Cell Cycle, Cell Size Regulation

2013 ◽  
pp. 343-346 ◽  
Author(s):  
Ákos Sveiczer ◽  
Anna Rácz-Mónus
Keyword(s):  
Cell Cycle ◽  
Cell Size ◽  
Size Regulation

Cell cycle and cell size regulation in Down Syndrome cells

2003 ◽  
pp. 51-58 ◽  
Author(s):  
M. Rosner ◽  
A. Kowalska ◽  
A. Freilinger ◽  
A-R. Prusa ◽  
E. Marton ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Down Syndrome ◽  
Cell Size ◽  
Size Regulation

scholarly journals Molecular Analysis of Fruit Size Regulation in Apple

HortScience ◽  
2004 ◽  
Vol 39 (4) ◽  
pp. 868C-868
Author(s):  
Anish Malladi* ◽  
Peter Hirst
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Size ◽  
Fruit Size ◽  
Cell Number ◽  
Size Analysis ◽  
Cell Cycle Gene ◽  
Cell Cycle Regulators ◽  
Size Regulation ◽  
Molecular Aspects

Fruit size is a commercially valuable trait. Although several factors are known to affect fruit size in apple, insights into the molecular aspects of its regulation are lacking. Our research aims to understand fruit size regulation using a combination of approaches. Analysis of a large fruited mutant of `Gala', `Grand Gala' (GG), showed that it was 40% heavier than `Gala' at harvest. Increase in size of GG fruit was caused by an increase in the cell size apparent at full bloom. Flow cytometry revealed the presence of multiple levels of ploidy (up to 16C) in GG during early fruit development. Increase in ploidy of GG is hypothesized to be due to endoreduplication, a process normally absent in apple. Endoreduplication is a modification of the cell cycle where DNA replication is not followed by cell division, resulting in increased DNA content accompanied by increased cell size. To understand if the cell cycle is altered in GG, four key cell cycle regulators, MdCDKA1, MdCDKB1, MdCYCB2 and MdCYCD3 have been partially cloned from apple using RT-PCR and RACE. As cell number at the end of the cell division phase is correlated with fruit size at harvest, expression analysis of these genes can provide valuable insights into their role in the regulation of cell number and fruit size. Analysis of cell cycle gene expression in GG may provide key insights into the altered molecular regulation that leads to endoreduplication in the mutant. Parallel approaches being employed to study whether environmental and cultural factors regulate fruit size through an influence on the cell cycle will also be discussed.

scholarly journals Cell size and growth regulation in theArabidopsis thalianaapical stem cell niche

2016 ◽  
Vol 113 (51) ◽  
pp. E8238-E8246 ◽  
Author(s):  
Lisa Willis ◽  
Yassin Refahi ◽  
Raymond Wightman ◽  
Benoit Landrein ◽  
José Teles ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Size ◽  
Growth Regulation ◽  
Critical Size ◽  
Single Cells ◽  
Growth Control ◽  
Fixed Time ◽  
Cell Contact ◽  
Size Regulation ◽  
4D Imaging

Cell size and growth kinetics are fundamental cellular properties with important physiological implications. Classical studies on yeast, and recently on bacteria, have identified rules for cell size regulation in single cells, but in the more complex environment of multicellular tissues, data have been lacking. In this study, to characterize cell size and growth regulation in a multicellular context, we developed a 4D imaging pipeline and applied it to track and quantify epidermal cells over 3–4 d inArabidopsis thalianashoot apical meristems. We found that a cell size checkpoint is not the trigger for G2/M or cytokinesis, refuting the unexamined assumption that meristematic cells trigger cell cycle phases upon reaching a critical size. Our data also rule out models in which cells undergo G2/M at a fixed time after birth, or by adding a critical size increment between G2/M transitions. Rather, cell size regulation was intermediate between the critical size and critical increment paradigms, meaning that cell size fluctuations decay by ∼75% in one generation compared with 100% (critical size) and 50% (critical increment). Notably, this behavior was independent of local cell–cell contact topologies and of position within the tissue. Cells grew exponentially throughout the first >80% of the cell cycle, but following an asymmetrical division, the small daughter grew at a faster exponential rate than the large daughter, an observation that potentially challenges present models of growth regulation. These growth and division behaviors place strong constraints on quantitative mechanistic descriptions of the cell cycle and growth control.

scholarly journals The cell cycle-associated protein kinase WEE1 regulates cell size in relation to endoreduplication in developing tomato fruit

2007 ◽  
Vol 51 (4) ◽  
pp. 642-655 ◽  
Author(s):  
Nathalie Gonzalez ◽  
Frédéric Gévaudant ◽  
Michel Hernould ◽  
Christian Chevalier ◽  
Armand Mouras
Keyword(s):  
Cell Cycle ◽  
Protein Kinase ◽  
Cell Size ◽  
Tomato Fruit

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.

scholarly journals Cell growth dilutes the cell cycle inhibitor Rb to trigger cell division

