scholarly journals Resistance is futile: Centering forces yield for asymmetric cell division

2019 ◽  
Vol 218 (3) ◽  
pp. 727-728
Author(s):  
Joshua Alper ◽  
Marija Zanic
Keyword(s):  
Cell Division ◽  
Sea Urchin ◽  
Asymmetric Cell Division ◽  
Asymmetric Division ◽  
Magnetic Tweezers ◽  
Time Dependent ◽  
Mitotic Apparatus ◽  
Cell Biol

Asymmetric cell division relies on microtubule-based forces to asymmetrically position the mitotic apparatus. In this issue, Sallé et al. (2019. J. Cell Biol. https://doi.org/10.1083/jcb.201807102) use magnetic tweezers to induce asymmetric division in sea urchin zygotes, demonstrating that asymmetry could arise from a time-dependent weakening of centering forces.

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 A Quantitative Description of Protoplasmic Movement During Cleavage in the Sea-Urchin Egg

1958 ◽  
Vol 35 (2) ◽  
pp. 407-424
Author(s):  
Y. HIRAMOTO
Keyword(s):  
Cell Division ◽  
Sea Urchin ◽  
Quantitative Description ◽  
Motive Force ◽  
Mitotic Apparatus ◽  
Band Theory ◽  
Cytoplasmic Granules ◽  
Carbon Particles ◽  
Sea Urchin Egg ◽  
Protoplasmic Movement

1. Protoplasmic movements during cleavage in the eggs of the heart-urchin Clypeaster japonicus have been followed by tracing the movements of cytoplasmic granules and of carbon particles adhering to the surface. 2. These movements are quantitatively described in normal eggs and in eggs whose mitotic apparatus has been destroyed by colchicine. 3. The results obtained are qualitatively similar to those obtained by Spek and by Dan and his collaborators. 4. Endoplasmic movement and changes in the length and shape of the astral rays are readily explained by the contracting-ring (band) theory. 5. The location of the motive force of cell division is discussed.

Obligatory Asymmetric Cell Division Regulates Self-Renewal In Hematopoietic Progenitor/Stem Cells

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 571-571
Author(s):  
William T. Tse ◽  
Livana Soetedjo ◽  
Timothy Lax ◽  
Lei Wang ◽  
Patrick J. Kennedy
Keyword(s):  
Cell Division ◽  
Daughter Cell ◽  
Asymmetric Cell Division ◽  
Bone Marrow Cells ◽  
Asymmetric Division ◽  
Mouse Bone Marrow ◽  
Hematopoietic Progenitor ◽  
Self Renewal ◽  
Daughter Cells ◽  
Dividing Cells

