Apical Constriction Reversal upon Mitotic Entry Underlies Different Morphogenetic Outcomes of Cell Division

2019 ◽  
Author(s):  
Grace Lim
Keyword(s):  
Cell Division ◽  
Apical Constriction ◽  
Mitotic Entry

scholarly journals Apical Constriction Reversal upon Mitotic Entry Underlies Different Morphogenetic Outcomes of Cell Division

2019 ◽  
Author(s):  
Clint S. Ko ◽  
Prateek Kalakuntla ◽  
Adam C. Martin
Keyword(s):  
Cell Division ◽  
Cell Shape ◽  
Mitotic Cell ◽  
Signal Interference ◽  
Apical Constriction ◽  
Mitotic Entry ◽  
Cell Divisions ◽  
Cell Shape Changes ◽  
Shape Changes ◽  
Mitotic Cells

AbstractDuring development, coordinated cell shape changes and cell divisions sculpt tissues. While these individual cell behaviors have been extensively studied, how cell shape changes and cell divisions that occur concurrently in epithelia influence tissue shape is less understood. We addressed this question in two contexts of the early Drosophila embryo: premature cell division during mesoderm invagination, and native ectodermal cell divisions with ectopic activation of apical contractility. Using quantitative live-cell imaging, we demonstrated that mitotic entry reverses apical contractility by interfering with medioapical RhoA signaling. While premature mitotic entry inhibits mesoderm invagination, which relies on apical constriction, mitotic entry in an artificially contractile ectoderm induced ectopic tissue invaginations. Ectopic invaginations resulted from medioapical myosin loss in neighboring mitotic cells. This myosin loss enabled non-mitotic cells to apically constrict through mitotic cell stretching. Thus, the spatial pattern of mitotic entry can differentially regulate tissue shape through signal interference between apical contractility and mitosis.

scholarly journals Apical Constriction Reversal upon Mitotic Entry Underlies Different Morphogenetic Outcomes of Cell Division

2020 ◽  
Vol 31 (16) ◽  
pp. 1663-1674 ◽  
Author(s):  
Clint S. Ko ◽  
Prateek Kalakuntla ◽  
Adam C. Martin
Keyword(s):  
Cell Division ◽  
Tissue Level ◽  
Spatiotemporal Patterns ◽  
Force Generation ◽  
Tissue Morphogenesis ◽  
Apical Constriction ◽  
Mitotic Entry ◽  
Cell Divisions

Cell divisions can either promote or inhibit tissue morphogenesis. In contractile epithelia, mitotic entry disrupts medioapical myosin activation and reverses apical constriction. We found that different spatiotemporal patterns of mitotic entry and the resultant changes in force generation at the tissue level dictate distinct tissue shape outcomes.

scholarly journals A Nodal/Eph signalling relay drives the transition from apical constriction to apico-basal shortening in ascidian endoderm invagination

Development ◽  
2020 ◽  
Vol 147 (15) ◽  
pp. dev186965
Author(s):  
Ulla-Maj Fiuza ◽  
Takefumi Negishi ◽  
Alice Rouan ◽  
Hitoyoshi Yasuo ◽  
Patrick Lemaire
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Ciona Intestinalis ◽  
Precursor Cells ◽  
Endodermal Cell ◽  
Apical Constriction ◽  
Fate Specification ◽  
Endoderm Cell ◽  
Ascidian Species ◽  
Morphogenetic Event

ABSTRACTGastrulation is the first major morphogenetic event during animal embryogenesis. Ascidian gastrulation starts with the invagination of 10 endodermal precursor cells between the 64- and late 112-cell stages. This process occurs in the absence of endodermal cell division and in two steps, driven by myosin-dependent contractions of the acto-myosin network. First, endoderm precursors constrict their apex. Second, they shorten apico-basally, while retaining small apical surfaces, thereby causing invagination. The mechanisms that prevent endoderm cell division, trigger the transition between step 1 and step 2, and drive apico-basal shortening have remained elusive. Here, we demonstrate a conserved role for Nodal and Eph signalling during invagination in two distantly related ascidian species, Phallusia mammillata and Ciona intestinalis. Specifically, we show that the transition to step 2 is triggered by Nodal relayed by Eph signalling. In addition, our results indicate that Eph signalling lengthens the endodermal cell cycle, independently of Nodal. Finally, we find that both Nodal and Eph signals are dispensable for endoderm fate specification. These results illustrate commonalities as well as differences in the action of Nodal during ascidian and vertebrate gastrulation.