2018 ◽  
Author(s):  
Evgeny Zatulovskiy ◽  
Daniel F. Berenson ◽  
Benjamin R. Topacio ◽  
Jan M. Skotheim
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Growth ◽  
Cell Size ◽  
Mammalian Cells ◽  
Molecular Mechanisms ◽  
Inverse Correlation ◽  
Cell Types ◽  
Similar Amount ◽  
Cell Cycle Inhibitor

Cell size is fundamental to function in different cell types across the human body because it sets the scale of organelle structures, biosynthesis, and surface transport1,2. Tiny erythrocytes squeeze through capillaries to transport oxygen, while the million-fold larger oocyte divides without growth to form the ~100 cell pre-implantation embryo. Despite the vast size range across cell types, cells of a given type are typically uniform in size likely because cells are able to accurately couple cell growth to division3–6. While some genes whose disruption in mammalian cells affects cell size have been identified, the molecular mechanisms through which cell growth drives cell division have remained elusive7–12. Here, we show that cell growth acts to dilute the cell cycle inhibitor Rb to drive cell cycle progression from G1 to S phase in human cells. In contrast, other G1/S regulators remained at nearly constant concentration. Rb is a stable protein that is synthesized during S and G2 phases in an amount that is independent of cell size. Equal partitioning to daughter cells of chromatin bound Rb then ensures that all cells at birth inherit a similar amount of Rb protein. RB overexpression increased cell size in tissue culture and a mouse cancer model, while RB deletion decreased cell size and removed the inverse correlation between cell size at birth and the duration of G1 phase. Thus, Rb-dilution by cell growth in G1 provides a long-sought cell autonomous molecular mechanism for cell size homeostasis.

scholarly journals Size uniformity of animal cells is actively maintained by a p38 MAPK-dependent regulation of G1-length

2017 ◽  
Author(s):  
Shixuan Liu ◽  
Miriam B. Ginzberg ◽  
Nish Patel ◽  
Marc Hild ◽  
Bosco Leung ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Size ◽  
P38 Mapk ◽  
Cell Cycle Progression ◽  
Molecular Mechanisms ◽  
Mapk Pathway ◽  
Small Cells ◽  
Animal Cells ◽  
Cycle Progression ◽  
Size Uniformity

AbstractAnimal cells within a tissue typically display a striking regularity in their size. To date, the molecular mechanisms that control this uniformity are still unknown. We have previously shown that size uniformity in animal cells is promoted, in part, by size-dependent regulation of G1 length. To identify the molecular mechanisms underlying this process, we performed a large-scale small molecule screen and found that the p38 MAPK pathway is involved in coordinating cell size and cell cycle progression. Small cells display higher p38 activity and spend more time in G1 than larger cells. Inhibition of p38 MAPK leads to loss of the compensatory G1 length extension in small cells, resulting in faster proliferation, smaller cell size and increased size heterogeneity. We propose a model wherein the p38 pathway responds to changes in cell size and regulates G1 exit accordingly, to increase cell size uniformity.One-sentence summaryThe p38 MAP kinase pathway coordinates cell growth and cell cycle progression by lengthening G1 in small cells, allowing them more time to grow before their next division.

scholarly journals Single-Cell Analysis of the Impact of Host Cell Heterogeneity on Infection with Foot-and-Mouth Disease Virus

2018 ◽  
Vol 92 (9) ◽  
pp. e00179-18 ◽  
Author(s):  
Xiu Xin ◽  
Hailong Wang ◽  
Lingling Han ◽  
Mingzhen Wang ◽  
Hui Fang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Single Cell ◽  
Host Cell ◽  
Cell Size ◽  
Single Cell Analysis ◽  
Foot And Mouth Disease ◽  
Cell Analysis ◽  
Cell Heterogeneity ◽  
Mouth Disease Virus ◽  
Foot And Mouth

ABSTRACTViral infection and replication are affected by host cell heterogeneity, but the mechanisms underlying the effects remain unclear. Using single-cell analysis, we investigated the effects of host cell heterogeneity, including cell size, inclusion, and cell cycle, on foot-and-mouth disease virus (FMDV) infection (acute and persistent infections) and replication. We detected various viral genome replication levels in FMDV-infected cells. Large cells and cells with a high number of inclusions generated more viral RNA copies and viral protein and a higher proportion of infectious cells than other cells. Additionally, we found that the viral titer was 10- to 100-fold higher in cells in G2/M than those in other cell cycle phases and identified a strong correlation between cell size, inclusion, and cell cycle heterogeneity, which all affected the infection and replication of FMDV. Furthermore, we demonstrated that host cell heterogeneity influenced the adsorption of FMDV due to differences in the levels of FMDV integrin receptors expression. Collectively, these results further our understanding of the evolution of a virus in a single host cell.IMPORTANCEIt is important to understand how host cell heterogeneity affects viral infection and replication. Using single-cell analysis, we found that viral genome replication levels exhibited dramatic variability in foot-and-mouth disease virus (FMDV)-infected cells. We also found a strong correlation between heterogeneity in cell size, inclusion number, and cell cycle status and that all of these characteristics affect the infection and replication of FMDV. Moreover, we found that host cell heterogeneity influenced the viral adsorption as differences in the levels of FMDV integrin receptors' expression. This study provided new ideas for the studies of correlation between FMDV infection mechanisms and host cells.

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