scholarly journals Asymmetry and Aging of Mycobacterial Cells Lead to Variable Growth and Antibiotic Susceptibility

Science ◽  
2011 ◽  
Vol 335 (6064) ◽  
pp. 100-104 ◽  
Author(s):  
Bree B. Aldridge ◽  
Marta Fernandez-Suarez ◽  
Danielle Heller ◽  
Vijay Ambravaneswaran ◽  
Daniel Irimia ◽  
...  
Keyword(s):  
Cell Division ◽  
Environmental Stress ◽  
Cell Size ◽  
Antibiotic Susceptibility ◽  
Mother Cell ◽  
Elongation Rate ◽  
Cell Heterogeneity ◽  
Clonal Population ◽  
Daughter Cells ◽  
Asymmetric Growth

Cells use both deterministic and stochastic mechanisms to generate cell-to-cell heterogeneity, which enables the population to better withstand environmental stress. Here we show that, within a clonal population of mycobacteria, there is deterministic heterogeneity in elongation rate that arises because mycobacteria grow in an unusual, unipolar fashion. Division of the asymmetrically growing mother cell gives rise to daughter cells that differ in elongation rate and size. Because the mycobacterial cell division cycle is governed by time, not cell size, rapidly elongating cells do not divide more frequently than slowly elongating cells. The physiologically distinct subpopulations of cells that arise through asymmetric growth and division are differentially susceptible to clinically important classes of antibiotics.

scholarly journals A new class of cyclin dependent kinase in Chlamydomonas is required for coupling cell size to cell division

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Yubing Li ◽  
Dianyi Liu ◽  
Cristina López-Paz ◽  
Bradley JSC Olson ◽  
James G Umen
Keyword(s):  
Cell Division ◽  
Cell Size ◽  
Mother Cell ◽  
Size Control ◽  
Mitotic Division ◽  
General Mechanism ◽  
Cell Cycle Regulators ◽  
Proliferating Cells ◽  
Multiple Fission ◽  
Division Number

Proliferating cells actively control their size by mechanisms that are poorly understood. The unicellular green alga Chlamydomonas reinhardtii divides by multiple fission, wherein a ‘counting’ mechanism couples mother cell-size to cell division number allowing production of uniform-sized daughters. We identified a sizer protein, CDKG1, that acts through the retinoblastoma (RB) tumor suppressor pathway as a D-cyclin-dependent RB kinase to regulate mitotic counting. Loss of CDKG1 leads to fewer mitotic divisions and large daughters, while mis-expression of CDKG1 causes supernumerous mitotic divisions and small daughters. The concentration of nuclear-localized CDKG1 in pre-mitotic cells is set by mother cell size, and its progressive dilution and degradation with each round of cell division may provide a link between mother cell-size and mitotic division number. Cell-size-dependent accumulation of limiting cell cycle regulators such as CDKG1 is a potentially general mechanism for size control.

Relative daughter cell volume and position of the division furrow in Tetrahymena

1983 ◽  
Vol 61 (1) ◽  
pp. 273-287
Author(s):  
K.K. Hjelm
Keyword(s):  
Cell Division ◽  
Cell Surface ◽  
Cell Volume ◽  
Mother Cell ◽  
Daughter Cell ◽  
Tetrahymena Pyriformis ◽  
Posterior Pole ◽  
Live Cells ◽  
Final Position ◽  
Daughter Cells

The relative daughter cell volume (RDCV) values for Tetrahymena pyriformis were determined at division on live cells. It was found that the anterior cell is generally larger than the posterior cell, and that the RDCV values are distributed in groups 5–6% apart. The RDCV value was found to be independent of predivision cell volume, indicating that the mother cell is divided into proportional volumes. The cells seem, however, not to assess volume directly but rather a parameter related to the cell volume. Furthermore, the RDCV value was found to increase during cell division, so that the final value is not reached until actual separation of daughter cells. It is suggested that the division furrow is positioned so that the area of the cell surface lying between the old oral apparatus and the posterior pole of the cell is divided into equal parts. It is further suggested that several alternative values of the RDCV are possible, only one of which is expressed in each cell. The early division furrow is placed anteriorly to its final position, and its location is adjusted during cytokinesis.

