin-dependent mitotic spindle orientation. Live cell imaging of HeLa cells expressing green fluorescent protein-tubulin also revealed that reduced Ric-8A expression prolonged mitosis, caused occasional mitotic arrest, and decreased mitotic spindle movements. These data indicate that Ric-8A signaling leads to assembly of a cortical signaling complex that functions to orient the mitotic spindle.
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Siletti, Kimberly, Basile Tarchini, and A. J. Hudspeth. "Daple coordinates organ-wide and cell-intrinsic polarity to pattern inner-ear hair bundles." Proceedings of the National Academy of Sciences 114, no. 52 (December 11, 2017): E11170—E11179. http://dx.doi.org/10.1073/pnas.1716522115.

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The establishment of planar polarization by mammalian cells necessitates the integration of diverse signaling pathways. In the inner ear, at least two systems regulate the planar polarity of sensory hair bundles. The core planar cell polarity (PCP) proteins coordinate the orientations of hair cells across the epithelial plane. The cell-intrinsic patterning of hair bundles is implemented independently by the G protein complex classically known for orienting the mitotic spindle. Although the primary cilium also participates in each of these pathways, its role and the integration of the two systems are poorly understood. We show that Dishevelled-associating protein with a high frequency of leucine residues (Daple) interacts with PCP and cell-intrinsic signals. Regulated by the cell-intrinsic pathway, Daple is required to maintain the polarized distribution of the core PCP protein Dishevelled and to position the primary cilium at the abneural edge of the apical surface. Our results suggest that the primary cilium or an associated structure influences the domain of cell-intrinsic signals that shape the hair bundle. Daple is therefore essential to orient and pattern sensory hair bundles.
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Giansanti, M. G., M. Gatti, and S. Bonaccorsi. "The role of centrosomes and astral microtubules during asymmetric division of Drosophila neuroblasts." Development 128, no. 7 (April 1, 2001): 1137–45. http://dx.doi.org/10.1242/dev.128.7.1137.

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Drosophila neuroblasts are stem cells that divide asymmetrically to produce another large neuroblast and a smaller ganglion mother cell (GMC). During neuroblast division, several cell fate determinants, such as Miranda, Prospero and Numb, are preferentially segregated into the GMC, ensuring its correct developmental fate. The accurate segregation of these determinants relies on proper orientation of the mitotic spindle within the dividing neuroblast, and on the correct positioning of the cleavage plane. In this study we have analyzed the role of centrosomes and astral microtubules in neuroblast spindle orientation and cytokinesis. We examined neuroblast division in asterless (asl) mutants, which, although devoid of functional centrosomes and astral microtubules, form well-focused anastral spindles that undergo anaphase and telophase. We show that asl neuroblasts assemble a normal cytokinetic ring around the central spindle midzone and undergo unequal cytokinesis. Thus, astral microtubules are not required for either signaling or positioning cytokinesis in Drosophila neuroblasts. Our results indicate that the cleavage plane is dictated by the positioning of the central spindle midzone within the cell, and suggest a model on how the central spindle attains an asymmetric position during neuroblast mitosis. We have also analyzed the localization of Miranda during mitotic division of asl neuroblasts. This protein accumulates in morphologically regular cortical crescents but these crescents are mislocalized with respect to the spindle orientation. This suggests that astral microtubules mediate proper spindle rotation during neuroblast division.
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Dissertations / Theses on the topic "Mitotic spindle orientations"

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Dunsch, Anja Katrin. "Control of the mitotic spindle by dynein light chain 1 complexes." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:b2fd5670-a035-42ca-aaef-78a30aeaa084.