Abstract Abstract 571 Asymmetric cell division, a proposed mechanism by which hematopoietic progenitor/stem cells (HPSC) maintain a balance between self-renewal and differentiation, has rarely been observed. Here we report the surprising finding that cultured mouse primary HPSC routinely generate pairs of daughter cells with 2 distinct phenotypes after a single round of cell division. Mouse bone marrow cells were cultured on chamber slides in the presence of stem cell factor (SCF). BrdU was added overnight to label dividing cells, and the cells were examined by immunofluorescence microscopy on day 2–4 of culture. In each BrdU+c-Kit+ divided cell doublet, c-Kit was invariably expressed in only 1 of the 2 daughter cells. In contrast, the other daughter cell was negative for c-Kit but positive for the asymmetric cell fate determinant Numb and mature myeloid markers Mac1, Gr1, M-CSFR and F4/80. Similarly, in each BrdU+Sca1+ cell doublet, 1 daughter cell was positive for the stem cell markers Sca1, c-Kit, CD150 and CD201, whereas the other cell was negative for these markers but positive for Numb and the mature myeloid markers. Analysis of 400 such doublets showed that the probability of HPSC undergoing asymmetric division was 99.5% (95% confidence interval 98–100%), indicating that asymmetric division in HPSC is in fact not rare but obligatory. In other model systems, it has been shown that activation of the atypical protein kinase C (aPKC)-Par6-Par3 cell polarity complex and realignment of the microtubule cytoskeleton precede asymmetric cell division. We asked whether similar steps are involved in the asymmetric division of HPSC. We found that c-Kit receptors, upon stimulation by SCF, rapidly capped at an apical pole next to the microtubule-organizing center, followed by redistribution to the same pole of the aPKC-Par6-Par3 complex and microtubule-stabilizing proteins APC, β-catenin, EB1 and IQGAP1. Strikingly, after cell division, the aPKC-Par6-Par3 complex and other polarity markers all partitioned only into the c-Kit+/Sca1+ daughter cell and not the mature daughter cell. The acetylated and detyrosinated forms of stabilized microtubules were also present only in the c-Kit+/Sca1+ cell, as were the Aurora A and Polo-like kinases, 2 mitotic kinases associated with asymmetric cell division. To understand how c-Kit activation triggers downstream polarization events, we studied the role of lipid rafts, cholesterol-enriched microdomains in the cell membrane that serve as organization centers of signaling complexes. These are enriched in phosphatidylinositol 4,5-bisphosphate and annexin 2, putative attachment sites for the aPKC-Par6-Par3 complex. We found that SCF stimulation led to coalescence of lipid raft components at the site of the c-Kit cap, and treatment with a wide range of inhibitors that blocked lipid raft formation abrogated polarization of the aPKC-Par6-Par3 complex and division of the c-Kit+/Sca1+ cells. Because obligatory asymmetric division in cultured HPSC would prevent a net increase in their number, we sought a way to bypass its mechanism. We tested whether inhibition of protein phosphatase 2A (PP2A), a physiological antagonist of aPKC, would enhance aPKC activity and promote self-renewal of HPSC. Treatment of cultured HPSC with okadaic acid or calyculin, 2 well-characterized PP2A inhibitors, increased the percent of c-Kit+/Sca1+ cells undergoing symmetric division from 0% to 23.3% (p<0.001). In addition, small colonies comprised of symmetrically dividing cells uniformly positive for Sca1, c-Kit, CD150 and CD201 were noted in the culture. To functionally characterize the effect of PP2A inhibition, mouse bone marrow cells were cultured in the absence or presence of PP2A inhibitors and transplanted into irradiated congenic mice in a competitive repopulation assay. At 4–8 weeks post-transplant, the donor engraftment rate increased from ∼1 in mice transplanted with untreated cells to >30% in mice transplanted with PP2A inhibitor-treated cells. This dramatic increase indicates that PP2A inhibition can effectively perturb the mechanism of asymmetric cell division and promote the self-renewal of HPSC. In summary, our data showed that obligatory asymmetric cell division works to maintain a strict balance between self-renewal and differentiation in HPSC and pharmacological manipulation of the cell polarity machinery could potentially be used to expand HPSC for clinical use. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Effects of caffeine and other methylxanthines on the development and metabolism of sea urchin eggs. Involvement of NADP and glutathione.

1976 ◽  
Vol 68 (3) ◽  
pp. 440-450 ◽  
Author(s):  
J Nath ◽  
J I Rebhun
Keyword(s):  
Cell Division ◽  
Sea Urchin ◽  
Reductase Activity ◽  
Inhibitory Effect ◽  
Pentose Phosphate ◽  
Nad Kinase ◽  
Mitotic Apparatus ◽  
Sea Urchin Eggs ◽  
Glutathione Reductase Activity

Methylxanthines (MX) inhibit cell division in sea urchin and clam eggs. This inhibitory effect is not mediated via cAMP. MX also inhibit respiration in marine eggs, at concentrations which inhibit cleavage. Studies showed that no changes occurred in ATP and ADP levels in the presence of inhibitory concentrations of MX, indicating an extra-mitochondrial site of action for the drug. Subsequent studies revealed decreased levels of NADP+ and NADPH, when eggs were incubated with inhibitory concentrations of MX, but no change in levels of NAD+ and NADH. MX did not affect the pentose phosphate shunt pathway and did not have any effect on the enzyme NAD+ -kinase. Further studies showed a marked inhibitory effect on the glutathione reductase activity of MX-treated eggs. Reduced glutathione (GSH) could reverse the cleavage inhibitory effect of MX. Moreover, diamide, a thiol-oxidizing agent specific for GSH in living cells, caused inhibition of cell division in sea urchin eggs. Diamide added to eggs containing mitotic apparatus (MA) could prevent cleavage by causing a dissolution of the formed MA. Both MX and diamide inhibit a Ca2+-activated ATPase in whole eggs. The enzyme can be reactivated by sulfhydryl reducing agents added in the assay mixture. In addition, diamide causes an inhibition of microtubule polymerization, reversible with dithioerythritol. All experimental evidence so far suggests that inhibition of mitosis in sea urchin eggs by MX is mediated by perturbations of the in vivo thiol-disulfide status of target systems, with a primary effect on glutathione levels.

scholarly journals Roles of kinesin and kinesin-like proteins in sea urchin embryonic cell division: evaluation using antibody microinjection.