Cell Volume and the Control of the Chlamydomonas Cell Cycle

1982 ◽  
Vol 54 (1) ◽  
pp. 173-191 ◽  
Author(s):  
R. A. CRAIGIE ◽  
T. CAVALIER-SMITH
Keyword(s):  
Cell Cycle ◽  
Cell Wall ◽  
Cell Division ◽  
Simple Model ◽  
Cell Volume ◽  
Mother Cell ◽  
Dark Period ◽  
Size Fractions ◽  
Daughter Cells ◽  
Mother Cell Wall

Chlamydomonas reinhardii divides by multiple fission to produce 2n daughter cells per division burst, where n is an integer. By separating predivision cells from synchronous cultures into fractions of differing mean cell volumes, and electronically measuring the numbers and volume distributions of the daughter cells produced by the subsequent division burst, we have shown that n is determined by the volume of the parent cell. Control of n can occur simply, if after every cell division the daughter cells monitor their volume and divide again if, and only if, their volume is greater than a fixed minimum value. In cultures synchronized by 12-h light/12-h dark cycles, the larger parent cells divide earlier in the dark period than do smaller cells. This has been shown by two independent methods: (1) by separating cells into different size fractions by Percoll density-gradient centrifugation and using the light microscope to see when they divide; and (2) by studying changes in the cell volume distribution of unfractioned cultures. Since daughter cells remain within the mother-cell wall for some hours after cell division, and cell division causes an overall swelling of the mother-cell wall, the timing of division can be determined electronically by measuring this increase in cell volume that occurs in the dark period in the absence of growth; we find that cells at the large end of the size distribution range undergo this swelling first, and are then followed by successively smaller size fractions. A simple model embodying a sizer followed by a timer gives a good quantitative fit to these data for 12-h light/12-h dark cycles if cell division occurs 12-h after attaining a critical volume of approximately 140 μm3. However, this simple model is called into question by our finding that alterations in the length of the light period alter the rate of progress towards division even of cells that have attained their critical volume. We discuss the relative roles of light and cell volume in the control of division timing in the Chlamydomonas cell cycle.

scholarly journals Asymmetric localization of the cell division machinery during Bacillus subtilis sporulation

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Kanika Khanna ◽  
Javier Lopez Garrido ◽  
Joseph Sugie ◽  
Kit Pogliano ◽  
Elizabeth Villa
Keyword(s):  
Bacillus Subtilis ◽  
Cell Division ◽  
Mother Cell ◽  
Electron Tomography ◽  
Leading Edge ◽  
Specific Protein ◽  
Bacterial Cell Division ◽  
Daughter Cells ◽  
Septal Thickness ◽  
Cryo Electron Tomography

The Gram-positive bacterium Bacillus subtilis can divide via two modes. During vegetative growth, the division septum is formed at the midcell to produce two equal daughter cells. However, during sporulation, the division septum is formed closer to one pole to yield a smaller forespore and a larger mother cell. Using cryo-electron tomography, genetics and fluorescence microscopy, we found that the organization of the division machinery is different in the two septa. While FtsAZ filaments, the major orchestrators of bacterial cell division, are present uniformly around the leading edge of the invaginating vegetative septa, they are only present on the mother cell side of the invaginating sporulation septa. We provide evidence suggesting that the different distribution and number of FtsAZ filaments impact septal thickness, causing vegetative septa to be thicker than sporulation septa already during constriction. Finally, we show that a sporulation-specific protein, SpoIIE, regulates asymmetric divisome localization and septal thickness during sporulation.

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 A Spatiotemporal Molecular Switch Governs Plant Asymmetric Cell Division

2020 ◽  
Author(s):  
Xiaoyu Guo ◽  
Chan Ho Park ◽  
Zhi-Yong Wang ◽  
Bryce E. Nickels ◽  
Juan Dong
Keyword(s):  
Cell Division ◽  
Cell Fate ◽  
Mother Cell ◽  
Asymmetric Cell Division ◽  
Molecular Switch ◽  
Cell Fate Determination ◽  
Stomatal Development ◽  
Division Plane ◽  
Daughter Cells ◽  
Commitment To Cell Division