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Robust control mechanisms ensure faithful inheritance of an intact genome through the processes of mitosis and cytokinesis. Different populations of the cytoplasmic dynein motor defined by specific dynein adaptor complexes are required for the formation of a stable bipolar mitotic spindle. This study analysed how different dynein subcomplexes contribute to spindle formation and orientation. Various dynein subpopulations were identified by mass spectrometry. I have shown that the dynein light chain 1 (DYNLL1) directly interacts with the kinetochore localised Astrin-Kinastrin complex as well as the spindle microtubule associated complex formed by CHICA and HMMR. I have characterised both complexes and identified unique functions in chromosome alignment and mitotic spindle orientation, respectively. I have found that Kinastrin (C15orf23) is the major Astrin-interacting protein in mitotic cells and is required for Astrin targeting to microtubule plus ends proximal to the plus tip tracking protein EB1. Fixed cell microscopy revealed that cells over-expressing or depleted of Kinastrin mislocalise Astrin. Additionally, depletion of the Astrin-Kinastrin complex delays chromosome alignment and causes the loss of normal spindle architecture and sister chromatid cohesion before anaphase onset (Dunsch et al., 2011). Using immunoprecipitation and microtubule binding assays, I have shown that CHICA and HMMR interact with one another, and target to the spindle by a microtubule-binding site in the amino-terminal region of HMMR. CHICA interacts with DYNLL1 by a series of conserved TQT motifs in the carboxy-terminal region. Depletion of DYNLL1, CHICA or HMMR causes a slight increase in mitotic index but has little effect on spindle formation or checkpoint function. Fixed and live cell microscopy reveal, however, that the asymmetric distribution of cor tical dynein is lost and the spindle in these cells fails to orient correctly in relation to the culture surface (Dunsch et al., 2012). These findings presented here suggest that the Astrin-Kinastrin complex is required for normal spindle architecture and chromosome alignment, and that per turbations of this pathway result in delayed mitosis and non-physiological separase activation, whereas HMMR and CHICA act as par t of a dynein-DYNLL1 complex with a specific function defining or controlling spindle orientation.
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Hüls, Daniela. "Structural and functional studies on mitotic spindle orientation in Saccharomyces cerevisiae." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-141524.

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Golub, Ognjen. "Molecular Mechanisms Regulating Subcellular Localization and Function of Mitotic Spindle Orientation Determinants." Thesis, University of Oregon, 2016. http://hdl.handle.net/1794/20711.

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Proper orientation of the mitotic spindle is essential during animal development for the generation of cell diversity and organogenesis. To understand the molecular mechanisms regulating this process, genetic studies have implicated evolutionarily conserved proteins that function in diverse cell types to align the spindle along an intrinsic cellular polarity axis. This activity is achieved through physical contacts between astral microtubules of the spindle and a distinct domain of force generating proteins on the cell cortex. In this work, I shed light on how these proteins form distinct cortical domains, how their activity is coupled to their subcellular localization, and how they provide cytoskeletal and motor protein connections that are required to generate the forces necessary to position the mitotic spindle. I first discuss the mechanisms by which Mushroom body defect (Mud; NuMA in mammals), provides spindle orientation cues from various subcellular locations. Aside from its known role at the cortex as an adapter for the Dynein motor, I reveal novel isoform-dependent Mud functions at the spindle poles during assembly of the mitotic spindle and astral microtubules, thus implicating Mud in spindle orientation pathways away from the cell cortex. Moreover, through collaborative efforts with former lab members, I describe molecular regulation and assembly of two ‘accessory’ pathways that activate cortical Mud-Dynein, one through the tumor suppressor protein Discs large (Dlg), and another through the signaling protein Dishevelled (Dsh). I demonstrate that the Dlg pathway is spatially regulated by the polarity kinase atypical Protein Kinase C (aPKC) through direct phosphorylation of Dlg. This signal relieves Dlg autoinhibition to promote cortical recruitment of the Dlg-ligand Gukholder (Gukh), a novel microtubule-binding protein that provides an additional connection between astral microtubules and the cortex that is essential for activity of the Dlg pathway. Lastly, I determine that the Dsh accessory pathway provides an alternative cytoskeletal cue by recruiting Diaphanous (Dia), an actin nucleating protein. By demonstrating interchangeability between the two accessory pathways, we conclude that Mud-Dynein is activated by various cytoskeletal cues and that the mode of activation is cell-context dependent. This dissertation includes unpublished and previously published co-authored material.
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Lu, Michelle. "The Construction and Deconstruction of Signaling Systems that Regulate Mitotic Spindle Positioning." Thesis, University of Oregon, 2013. http://hdl.handle.net/1794/12955.

