scholarly journals Spatiotemporally controlled Myosin relocalization and internal pressure cause biased cortical extension to generate sibling cell size asymmetry

2018 ◽  
Author(s):  
Tri Thanh Pham ◽  
Arnaud Monnard ◽  
Jonne Helenius ◽  
Erik Lund ◽  
Nicole Lee ◽  
...  
Keyword(s):  
Cell Division ◽  
Hydrostatic Pressure ◽  
Cell Size ◽  
Asymmetric Cell Division ◽  
Apical Cell ◽  
Basal Membrane ◽  
Cell Cortex ◽  
Subsequent Increase ◽  
Biophysical Forces ◽  
Size Asymmetry

AbstractMetazoan cells can generate unequal sized sibling cells during cell division. This form of asymmetric cell division depends on spindle geometry and Myosin distribution but the underlying mechanics are unclear. Here, we use atomic force microscopy and live cell imaging to elucidate the biophysical forces involved in the establishment of physical asymmetry in Drosophila neural stem cells. We show that the force driving initial apical membrane expansion is provided by hydrostatic pressure, peaking shortly after anaphase onset, and enabled by a relieve of actomyosin contractile tension on the apical cell cortex. The subsequent increase in contractile forces at the cleavage furrow, combined with the relocalization of basally located Myosin results in basal membrane extension and sustained apical expansion. We propose that spatiotemporally controlled actomyosin contractile tension and hydrostatic pressure enables stereotypic biased membrane expansion to generate sibling cell size asymmetry.

scholarly journals Moesin is involved in polarity maintenance and cortical remodeling during asymmetric cell division

2018 ◽  
Vol 29 (4) ◽  
pp. 419-434 ◽  
Author(s):  
Namal Abeysundara ◽  
Andrew J. Simmonds ◽  
Sarah C. Hughes
Keyword(s):  
Cell Division ◽  
Cell Size ◽  
Asymmetric Cell Division ◽  
Developing Brain ◽  
Actin Binding ◽  
Cell Cortex ◽  
Asymmetric Distribution ◽  
Mitotic Progression ◽  
Apical Polarity ◽  
Size Asymmetry

An intact actomyosin network is essential for anchoring polarity proteins to the cell cortex and maintaining cell size asymmetry during asymmetric cell division of Drosophila neuroblasts (NBs). However, the mechanisms that control changes in actomyosin dynamics during asymmetric cell division remain unclear. We find that the actin-binding protein, Moesin, is essential for NB proliferation and mitotic progression in the developing brain. During metaphase, phosphorylated Moesin (p-Moesin) is enriched at the apical cortex, and loss of Moesin leads to defects in apical polarity maintenance and cortical stability. This asymmetric distribution of p-Moesin is determined by components of the apical polarity complex and Slik kinase. During later stages of mitosis, p-Moesin localization shifts more basally, contributing to asymmetric cortical extension and myosin basal furrow positioning. Our findings reveal Moesin as a novel apical polarity protein that drives cortical remodeling of dividing NBs, which is essential for polarity maintenance and initial establishment of cell size asymmetry.

scholarly journals Phases of cortical actomyosin dynamics coupled to the neuroblast polarity cycle

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Chet Huan Oon ◽  
Kenneth E Prehoda
Keyword(s):  
Cell Division ◽  
Cell Size ◽  
Daughter Cell ◽  
Asymmetric Cell Division ◽  
Tightly Coupled ◽  
Size Asymmetry ◽  
Early Mitosis

The Par complex dynamically polarizes to the apical cortex of asymmetrically dividing Drosophila neuroblasts where it directs fate determinant segregation. Previously we showed that apically directed cortical movements that polarize the Par complex require F-actin (Oon and Prehoda, 2019). Here we report the discovery of cortical actomyosin dynamics that begin in interphase when the Par complex is cytoplasmic but ultimately become tightly coupled to cortical Par dynamics. Interphase cortical actomyosin dynamics are unoriented and pulsatile but rapidly become sustained and apically-directed in early mitosis when the Par protein aPKC accumulates on the cortex. Apical actomyosin flows drive the coalescence of aPKC into an apical cap that is depolarized in anaphase when the flow reverses direction. Together with the previously characterized role of anaphase flows in specifying daughter cell size asymmetry, our results indicate that multiple phases of cortical actomyosin dynamics regulate asymmetric cell division.

