Faculty Opinions recommendation of Myosin concentration underlies cell size-dependent scalability of actomyosin ring constriction.

2016 ◽  
Author(s):  
Meritxell Riquelme
Keyword(s):  
Cell Size ◽  
Size Dependent ◽  
Ring Constriction

Spindle scaling mechanisms

2020 ◽  
Vol 64 (2) ◽  
pp. 383-396
Author(s):  
Lara K. Krüger ◽  
Phong T. Tran
Keyword(s):  
Cell Size ◽  
Spindle Assembly ◽  
Dependent Manner ◽  
Post Translational Modification ◽  
Size Dependent ◽  
A Cell ◽  
Chromosome Separation ◽  
Spindle Elongation ◽  
Protein Gradients ◽  
Spindle Structure

Abstract The mitotic spindle robustly scales with cell size in a plethora of different organisms. During development and throughout evolution, the spindle adjusts to cell size in metazoans and yeast in order to ensure faithful chromosome separation. Spindle adjustment to cell size occurs by the scaling of spindle length, spindle shape and the velocity of spindle assembly and elongation. Different mechanisms, depending on spindle structure and organism, account for these scaling relationships. The limited availability of critical spindle components, protein gradients, sequestration of spindle components, or post-translational modification and differential expression levels have been implicated in the regulation of spindle length and the spindle assembly/elongation velocity in a cell size-dependent manner. In this review, we will discuss the phenomenon and mechanisms of spindle length, spindle shape and spindle elongation velocity scaling with cell size.

scholarly journals Large cells activate global protein degradation to maintain cell size homeostasis

2021 ◽  
Author(s):  
Shixuan Liu ◽  
Ceryl Tan ◽  
Chloe Melo-Gavin ◽  
Kevin G. Mark ◽  
Miriam Bracha Ginzberg ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Protein Synthesis ◽  
Protein Degradation ◽  
Cell Size ◽  
Cell Cycle Progression ◽  
Mapk Pathway ◽  
Cellular Growth ◽  
Small Cells ◽  
Animal Cells ◽  
Size Dependent

Proliferating animal cells maintain a stable size distribution over generations despite fluctuations in cell growth and division size. This tight control of cell size involves both cell size checkpoints (e.g., delaying cell cycle progression for small cells) and size-dependent compensation in rates of mass accumulation (e.g., slowdown of cellular growth in large cells). We previously identified that the mammalian cell size checkpoint is mediated by a selective activation of the p38 MAPK pathway in small cells. However, mechanisms underlying the size-dependent compensation of cellular growth remain unknown. In this study, we quantified global rates of protein synthesis and degradation in naturally large and small cells, as well as in conditions that trigger a size-dependent compensation in cellular growth. Rates of protein synthesis increase proportionally with cell size in both perturbed and unperturbed conditions, as well as across cell cycle stages. Additionally, large cells exhibit elevated rates of global protein degradation and increased levels of activated proteasomes. Conditions that trigger a large-size-induced slowdown of cellular growth also promote proteasome-mediated global protein degradation, which initiates only after growth rate compensation occurs. Interestingly, the elevated rates of global protein degradation in large cells were disproportionately higher than the increase in size, suggesting activation of protein degradation pathways. Large cells at the G1/S transition show hyperactivated levels of protein degradation, even higher than similarly sized or larger cells in S or G2, coinciding with the timing of the most stringent size control in animal cells. Together, these findings suggest that large cells maintain cell size homeostasis by activating global protein degradation to induce a compensatory slowdown of growth.

The expected population size in a cell-size-dependent branching process

1981 ◽  
Vol 18 (01) ◽  
pp. 65-75 ◽  
Author(s):  
Aidan Sudbury
Keyword(s):  
Cell Size ◽  
Exponential Growth ◽  
Branching Process ◽  
Expected Number ◽  
Size Dependent ◽  
Daughter Cells ◽  
Rate Of Increase ◽  
A Cell ◽  
Dependent Growth ◽  
Number Of Cells

In cell-size-dependent growth the probabilistic rate of division of a cell into daughter-cells and the rate of increase of its size depend on its size. In this paper the expected number of cells in the population at time t is calculated for a variety of models, and it is shown that population growths slower and faster than exponential are both possible. When the cell sizes are bounded conditions are given for exponential growth.

Some results for general cell-size-dependent branching processes

1973 ◽  
Vol 10 (2) ◽  
pp. 289-298 ◽  
Author(s):  
Aidan Sudbury ◽  
Peter Clifford
Keyword(s):  
Growth Rate ◽  
Cell Size ◽  
Wide Class ◽  
General Model ◽  
Branching Processes ◽  
Size Dependent ◽  
Sister Cells

A general model for the growth and division of cells in which the growth rate and division probability at any instant depend only on their size at that time is introduced. Conditions under which (a) the distribution of cell-size at division converges ergodically, (b) the sizes tend to 0 or ∞, are exhibited, and bounds to the correlation between the sizes at division of sister cells are given in a wide class of cases.

scholarly journals Modelling sediment clasts transport during landscape evolution