SummaryAsymmetric cell division (ACD) often requires protein polarization in the mother cell to produce daughter cells with distinct identities (“cell-fate asymmetry”). Here, we define a previously undocumented mechanism for establishing cell-fate asymmetry in Arabidopsis stomatal stem cells. In particular, we show that polarization of BSL protein phosphatases promotes stomatal ACD by establishing a “kinase-based signaling asymmetry” in the two daughter cells. BSL polarization in the stomatal ACD mother cell is triggered upon commitment to cell division. Polarized BSL is inherited by the differentiating daughter cell where it suppresses cell division and promotes cell-fate determination. Plants lacking BSL exhibit stomatal over-proliferation, demonstrating BSL plays an essential role in stomatal development. Our findings establish that BSL polarization provides a spatiotemporal molecular switch that enables cell-fate asymmetry in stomatal ACD daughter cells. We propose BSL polarization is triggered by an ACD “checkpoint” in the mother cell that monitors establishment of division-plane asymmetry.

scholarly journals Comparing Cell Division- and Cell Reproduction-based Cell Lineage Analysis for Early Embryogenesis of Caenorhabditis elegans

2017 ◽  
Author(s):  
Shi V. Liu
Keyword(s):  
Cell Division ◽  
Caenorhabditis Elegans ◽  
Mother Cell ◽  
Cell Lineage ◽  
Early Embryogenesis ◽  
Reconstruction Method ◽  
Daughter Cells ◽  
Cell Reproduction ◽  
A Cell ◽  
Lineage Analysis

ABSTRACTCell lineage analysis holds important stakes for understanding heredity and cell differentiation. Conventional cell lineages are reconstructed according to a cell division doctrine of one mother cell dividing into two daughter cells. An alternative cell lineage reconstruction method followed a cell reproduction discovery of multiple daughter cells reproduced from a same mother cell. To see which reconstruction method reflects reality of early embryogenesis of Caenorhabditis elegans, a side-by-side comparison was made between two methods. Here I show cell division-based lineage distorted reality and failed in revealing any true genealogy. Cell reproduction – based lineage conformed to reality with exact same number of cells in every developmental stage under examination and showed clear genealogical relationship. A paradigm-shift from cell division-to cell reproduction-based cell lineage analysis is necessary for correct understanding of developmental biology and will lead to a revolution in cell biology and life science.

scholarly journals A Mutation in the ATP2 Gene Abrogates the Age Asymmetry Between Mother and Daughter Cells of the Yeast Saccharomyces cerevisiae

Genetics ◽  
2002 ◽  
Vol 162 (1) ◽  
pp. 73-87 ◽  
Author(s):  
Chi-Yung Lai ◽  
Ewa Jaruga ◽  
Corina Borghouts ◽  
S Michal Jazwinski
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Division ◽  
Life Span ◽  
Mother Cell ◽  
Yeast Cells ◽  
Mitochondrial Morphology ◽  
Temperature Sensitive ◽  
Yeast Saccharomyces Cerevisiae ◽  
Daughter Cells ◽  
Mother And Daughter

Abstract The yeast Saccharomyces cerevisiae reproduces by asymmetric cell division, or budding. In each cell division, the daughter cell is usually smaller and younger than the mother cell, as defined by the number of divisions it can potentially complete before it dies. Although individual yeast cells have a limited life span, this age asymmetry between mother and daughter ensures that the yeast strain remains immortal. To understand the mechanisms underlying age asymmetry, we have isolated temperature-sensitive mutants that have limited growth capacity. One of these clonal-senescence mutants was in ATP2, the gene encoding the β-subunit of mitochondrial F1, F0-ATPase. A point mutation in this gene caused a valine-to-isoleucine substitution at the ninetieth amino acid of the mature polypeptide. This mutation did not affect the growth rate on a nonfermentable carbon source. Life-span determinations following temperature shift-down showed that the clonal-senescence phenotype results from a loss of age asymmetry at 36°, such that daughters are born old. It was characterized by a loss of mitochondrial membrane potential followed by the lack of proper segregation of active mitochondria to daughter cells. This was associated with a change in mitochondrial morphology and distribution in the mother cell and ultimately resulted in the generation of cells totally lacking mitochondria. The results indicate that segregation of active mitochondria to daughter cells is important for maintenance of age asymmetry and raise the possibility that mitochondrial dysfunction may be a normal cause of aging. The finding that dysfunctional mitochondria accumulated in yeasts as they aged and the propensity for old mother cells to produce daughters depleted of active mitochondria lend support to this notion. We propose, more generally, that age asymmetry depends on partition of active and undamaged cellular components to the progeny and that this “filter” breaks down with age.