Asymmetric cell division in fucoid algae: a role for cortical adhesions in alignment of the mitotic apparatus

2001 ◽  
Vol 114 (23) ◽  
pp. 4319-4328
Author(s):  
Sherryl R. Bisgrove ◽  
Darryl L. Kropf
Keyword(s):  
Cell Division ◽  
Asymmetric Cell Division ◽  
Cell Cortex ◽  
Mitotic Apparatus ◽  
Pharmacological Agents ◽  
Division Plane ◽  
Adhesion Sites ◽  
Spindle Poles ◽  
Pelvetia Compressa ◽  
Two Phases

The first cell division in zygotes of the fucoid brown alga Pelvetia compressa is asymmetric and we are interested in the mechanism controlling the alignment of this division. Since the division plane bisects the mitotic apparatus, we investigated the timing and mechanism of spindle alignments. Centrosomes, which give rise to spindle poles, aligned with the growth axis in two phases – a premetaphase rotation of the nucleus and centrosomes followed by a postmetaphase alignment that coincided with the separation of the mitotic spindle poles during anaphase and telophase. The roles of the cytoskeleton and cell cortex in the two phases of alignment were analyzed by treatment with pharmacological agents. Treatments that disrupted cytoskeleton or perturbed cortical adhesions inhibited pre-metaphase alignment and we propose that this rotational alignment is effected by microtubules anchored at cortical adhesion sites. Postmetaphase alignment was not affected by any of the treatments tested, and may be dependent on asymmetric cell morphology.

scholarly journals Asymmetric cell division: microtubule dynamics and spindle asymmetry

2002 ◽  
Vol 115 (11) ◽  
pp. 2257-2264 ◽  
Author(s):  
Julia A. Kaltschmidt ◽  
Andrea H. Brand
Keyword(s):  
Cell Division ◽  
Cell Size ◽  
Mitotic Spindle ◽  
Asymmetric Cell Division ◽  
Model Organisms ◽  
Complex Nature ◽  
Daughter Cells ◽  
Cytoskeletal Dynamics ◽  
Insight Into

Asymmetric cell division can produce daughter cells with different developmental fates and is often accompanied by a difference in cell size. A number of recent genetic and in vivo imaging studies in Drosophilaand Caenorhabditis elegans have begun to elucidate the mechanisms underlying the rearrangements of the cytoskeleton that result in eccentrically positioned cleavage planes. As a result, we are starting to gain an insight into the complex nature of the signals controlling cytoskeletal dynamics in the dividing cell. In this commentary we discuss recent findings on how the mitotic spindle is positioned and on cleavage site induction and place them in the context of cell size asymmetry in different model organisms.

scholarly journals PLK-1 Regulation of Asymmetric Cell Division in the Early C. elegans Embryo

2021 ◽  
Vol 8 ◽  
Author(s):  
Amelia J. Kim ◽  
Erik E. Griffin
Keyword(s):  
Cell Division ◽  
Cell Fate ◽  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Asymmetric Cell Division ◽  
Critical Role ◽  
Cell Cortex ◽  
C Elegans ◽  
Mitotic Kinase ◽  
Centrosome Separation

PLK1 is a conserved mitotic kinase that is essential for the entry into and progression through mitosis. In addition to its canonical mitotic functions, recent studies have characterized a critical role for PLK-1 in regulating the polarization and asymmetric division of the one-cell C. elegans embryo. Prior to cell division, PLK-1 regulates both the polarization of the PAR proteins at the cell cortex and the segregation of cell fate determinants in the cytoplasm. Following cell division, PLK-1 is preferentially inherited to one daughter cell where it acts to regulate the timing of centrosome separation and cell division. PLK1 also regulates cell polarity in asymmetrically dividing Drosophila neuroblasts and during mammalian planar cell polarity, suggesting it may act broadly to connect cell polarity and cell cycle mechanisms.

scholarly journals Tumor suppressor APC is an attenuator of spindle-pulling forces during C. elegans asymmetric cell division

2018 ◽  
Vol 115 (5) ◽  
pp. E954-E963 ◽  
Author(s):  
Kenji Sugioka ◽  
Lars-Eric Fielmich ◽  
Kota Mizumoto ◽  
Bruce Bowerman ◽  
Sander van den Heuvel ◽  
...  
Keyword(s):  
Cell Division ◽  
Tumor Suppressor ◽  
Mitotic Spindle ◽  
Asymmetric Cell Division ◽  
Cell Cortex ◽  
Dependent Manner ◽  
C Elegans ◽  
Pulling Forces ◽  
Underlying Mechanisms ◽  
Pulling Force

