Amitosis

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Conly L Rieder - One of the best experts on this subject based on the ideXlab platform.

  • stuck in division or passing through what happens when cells cannot satisfy the spindle assembly checkpoint
    Developmental Cell, 2004
    Co-Authors: Conly L Rieder, Helder Maiato
    Abstract:

    Abstract Cells that cannot satisfy the spindle assembly checkpoint (SAC) are delayed in mitosis (D-mitosis), a fact that has useful clinical ramifications. However, this delay is seldom permanent, and in the presence of an active SAC most cells ultimately escape mitosis and enter the next G1 as tetraploid cells. This review defines and discusses the various factors that determine how long a cell remains in mitosis when it cannot satisfy the SAC and also discusses the cell's subsequent fate.

Wei Wang - One of the best experts on this subject based on the ideXlab platform.

  • subcellular localization and role of ran1 in tetrahymena thermophila amitotic macronucleus
    FEBS Journal, 2012
    Co-Authors: Haixia Liang, Jing Xu, Dan Zhao, Huaru Tian, Xuxia Yang, Aihua Liang, Wei Wang
    Abstract:

    Amitosis, a direct method of cell division is common in ciliated protozoan, fungi and some animal and plant cells. During Amitosis, intranuclear microtubules are reorganized into specified arrays which assist in separation of nucleus, despite lack of a bipolar spindle. However, the regulation of Amitosis is not understood. Here, we focused on the localization and role of mitotic spindle assembly regulator: Ran GTPase (Ran1) in macronuclear Amitosis in binucleated protozoan Tetrahymena thermophila. HA-tagged Ran1 was localized in the macronucleus throughout the cell cycle of Tetrahymena during vegetative growth, and the accessory factor binding domains of Ran1 contributed to its macronuclear localization. Incomplete somatic knockout of RAN1 resulted in aberrant intramacronuclear microtubule array formation, missegregation of macronuclear chromosomes and ultimately blocked macronuclei proliferation. When the Ran1 cycle was perturbed by overexpression of Ran1T25N (GDP-bound Ran1-mimetic) or Ran1Q70L (GTP-bound Ran1-mimetic), intramacronuclear microtubule assembly was inhibited or multi-micronucleate cells formed. These results suggest that Ran GTPase pathway is involved in assembly of a specialized intramacronuclear microtubule network and coordinates amitotic progression in Tetrahymena.

Andre R. O. Cavalcanti - One of the best experts on this subject based on the ideXlab platform.

  • Amitotic chromosome loss predicts distinct patterns of senescence and non-senescence in ciliates.
    Protist, 2015
    Co-Authors: David W. Morgens, Andre R. O. Cavalcanti
    Abstract:

    Over time and repeated asexual divisions, many ciliate species display the characteristics of senescence, reduced fecundity and increased mortality. Their only path to recovery is sexual conjugation or autogamy. While more traditional models of cellular aging have been proposed, one of the most accepted explanations relies on the faulty mechanism by which ciliates duplicate their somatic nucleus, a process referred to as Amitosis. Amitosis involves the random segregation of chromosomes with no consideration for homology. Over subsequent divisions, chromosome copy numbers will fluctuate until an entire chromosome is lost, resulting in death. Via simulations of this process, we find that senescence and death via chromosome loss is not the only possible result of Amitosis. Random chromosome loss is less damaging to populations than previously thought, and strict adherence to the model predicts that Paramecium tetraurelia would not senesce. A combination of the reciprocal nature of Amitosis and lethal selection against low-copy number chromosomes is responsible for this startling prediction. Additionally, our results provide an alternate explanation to recent evidence for selection on chromosome copy number in Tetrahymena thermophila and peculiar patterns of senescence in Tetrahymena pyriformis.

Osamu Numata - One of the best experts on this subject based on the ideXlab platform.

  • Kinesin-14 is Important for Chromosome Segregation During Mitosis and Meiosis in the Ciliate Tetrahymena thermophila.
    The Journal of eukaryotic microbiology, 2016
    Co-Authors: Yasuharu Kushida, Masak Takaine, Kentaro Nakano, Toshiro Sugai, Krishna Kumar Vasudevan, Mayukh Guha, Yu-yang Jiang, Jacek Gaertig, Osamu Numata
    Abstract:

    Ciliates such as Tetrahymena thermophila have two distinct nuclei within one cell: the micronucleus that undergoes mitosis and meiosis and the macronucleus that undergoes Amitosis, a type of nuclear division that does not involve a bipolar spindle, but still relies on intranuclear microtubules. Ciliates provide an opportunity for the discovery of factors that specifically contribute to chromosome segregation based on a bipolar spindle, by identification of factors that affect the micronuclear but not the macronuclear division. Kinesin-14 is a conserved minus end-directed microtubule motor that crosslinks microtubules and contributes to the bipolar spindle sizing and organization. Here we use homologous DNA recombination to knock out genes that encode kinesin-14 orthologues (KIN141, KIN142) in Tetrahymena. A loss of KIN141 led to severe defects in the chromosome segregation during both mitosis and meiosis but did not affect Amitosis. A loss of KIN141 altered the shape of the meiotic spindle in a way consistent with the KIN141′s contribution to the organization of the spindle poles. EGFP-tagged KIN141 preferentially accumulated at the spindle poles during the meiotic prophase and metaphase I. Thus, in ciliates, kinesin-14 is important for nuclear divisions that involve a bipolar spindle. This article is protected by copyright. All rights reserved.

  • Amitosis requires γ-tubulin-mediated microtubule assembly in Tetrahymena thermophila.
    Cytoskeleton (Hoboken N.J.), 2010
    Co-Authors: Yasuharu Kushida, Kentaro Nakano, Osamu Numata
    Abstract:

    To reveal the molecular systems involved in the division of a cell and its contents during cell proliferation is one of the major subjects in cell biology. Although cytoskeletal organization during mitosis has been well studied, consensus on the molecular basis of Amitosis has not been achieved. Here we adapted an immunofluorescence method and investigated the cellular localization of γ-tubulin and microtubules (MTs) in dividing Tetrahymena. Although the macronucleus (Mac) lacks a bipolar spindle, γ-tubulin and MTs are specifically detected in the dividing Mac and show a marked change in the pattern of localization. First, γ-tubulin and MTs appear in whole Mac, then, γ-tubulin gathers at the center of the Mac where the aster-like structure of MTs forms. On Mac expansion, MTs associated with numerous dots of γ-tubulin are reorganized into longitudinally arranged bundles, suggesting that the mutual sliding of each filament and polymerization of MTs may induce Mac expansion. Moreover, normal Mac expansion and equal segregation of the Mac are severely disturbed when γ-tubulin is shut off. We propose that γ-tubulin-mediated MT assembly is required in Mac Amitosis of Tetrahymena. © 2010 Wiley-Liss, Inc.

Domenico Grieco - One of the best experts on this subject based on the ideXlab platform.

  • the fcp1 wee1 cdk1 axis affects spindle assembly checkpoint robustness and sensitivity to antimicrotubule cancer drugs
    Cell Death & Differentiation, 2015
    Co-Authors: Roberta Visconti, Luca Palazzo, Rosa Della Monica, Francesca Dalessio, Maddalena Raia, S Improta, L Del Vecchio, M R Villa, Domenico Grieco
    Abstract:

    To grant faithful chromosome segregation, the spindle assembly checkpoint (SAC) delays mitosis exit until mitotic spindle assembly. An exceedingly prolonged mitosis, however, promotes cell death and by this means antimicrotubule cancer drugs (AMCDs), that impair spindle assembly, are believed to kill cancer cells. Despite malformed spindles, cancer cells can, however, slip through SAC, exit mitosis prematurely and resist killing. We show here that the Fcp1 phosphatase and Wee1, the cyclin B-dependent kinase (cdk) 1 inhibitory kinase, play a role for this slippage/resistance mechanism. During AMCD-induced prolonged mitosis, Fcp1-dependent Wee1 reactivation lowered cdk1 activity, weakening SAC-dependent mitotic arrest and leading to mitosis exit and survival. Conversely, genetic or chemical Wee1 inhibition strengthened the SAC, further extended mitosis, reduced antiapoptotic protein Mcl-1 to a minimum and potentiated killing in several, AMCD-treated cancer cell lines and primary human adult lymphoblastic leukemia cells. Thus, the Fcp1-Wee1-Cdk1 (FWC) axis affects SAC robustness and AMCDs sensitivity.

  • The end of mitosis from a phosphatase perspective.
    Cell Cycle, 2012
    Co-Authors: Roberta Visconti, Luca Palazzo, Rosa Della Monica, Anna Pepe, Domenico Grieco
    Abstract:

    Transition through mitosis, the cell division cycle phase deputed to segregate replicated chromosomes, requires a wave of protein phosphorylation. While in the past decades a wealth of information has been gathered on the major kinase activities responsible for the onset of mitosis, only recently has a picture emerged of how their effects are reversed by protein phosphatases at the end of mitosis. Here, we summarized some recent data on the relevance for protein phosphatases in the reversal of mitotic phosphorylation required to complete mitosis in vertebrate cells.