scholarly journals Cortical regulation of cell size by a sizer cdr2p

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Kally Z Pan ◽  
Timothy E Saunders ◽  
Ignacio Flor-Parra ◽  
Martin Howard ◽  
Fred Chang
Keyword(s):  
Cell Division ◽  
Protein Kinase ◽  
Cell Surface ◽  
Surface Area ◽  
Control Mechanism ◽  
Size Control ◽  
Mitotic Entry ◽  
Medial Cortex ◽  
Peripheral Membrane Protein ◽  
Dose Dependent

Cells can, in principle, control their size by growing to a specified size before commencing cell division. How any cell actually senses its own size remains poorly understood. The fission yeast Schizosaccharomyces pombe are rod-shaped cells that grow to ∼14 µm in length before entering mitosis. In this study, we provide evidence that these cells sense their surface area as part of this size control mechanism. We show that cells enter mitosis at a certain surface area, as opposed to a certain volume or length. A peripheral membrane protein kinase cdr2p has properties of a dose-dependent ‘sizer’ that controls mitotic entry. As cells grow, the local cdr2p concentration in nodes at the medial cortex accumulates as a measure of cell surface area. Our findings, which challenge a previously proposed pom1p gradient model, lead to a new model in which cells sense their size by using cdr2p to probe the surface area over the whole cell and relay this information to the medial cortex.

scholarly journals Anisotropy of cell division and epithelial sheet bending via apical constriction shape the complex folding pattern of beetle horn primordia

2018 ◽  
Vol 152 ◽  
pp. 32-37 ◽  
Author(s):  
Haruhiko Adachi ◽  
Keisuke Matsuda ◽  
Teruyuki Niimi ◽  
Yasuhiro Inoue ◽  
Shigeru Kondo ◽  
...  
Keyword(s):  
Cell Division ◽  
Apical Constriction ◽  
Folding Pattern ◽  
Sheet Bending ◽  
Epithelial Sheet

scholarly journals CDK1 and PLK1 co-ordinate the disassembly and re-assembly of the Nuclear Envelope in vertebrate mitosis

2017 ◽  
Author(s):  
Ines J de Castro ◽  
Raquel Sales Gil ◽  
Lorena Ligammari ◽  
Maria Laura Di Giacinto ◽  
Paola Vagnarelli
Keyword(s):  
Dna Repair ◽  
Cell Division ◽  
Nuclear Envelope ◽  
Genetic Instability ◽  
Nuclear Pore ◽  
Lamin A ◽  
Nuclear Pore Complexes ◽  
Regulatory Pathways ◽  
Mitotic Entry ◽  
Pore Complexes

ABSTRACTMicronuclei (MN) arise from chromosomes or fragments that fail to be incorporated into the primary nucleus after cell division. These structures are a major source of genetic instability caused by DNA repair and replication defects coupled to aberrant Nuclear Envelope (NE). These problems ultimately lead to a spectrum of chromosome rearrangements called chromothripsis, a phenomenon that is a hallmark of several cancers. Despite its importance, the molecular mechanism at the origin of this instability is still not understood. Here we show that lagging chromatin, although it can efficiently assemble Lamin A/C, always fails to recruit Nuclear Pore Complexes (NPCs) proteins and that Polo-Like Kinase (PLK1) negatively regulates the NPC assembly. We also provide evidence for the requirement of PLK1 activity for the disassembly of NPCs, but not Lamina (A/C), at mitotic entry. Altogether this study reveals the existence of independent regulatory pathways for Lamin A/C and NPC reorganization during mitosis where Lamin A targeting to the chromatin is controlled by CDK1 activity (a clock-based model) while the NPC loading is also spatially monitored by PLK1.

scholarly journals Dissociation of membrane–chromatin contacts is required for proper chromosome segregation in mitosis

2019 ◽  
Vol 30 (4) ◽  
pp. 427-440 ◽  
Author(s):  
Lysie Champion ◽  
Sumit Pawar ◽  
Naemi Luithle ◽  
Rosemarie Ungricht ◽  
Ulrike Kutay
Keyword(s):  
Cell Division ◽  
Nuclear Envelope ◽  
Chromosome Segregation ◽  
Nuclear Periphery ◽  
Metaphase Plate ◽  
Chromatin Organization ◽  
Mitotic Entry ◽  
Chromatin Interactions ◽  
Membrane Attachment ◽  
Mitotic Chromatin