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Signaling systems regulate the flow of cellular information by organizing proteins in space and time to coordinate a variety of cellular activities that are critical for the proper development, function, and maintenance of cells. Signaling molecules can exhibit several levels of complexity through the utilization of modular protein interactions, which can generate simple linear behaviors or complex behaviors such as ultrasensitivity. Protein modularity also serves as the basis for the vast protein networks that form the regulatory networks that govern several biological activities. My work focuses on the importance of protein modularity in complex biological systems, in particular the regulatory pathways of spindle positioning. The first part of my work involves the construction of a synthetic regulatory network using modular protein interactions in an effort to understand the complex behavior of the natural spindle orientation regulator Pins. Utilizing well-characterized protein domains and their binding partners, I built an autoinhibited protein switch that can be activated by a small protein domain. We found that the input-output relationship of the synthetic protein switch could be tuned by the simple addition of "decoy" domains, domains that bind and sequester input signal, thereby impeding the onset of the output response to generate an input threshold. By varying the number and affinities of the decoy domains, we found that we could transform a simple linear response into a complex, ultrasensitive one. Thus, modular protein interactions can serve as a source of complex behaviors. The second part of my work focuses on elucidating the molecular mechanisms underlying spindle positioning in the Drosophila neuroblast. I found that Pins orients the mitotic spindle by coordinating two opposite-polarity microtubule motors Dynein and Kinesin-73 through its multiple domains. Kinesin-73 also relies on its modular domain architecture to perform its duties in Pins-mediated spindle positioning, where its N-terminal half functions in coordinating cortical-microtubule capture while its C-terminal half functions as a region necessary for the activation of Dynein. Thus, modular protein design allows for the organization of spindle orientation regulators in space to achieve the complex biological activity that is spindle positioning. This dissertation includes previously published and unpublished coauthored material.
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Lopes, Cláudia Sofia de Jesus. "Molecular partners for Bud6p-mediated orientation of the mitotic spindle in S. cerevisiae." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608848.

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Vodicska, Barbara [Verfasser], and Ingrid [Akademischer Betreuer] Hoffmann. "Deciphering the function of MISP in mitotic spindle orientation / Barbara Vodicska ; Betreuer: Ingrid Hoffmann." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/117704370X/34.

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Fernández, Baldovinos Javier [Verfasser], and Thomas [Akademischer Betreuer] Worzfeld. "Mechanisms of Mitotic Spindle Orientation by Plexin-B2 / Javier Fernández Baldovinos ; Betreuer: Thomas Worzfeld." Marburg : Philipps-Universität Marburg, 2021. http://d-nb.info/1228535744/34.

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Penisson, Maxime. "Mécanismes de LIS1 dans les progéniteurs neuraux contribuant aux malformations de développement du cortex." Electronic Thesis or Diss., Sorbonne université, 2020. http://www.theses.fr/2020SORUS415.