Stimulated Virus Production in Vinblastine and Cytochalasin-Induced Multinucleate Cells

1970 ◽  
Vol 28 ◽  
pp. 186-187
Author(s):  
Krishan Awtar
Keyword(s):  
Cell Division ◽  
Normal Cell ◽  
Virus Production ◽  
Multinucleate Cells ◽  
Daughter Cells ◽  
Cell Divisions ◽  
Nuclear Membranes ◽  
Division 2 ◽  
Vinblastine Sulfate

Exposure of cells to low sublethal but mitosis-arresting doses of vinblastine sulfate (Velban) results in the initial arrest of cells in mitosis followed by their subsequent return to an “interphase“-like stage. A large number of these cells reform their nuclear membranes and form large multimicronucleated cells, some containing as many as 25 or more micronuclei (1). Formation of large multinucleate cells is also caused by cytochalasin, by causing the fusion of daughter cells at the end of an otherwise .normal cell division (2). By the repetition of this process through subsequent cell divisions, large cells with 6 or more nuclei are formed.

scholarly journals Interdependent YpsA- and YfhS-Mediated Cell Division and Cell Size Phenotypes in Bacillus subtilis

mSphere ◽  
2020 ◽  
Vol 5 (4) ◽  
Author(s):  
Robert S. Brzozowski ◽  
Brooke R. Tomlinson ◽  
Michael D. Sacco ◽  
Judy J. Chen ◽  
Anika N. Ali ◽  
...  
Keyword(s):  
Bacillus Subtilis ◽  
Cell Division ◽  
Cell Size ◽  
Unknown Function ◽  
Suppressor Mutation ◽  
Gram Positive ◽  
Content Type ◽  
Suppressor Mutations ◽  
Extragenic Suppressor ◽  
Cell Division Inhibition

ABSTRACT Although many bacterial cell division factors have been uncovered over the years, evidence from recent studies points to the existence of yet-to-be-discovered factors involved in cell division regulation. Thus, it is important to identify factors and conditions that regulate cell division to obtain a better understanding of this fundamental biological process. We recently reported that in the Gram-positive organisms Bacillus subtilis and Staphylococcus aureus, increased production of YpsA resulted in cell division inhibition. In this study, we isolated spontaneous suppressor mutations to uncover critical residues of YpsA and the pathways through which YpsA may exert its function. Using this technique, we were able to isolate four unique intragenic suppressor mutations in ypsA (E55D, P79L, R111P, and G132E) that rendered the mutated YpsA nontoxic upon overproduction. We also isolated an extragenic suppressor mutation in yfhS, a gene that encodes a protein of unknown function. Subsequent analysis confirmed that cells lacking yfhS were unable to undergo filamentation in response to YpsA overproduction. We also serendipitously discovered that YfhS may play a role in cell size regulation. Finally, we provide evidence showing a mechanistic link between YpsA and YfhS. IMPORTANCE Bacillus subtilis is a rod-shaped Gram-positive model organism. The factors fundamental to the maintenance of cell shape and cell division are of major interest. We show that increased expression of ypsA results in cell division inhibition and impairment of colony formation on solid medium. Colonies that do arise possess compensatory suppressor mutations. We have isolated multiple intragenic (within ypsA) mutants and an extragenic suppressor mutant. Further analysis of the extragenic suppressor mutation led to a protein of unknown function, YfhS, which appears to play a role in regulating cell size. In addition to confirming that the cell division phenotype associated with YpsA is disrupted in a yfhS-null strain, we also discovered that the cell size phenotype of the yfhS knockout mutant is abolished in a strain that also lacks ypsA. This highlights a potential mechanistic link between these two proteins; however, the underlying molecular mechanism remains to be elucidated.

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