2015 ◽  
Vol 3 (4) ◽  
pp. 1221-1254 ◽  
Author(s):  
S. Carretier ◽  
P. Martinod ◽  
M. Reich ◽  
Y. Godderis
Keyword(s):  
Cell Size ◽  
Landscape Evolution ◽  
Transport Rate ◽  
Time Step ◽  
Size Dependent ◽  
Scattering Rate ◽  
Local Erosion ◽  
Model Cell ◽  
Scattering Time ◽  
Grain Properties

Abstract. Over thousands to millions of years, the landscape evolution is predicted by models based on fluxes of eroded, transported and deposited material. The laws describing these fluxes, corresponding to averages over many years, are difficult to prove with the available data. On the other hand, sediment dynamics are often tackled by studying the distribution of certain grain properties in the field (e.g. heavy metals, detrial zircons, 10Be in gravel, magnetic tracers, etc.). There is a gap between landscape evolution models based on fluxes and these field data on individual clasts, which prevent the latter from being used to calibrate the former. Here we propose an algorithm coupling the landscape evolution with mobile clasts. Our landscape evolution model predicts local erosion, deposition and transfer fluxes resulting from hillslope and river processes. Clasts of any size are initially spread in the basement and are detached, moved and deposited according to probabilities using these fluxes. Several river and hillslope laws are studied. Although the resulting mean transport rate of the clasts does not depend on the time step or the model cell size, our approach is limited by the fact that their scattering rate is cell-size dependent. Nevertheless, both their mean transport rate and the shape of the scattering-time curves fit the predictions. Different erosion-transport laws generate different clast movements. These differences show that studying the tracers in the field may provide a way to establish these laws on the hillslopes and in the rivers. Possible applications include the interpretation of cosmogenic nuclides in individual gravel deposits, provenance analyses, placers, sediment coarsening or fining, the relationship between magnetic tracers in rivers and the river planform, and the tracing of weathered sediment.

scholarly journals Cell size-dependent regulation of Wee1 localization by Cdr2 cortical nodes

2017 ◽  
Author(s):  
Corey A. H. Allard ◽  
Hannah E. Opalko ◽  
Ko-Wei Liu ◽  
Uche Medoh ◽  
James B. Moseley
Keyword(s):  
Cell Growth ◽  
Fission Yeast ◽  
Cell Size ◽  
Kinase Activity ◽  
Size Control ◽  
Small Cells ◽  
Mitotic Entry ◽  
Size Dependent ◽  
Biochemical Fractionation ◽  
Mitotic Inhibitor

AbstractCell size control requires mechanisms that link cell growth with Cdk1 activity. In fission yeast, the protein kinase Cdr2 forms cortical nodes that include the Cdk1 inhibitor Wee1, along with the Wee1-inhibitory kinase Cdr1. We investigated how nodes inhibit Wee1 during cell growth. Biochemical fractionation revealed that Cdr2 nodes were megadalton structures enriched for activated Cdr2, which increases in level during interphase growth. In live-cell TIRF movies, Cdr2 and Cdr1 remained constant at nodes over time, but Wee1 localized to nodes in short bursts. Recruitment of Wee1 to nodes required Cdr2 kinase activity and the noncatalytic N-terminus of Wee1. Bursts of Wee1 localization to nodes increased 20-fold as cells doubled in size throughout G2. Size-dependent signaling was due in part to the Cdr2 inhibitor Pom1, which suppressed Wee1 node bursts in small cells. Thus, increasing Cdr2 activity during cell growth promotes Wee1 localization to nodes, where inhibitory phosphorylation of Wee1 by Cdr1 and Cdr2 kinases promotes mitotic entry.SummaryCells turn off the mitotic inhibitor Wee1 to enter into mitosis. This study shows how cell growth progressively inhibits fission yeast Wee1 through dynamic bursts of localization to cortical node structures that contain Wee1 inhibitory kinases.

scholarly journals Hybrid systems approach to modeling stochastic dynamics of cell size

2016 ◽  
Author(s):  
Cesar Augusto Vargas-Garcia ◽  
Abhyudai Singh
Keyword(s):  
Growth Rate ◽  
Cell Size ◽  
Size Variation ◽  
Model Parameters ◽  
Constant Growth Rate ◽  
Division Rate ◽  
Size Dependent ◽  
Daughter Cells ◽  
Constant Growth ◽  
Over Time

A ubiquitous feature of all living cells is their growth over time followed by division into two daughter cells. How a population of genetically identical cells maintains size homeostasis, i.e., a narrow distribution of cell size, is an intriguing fundamental problem. We model size using a stochastic hybrid system, where a cell grows exponentially over time and probabilistic division events are triggered at discrete time intervals. Moreover, whenever these events occur, size is randomly partitioned among daughter cells. We first consider a scenario, where a timer (i.e., cell-cycle clock) that measures the time since the last division event regulates cellular growth and the rate of cell division. Analysis reveals that such a timer-driven system cannot achieve size homeostasis, in the sense that, the cell-to-cell size variation grows unboundedly with time. To explore biologically meaningful mechanisms for controlling size we consider three different classes of models: i) a size-dependent growth rate and timer-dependent division rate; ii) a constant growth rate and size-dependent division rate and iii) a constant growth rate and division rate that depends both on the cell size and timer. We show that each of these strategies can potentially achieve bounded intercellular size variation, and derive closed-form expressions for this variation in terms of underlying model parameters. Finally, we discuss how different organisms have adopted the above strategies for maintaining cell size homeostasis.

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