The nuclear envelope (NE) aids in organizing the interphase genome by tethering chromatin to the nuclear periphery. During mitotic entry, NE–chromatin contacts are broken. Here, we report on the consequences of impaired NE removal from chromatin for cell division of human cells. Using a membrane–chromatin tether that cannot be dissociated when cells enter mitosis, we show that a failure in breaking membrane–chromatin interactions impairs mitotic chromatin organization, chromosome segregation and cytokinesis, and induces an aberrant NE morphology in postmitotic cells. In contrast, chromosome segregation and cell division proceed successfully when membrane attachment to chromatin is induced during metaphase, after chromosomes have been singularized and aligned at the metaphase plate. These results indicate that the separation of membranes and chromatin is critical during prometaphase to allow for proper chromosome compaction and segregation. We propose that one cause of these defects is the multivalency of membrane–chromatin interactions.

scholarly journals NDEL1 Phosphorylation by Aurora-A Kinase Is Essential for Centrosomal Maturation, Separation, and TACC3 Recruitment

2006 ◽  
Vol 27 (1) ◽  
pp. 352-367 ◽  
Author(s):  
Daisuke Mori ◽  
Yoshihisa Yano ◽  
Kazuhito Toyo-oka ◽  
Noriyuki Yoshida ◽  
Masami Yamada ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Neuronal Migration ◽  
Mitotic Cell ◽  
Cytoplasmic Dynein ◽  
Aurora A Kinase ◽  
Aurora A ◽  
Microtubule Organization ◽  
Mitotic Entry ◽  
Binding Partner

ABSTRACT NDEL1 is a binding partner of LIS1 that participates in the regulation of cytoplasmic dynein function and microtubule organization during mitotic cell division and neuronal migration. NDEL1 preferentially localizes to the centrosome and is a likely target for cell cycle-activated kinases, including CDK1. In particular, NDEL1 phosphorylation by CDK1 facilitates katanin p60 recruitment to the centrosome and triggers microtubule remodeling. Here, we show that Aurora-A phosphorylates NDEL1 at Ser251 at the beginning of mitotic entry. Interestingly, NDEL1 phosphorylated by Aurora-A was rapidly downregulated thereafter by ubiquitination-mediated protein degradation. In addition, NDEL1 is required for centrosome targeting of TACC3 through the interaction with TACC3. The expression of Aurora-A phosphorylation-mimetic mutants of NDEL1 efficiently rescued the defects of centrosomal maturation and separation which are characteristic of Aurora-A-depleted cells. Our findings suggest that Aurora-A-mediated phosphorylation of NDEL1 is essential for centrosomal separation and centrosomal maturation and for mitotic entry.

scholarly journals A unified view of spatio-temporal control of mitotic entry: Polo kinase as the key

Open Biology ◽  
2018 ◽  
Vol 8 (8) ◽  
pp. 180114 ◽  
Author(s):  
Lionel Pintard ◽  
Vincent Archambault
Keyword(s):  
Cell Division ◽  
Temporal Control ◽  
Animal Cells ◽  
Mitotic Entry ◽  
Multiple Events ◽  
Polo Kinase ◽  
Unified View ◽  
Mechanistic Understanding ◽  
Spatio Temporal ◽  
Upstream Regulators

The Polo kinase is an essential regulator of cell division. Its ability to regulate multiple events at distinct subcellular locations and times during mitosis is remarkable. In the last few years, a much clearer mechanistic understanding of the functions and regulation of Polo in cell division has emerged. In this regard, the importance of coupling changes in activity with changes in localization is striking, both for Polo itself and for its upstream regulators. This review brings together several new pieces of the puzzle that are gradually revealing how Polo is regulated, in space and time, to enable its functions in the early stages of mitosis in animal cells. As a result, a unified view of how mitotic entry is spatio-temporally regulated is emerging.

The Ultrastructure of the Nuclear Events of Binary Fission in Paramecium bursaria and the Effects of Colchicine on Cell Division

1974 ◽  
Vol 32 ◽  
pp. 276-277
Author(s):  
L. M. Lewis
Keyword(s):  
Cell Division ◽  
Nuclear Envelope ◽  
Condensed Chromatin ◽  
Binary Fission ◽  
Paramecium Bursaria ◽  
Nuclear Events ◽  
Division Axis

The effects of colchicine on extranuclear microtubules associated with the macronucleus of Paramecium bursaria were studied to determine the possible role that these microtubules play in controlling the shape of the macronucleus. In the course of this study, the ultrastructure of the nuclear events of binary fission in control cells was also studied.During interphase in control cells, the micronucleus contains randomly distributed clumps of condensed chromatin and microtubular fragments. Throughout mitosis the nuclear envelope remains intact. During micronuclear prophase, cup-shaped microfilamentous structures appear that are filled with condensing chromatin. Microtubules are also present and are parallel to the division axis.

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