1993 ◽  
Vol 123 (3) ◽  
pp. 681-689 ◽  
Author(s):  
B D Wright ◽  
M Terasaki ◽  
J M Scholey
Keyword(s):  
Cell Division ◽  
Sea Urchin ◽  
Heavy Chain ◽  
Mammalian Cells ◽  
Embryonic Cell ◽  
Mitotic Apparatus ◽  
Specific Antibodies ◽  
Sea Urchin Embryos ◽  
Mitotic Figures

Previous studies suggest that kinesin heavy chain (KHC) is associated with ER-derived membranes that accumulate in the mitotic apparatus in cells of early sea urchin embryos (Wright, B. D., J. H. Henson, K. P. Wedaman, P. J. Willy, J. N. Morand, and J. M. Scholey. 1991. J. Cell Biol. 113:817-833). Here, we report that the microinjection of KHC-specific antibodies into these cells has no effect on mitosis or ER membrane organization, even though one such antibody, SUK4, blocks kinesin-driven motility in vitro and in mammalian cells. Microinjected SUK4 was localized to early mitotic figures, suggesting that it is able to access kinesin in spindles. In contrast to KHC-specific antibodies, two antibodies that react with kinesin-like proteins (KLPs), namely CHO1 and HD, disrupted mitosis and prevented subsequent cell division. CHO1 is thought to exert this effect by blocking the activity of a 110-kD KLP. The relevant target of HD, which was raised against the KHC motor domain, is unknown; HD may disrupt mitosis by interfering with an essential spindle KLP but not with KHC itself, as preabsorption of HD with KHC did not alter its ability to block mitosis. These data indicate that some KLPs have essential mitotic functions in early sea urchin embryos but KHC itself does not.

scholarly journals FURTHER STUDIES ON CELL DIVISION WITHOUT MITOTIC APPARATUS IN SEA URCHIN EGGS

1965 ◽  
Vol 25 (1) ◽  
pp. 161-167 ◽  
Author(s):  
Y. Hiramoto
Keyword(s):  
Cell Division ◽  
Sea Urchin ◽  
Sea Water ◽  
Sucrose Solution ◽  
Mitotic Apparatus ◽  
Sea Urchin Eggs ◽  
Paraffin Oil

A large quantity of paraffin oil, sucrose solution, or sea water was injected into the eggs of the heart urchin Clypeaster japonicus shortly before the onset of the first cleavage. The injected oil became spherical, pushing the mitotic apparatus aside. The sucrose solution mixed with the protoplasm and caused disintegration of the mitotic apparatus, and the sea water formed a vacuole at the center of the cell. In all these cases, cleavage may take place almost normally in spite of the absence of the mitotic apparatus or its displacement within the cell. In some eggs, furrowing may take place when more than fifty per cent of the endoplasm has been replaced with sea water before onset of cleavage.

scholarly journals Asymmetric division through a reduction of microtubule centering forces

2018 ◽  
Vol 218 (3) ◽  
pp. 771-782 ◽  
Author(s):  
Jérémy Sallé ◽  
Jing Xie ◽  
Dmitry Ershov ◽  
Milan Lacassin ◽  
Serge Dmitrieff ◽  
...  
Keyword(s):  
Cell Fate ◽  
Sea Urchin ◽  
Magnetic Particles ◽  
Force Measurement ◽  
Asymmetric Division ◽  
Time Dependent ◽  
Asymmetric Divisions ◽  
Dividing Cells ◽  
Size Diversity ◽  
Global Reduction

Asymmetric divisions are essential for the generation of cell fate and size diversity. They implicate cortical domains where minus end–directed motors, such as dynein, are activated to pull on microtubules to decenter asters attached to centrosomes, nuclei, or spindles. In asymmetrically dividing cells, aster decentration typically follows a centering phase, suggesting a time-dependent regulation in the competition between microtubule centering and decentering forces. Using symmetrically dividing sea urchin zygotes, we generated cortical domains of magnetic particles that spontaneously cluster endogenous dynein activity. These domains efficiently attract asters and nuclei, yielding marked asymmetric divisions. Remarkably, aster decentration only occurred after asters had first reached the cell center. Using intracellular force measurement and models, we demonstrate that this time-regulated imbalance results from a global reduction of centering forces rather than a local maturation of dynein activity at the domain. Those findings define a novel paradigm for the regulation of division asymmetry.