The adenomatous polyposis coli (APC) tumor suppressor has dual functions in Wnt/β-catenin signaling and accurate chromosome segregation and is frequently mutated in colorectal cancers. Although APC contributes to proper cell division, the underlying mechanisms remain poorly understood. Here we show that Caenorhabditis elegans APR-1/APC is an attenuator of the pulling forces acting on the mitotic spindle. During asymmetric cell division of the C. elegans zygote, a LIN-5/NuMA protein complex localizes dynein to the cell cortex to generate pulling forces on astral microtubules that position the mitotic spindle. We found that APR-1 localizes to the anterior cell cortex in a Par–aPKC polarity-dependent manner and suppresses anterior centrosome movements. Our combined cell biological and mathematical analyses support the conclusion that cortical APR-1 reduces force generation by stabilizing microtubule plus-ends at the cell cortex. Furthermore, APR-1 functions in coordination with LIN-5 phosphorylation to attenuate spindle-pulling forces. Our results document a physical basis for the attenuation of spindle-pulling force, which may be generally used in asymmetric cell division and, when disrupted, potentially contributes to division defects in cancer.

scholarly journals CLAMP/Spef1 regulates planar cell polarity signaling and asymmetric microtubule accumulation in the Xenopus ciliated epithelia

2018 ◽  
Vol 217 (5) ◽  
pp. 1633-1641 ◽  
Author(s):  
Sun K. Kim ◽  
Siwei Zhang ◽  
Michael E. Werner ◽  
Eva J. Brotslaw ◽  
Jennifer W. Mitchell ◽  
...  
Keyword(s):  
Cell Division ◽  
Epithelial Cells ◽  
Cell Signaling ◽  
Cell Polarity ◽  
Planar Cell Polarity ◽  
Protein Localization ◽  
Apical Cell ◽  
Cell Cortex ◽  
Pcp Signaling ◽  
Cell Cell

Most epithelial cells polarize along the axis of the tissue, a feature known as planar cell polarity (PCP). The initiation of PCP requires cell–cell signaling via the noncanonical Wnt/PCP pathway. Additionally, changes in the cytoskeleton both facilitate and reflect this polarity. We have identified CLAMP/Spef1 as a novel regulator of PCP signaling. In addition to decorating microtubules (MTs) and the ciliary rootlet, a pool of CLAMP localizes at the apical cell cortex. Depletion of CLAMP leads to the loss of PCP protein asymmetry, defects in cilia polarity, and defects in the angle of cell division. Additionally, depletion of CLAMP leads to a loss of the atypical cadherin-like molecule Celrs2, suggesting that CLAMP facilitates the stabilization of junctional interactions responsible for proper PCP protein localization. Depletion of CLAMP also affects the polarized organization of MTs. We hypothesize that CLAMP facilitates the establishment of cell polarity and promotes the asymmetric accumulation of MTs downstream of the establishment of proper PCP.

Asymmetric inheritance of mitochondria in yeast

2020 ◽  
Vol 401 (6-7) ◽  
pp. 779-791 ◽  
Author(s):  
Till Klecker ◽  
Benedikt Westermann
Keyword(s):  
Cell Division ◽  
Cell Cycle Progression ◽  
Asymmetric Cell Division ◽  
De Novo ◽  
Critical Role ◽  
Model Organism ◽  
Cellular Aging ◽  
Yeast Cells ◽  
Cell Cortex ◽  
Mitochondrial Inheritance

AbstractMitochondria are essential organelles of virtually all eukaryotic organisms. As they cannot be made de novo, they have to be inherited during cell division. In this review, we provide an overview on mitochondrial inheritance in Saccharomyces cerevisiae, a powerful model organism to study asymmetric cell division. Several processes have to be coordinated during mitochondrial inheritance: mitochondrial transport along the actin cytoskeleton into the emerging bud is powered by a myosin motor protein; cell cortex anchors retain a critical fraction of mitochondria in the mother cell and bud to ensure proper partitioning; and the quantity of mitochondria inherited by the bud is controlled during cell cycle progression. Asymmetric division of yeast cells produces rejuvenated daughter cells and aging mother cells that die after a finite number of cell divisions. We highlight the critical role of mitochondria in this process and discuss how asymmetric mitochondrial partitioning and cellular aging are connected.

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