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Les malformations du développement du cortex sont associées à des troubles de la prolifération des progéniteurs et de la migration neuronale. Les glies radiaires basales (bRGs), un type de progéniteur, sont limités dans les espèces lissencéphaliques mais abondants dans les cerveaux gyrencéphaliques. Le gène LIS1, codant pour un régulateur de la dynéine, est muté dans la lissencéphalie humaine. LIS1 a un rôle dans la division cellulaire et la migration neuronale. Dans cette étude, nous avons généré des cellules bRG-like dans le cerveau embryonnaire murin, pour étudier le rôle de Lis1 dans leur production. Ceci fut réalisé par électroporation in utero du gène hominoïde-spécifique TBC1D3 au jour embryonnaire (E) 14.5. Nous avons confirmé que l’expression de TBC1D3 dans des cerveaux WT induit un grand nombre de cellules bRG-like basales. Puis, nous avons étudié la production des bRGs-like dans des cerveaux murins hétérozygotes pour Lis1. Nos résultats novateurs montrent que la déplétion de Lis1 à partir de E9.5 empêche la production de cellules bRG-like induites par TBC1D3. La déplétion de Lis1 change l’orientation du fuseau mitotique, accroit le nombre de mitoses abventriculaires et altère l’expression de N-Cadhérine. Nous concluons que la perturbation du dosage de Lis1 pourrait perturber le nombre et la position corrects des progéniteurs, contribuant à la pathogenèse de Lis1
Human cortical malformations are associated with progenitor proliferation and neuronal migration abnormalities. Basal radial glia (bRGs), a type of progenitor cells, are limited in lissencephalic species (e.g. the mouse) but abundant in gyrencephalic brains. The LIS1 gene coding for a dynein regulator, is mutated in human lissencephaly, associated also in some cases with microcephaly. LIS1 was shown to be important during cell division and neuronal migration. Here, we generated bRG-like cells in the mouse embryonic brain, investigating the role of Lis1 in their formation. This was achieved by in utero electroporation of a hominoid-specific gene TBC1D3 at mouse embryonic day (E) 14.5. We first confirmed that TBC1D3 overexpression in WT brain generates numerous Pax6+ bRG-like cells that are basally localized. Second, we assessed the formation of these cells in heterozygote Lis1 mutant brains. Our novel results show that Lis1 depletion in the forebrain from E9.5 prevented subsequent TBC1D3-induced bRG-like cell amplification. Lis1 depletion changed mitotic spindle orientations at the ventricular surface, increased the proportion of abventricular mitoses, and altered N-Cadherin expression, altering TBC1D3 function. We conclude that perturbation of Lis1/LIS1 dosage is likely to be detrimental for appropriate progenitor number and position, contributing to lissencephaly pathogenesis
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Hüls, Daniela [Verfasser], and Klaus [Akademischer Betreuer] Förstemann. "Structural and functional studies on mitotic spindle orientation in Saccharomyces cerevisiae / Daniela Hüls. Betreuer: Klaus Förstemann." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2012. http://d-nb.info/1021307645/34.

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Quyn, Aaron J. "The role of the APC protein in mitotic spindle orientation and tissue organisation in gut epithelium." Thesis, University of Dundee, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505629.

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Book chapters on the topic "Mitotic spindle orientations"

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Glaubke, Elina, and Holger Bastians. "A Cell-Based Assay for Mitotic Spindle Orientation." In Methods in Molecular Biology, 67–75. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7847-2_5.

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Decarreau, Justin, Jonathan Driver, Charles Asbury, and Linda Wordeman. "Rapid Measurement of Mitotic Spindle Orientation in Cultured Mammalian Cells." In Methods in Molecular Biology, 31–40. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0329-0_2.

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Tadenev, Abigail L. D., and Basile Tarchini. "The Spindle Orientation Machinery Beyond Mitosis: When Cell Specialization Demands Polarization." In Advances in Experimental Medicine and Biology, 209–25. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57127-0_9.

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Sullivan, Kevin F. "A moveable feast: the centromere-kinetochore complex in cell division." In Dynamics of Cell Division, 124–63. Oxford University PressOxford, 1998. http://dx.doi.org/10.1093/oso/9780199636839.003.0005.

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Abstract The goal of cell division is to transmit the genome from one generation to the next. This occurs in two essential steps: the genome is first replicated in S phase and then during mitosis the two copies are separated and transported into separate cytoplasmic domains destined to become new cells. This transport function is specified primarily by the centromeres, specialized nucleoprotein domains present in a single copy on each chromosome (1). Centromeres direct assembly of the machinery for microtubule binding and motor activities, known as the kinetochore, at the surface of each sister chromatid, maintain cohesion between sister chromatids, and possess regulatory elements that integrate chromosome motility and spindle function with cell cycle control pathways. During mitosis the kinetochores interact with spindle microtubules first to bind the spindle in prometaphase, then to achieve the crucial bipolar orientation in metaphase and finally to drive poleward movement in anaphase. A parallel system of regulatory elements located within the centromere monitors kinetochore attachment and communicates with the spindle to control anaphase onset. On the other side of the anaphase switch, centromeres very probably function as targets for regulated proteolysis of the 'glue' that holds sister chromatids together.
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Conference papers on the topic "Mitotic spindle orientations"

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Thaiparambil, Jose T., and Adam I. Marcus. "Abstract 4687: Novel functions of the AMPK pathway to maintain spindle orientation during mitosis." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4687.

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