scholarly journals Cytoplasmic MTOCs control spindle orientation for asymmetric cell division in plants

2017 ◽  
Vol 114 (42) ◽  
pp. E8847-E8854 ◽  
Author(s):  
Ken Kosetsu ◽  
Takashi Murata ◽  
Moé Yamada ◽  
Momoko Nishina ◽  
Joanna Boruc ◽  
...  
Keyword(s):  
Cell Division ◽  
Asymmetric Cell Division ◽  
Physcomitrella Patens ◽  
De Novo ◽  
Critical Role ◽  
Fine Tuning ◽  
Spindle Orientation ◽  
Mitotic Apparatus ◽  
Division Plane ◽  
Division Axis

Proper orientation of the cell division axis is critical for asymmetric cell divisions that underpin cell differentiation. In animals, centrosomes are the dominant microtubule organizing centers (MTOC) and play a pivotal role in axis determination by orienting the mitotic spindle. In land plants that lack centrosomes, a critical role of a microtubular ring structure, the preprophase band (PPB), has been observed in this process; the PPB is required for orienting (before prophase) and guiding (in telophase) the mitotic apparatus. However, plants must possess additional mechanisms to control the division axis, as certain cell types or mutants do not form PPBs. Here, using live imaging of the gametophore of the moss Physcomitrella patens, we identified acentrosomal MTOCs, which we termed “gametosomes,” appearing de novo and transiently in the prophase cytoplasm independent of PPB formation. We show that gametosomes are dispensable for spindle formation but required for metaphase spindle orientation. In some cells, gametosomes appeared reminiscent of the bipolar MT “polar cap” structure that forms transiently around the prophase nucleus in angiosperms. Specific disruption of the polar caps in tobacco cells misoriented the metaphase spindles and frequently altered the final division plane, indicating that they are functionally analogous to the gametosomes. These results suggest a broad use of transient MTOC structures as the spindle orientation machinery in plants, compensating for the evolutionary loss of centrosomes, to secure the initial orientation of the spindle in a spatial window that allows subsequent fine-tuning of the division plane axis by the guidance machinery.

Molecular Mechanisms of Asymmetric Division in Oocytes

2013 ◽  
Vol 19 (4) ◽  
pp. 883-897 ◽  
Author(s):  
Shao-Chen Sun ◽  
Nam-Hyung Kim
Keyword(s):  
Cell Division ◽  
Molecular Mechanisms ◽  
Asymmetric Cell Division ◽  
Polar Body ◽  
Asymmetric Division ◽  
Small Gtpases ◽  
Cortical Reorganization ◽  
Actin Dynamics ◽  
Mammalian Oocyte ◽  
Pubmed Database

AbstractIn contrast to symmetric division in mitosis, mammalian oocyte maturation is characterized by asymmetric cell division that produces a large egg and a small polar body. The asymmetry results from oocyte polarization, which includes spindle positioning, migration, and cortical reorganization, and this process is critical for fertilization and the retention of maternal components for early embryo development. Although actin dynamics are involved in this process, the molecular mechanism underlying this remained unclear until the use of confocal microscopy and live cell imaging became widespread in recent years. Information obtained through a PubMed database search of all articles published in English between 2000 and 2012 that included the phrases “oocyte, actin, spindle migration,” “oocyte, actin, polar body,” or “oocyte, actin, asymmetric division” was reviewed. The actin nucleation factor actin-related protein 2/3 complex and its nucleation-promoting factors, formins and Spire, and regulators such as small GTPases, partitioning-defective/protein kinase C, Fyn, microRNAs, cis-Golgi apparatus components, myosin/myosin light-chain kinase, spindle stability regulators, and spindle assembly checkpoint regulators, play critical roles in asymmetric cell division in oocytes. This review summarizes recent findings on these actin-related regulators in mammalian oocyte asymmetric division and outlines a complete signaling pathway.

Sign in / Sign up

Export Citation Format

Share Document