A ‘Dynamic Adder Model’ For Cell Size Homeostasis in Dictyostelium Cells

2021 ◽  
Author(s):  
Masahito Tanaka ◽  
Shigehiko Yumura
Keyword(s):  
Cell Surface ◽  
Surface Area ◽  
Cell Size ◽  
Surface Membrane ◽  
Total Cell ◽  
Membrane Turnover ◽  
Cell Surface Area ◽  
Daughter Cells ◽  
A Cell ◽  
Original Size

Abstract After a cell divides into two daughter cells, the total cell surface area of the daughtercells should increase to the original size to maintain cell size homeostasis in a single cellcycle. Previously, three models have been proposed to explain the regulation of cell sizehomeostasis: sizer, timer, and adder models. Here, we precisely measured the total cellsurface area of Dictyostelium cells in a whole cell cycle by using the agar-overlaymethod, which eliminated the influence of surface membrane reservoirs, such asmicrovilli and membrane winkles. The total cell surface area linearly increased duringinterphase, slightly decreased at the metaphase, and then increased by approximately20% during cytokinesis. From the analysis of the added surface area, we concluded thatthe cell size was regulated by the near-adder model in interphase and by the timer modelin the mitotic phase. The adder model in the interphase is not caused by a simple cellmembrane addition, but is more dynamic due to the rapid cell membrane turnover. Wepropose a ‘dynamic adder model’ to explain cell size homeostasis in the interphase.

scholarly journals Regulation of the Total Cell Surface Area in Dividing Dictyostelium Cells

2020 ◽  
Vol 8 ◽  
Author(s):  
Masahito Tanaka ◽  
Koushiro Fujimoto ◽  
Shigehiko Yumura
Keyword(s):  
Cell Surface ◽  
Surface Area ◽  
Total Cell ◽  
Cell Surface Area

scholarly journals MiR-26a-5p inhibits GSK3β expression and promotes cardiac hypertrophy in vitro

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e10371
Author(s):  
Liqun Tang ◽  
Jianhong Xie ◽  
Xiaoqin Yu ◽  
Yangyang Zheng
Keyword(s):  
Cell Surface ◽  
Cardiac Hypertrophy ◽  
Surface Area ◽  
Myocardial Cell ◽  
Immunofluorescence Staining ◽  
Cell Surface Area ◽  
Direct Target

Background The role of miR-26a-5p expression in cardiac hypertrophy remains unclear. Herein, the effect of miR-26a-5p on cardiac hypertrophy was investigated using phenylephrine (PE)-induced cardiac hypertrophy in vitro and in a rat model of hypertension-induced hypertrophy in vivo. Methods The PE-induced cardiac hypertrophy models in vitro and vivo were established. To investigate the effect of miR-26a-5p activation on autophagy, the protein expression of autophagosome marker (LC3) and p62 was detected by western blot analysis. To explore the effect of miR-26a-5p activation on cardiac hypertrophy, the relative mRNA expression of cardiac hypertrophy related mark GSK3β was detected by qRT-PCR in vitro and vivo. In addition, immunofluorescence staining was used to detect cardiac hypertrophy related mark α-actinin. The cell surface area was measured by immunofluorescence staining. The direct target relationship between miR-26a-5p and GSK3β was confirmed by dual luciferase report. Results MiR-26a-5p was highly expressed in PE-induced cardiac hypertrophy. MiR-26a-5p promoted LC3II and decreased p62 expression in PE-induced cardiac hypertrophy in the presence or absence of lysosomal inhibitor. Furthermore, miR-26a-5p significantly inhibited GSK3β expression in vitro and in vivo. Dual luciferase report results confirmed that miR-26a-5p could directly target GSK3β. GSK3β overexpression significantly reversed the expression of cardiac hypertrophy-related markers including ANP, ACTA1 and MYH7. Immunofluorescence staining results demonstrated that miR-26a-5p promoted cardiac hypertrophy related protein α-actinin expression, and increased cell surface area in vitro and in vivo. Conclusion Our study revealed that miR-26a-5p promotes myocardial cell autophagy activation and cardiac hypertrophy by regulating GSK3β, which needs further research.

scholarly journals Ca2+-activated cleavage of ezrin visualised dynamically in living myeloid cells during cell surface area expansion

2020 ◽  
Vol 133 (5) ◽  
pp. jcs236968 ◽  
Author(s):  
Rhiannon E. Roberts ◽  
Marianne Martin ◽  
Sabrina Marion ◽  
Geetha L. Elumalai ◽  
Kimberly Lewis ◽  
...  
Keyword(s):  
Cell Surface ◽  
Surface Area ◽  
Myeloid Cells ◽  
Cell Surface Area ◽  
Area Expansion

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.

scholarly journals Abnormalities in the mechanical properties of red blood cells caused by Plasmodium falciparum

Blood ◽  
1989 ◽  
Vol 74 (2) ◽  
pp. 855-861 ◽  
Author(s):  
GB Nash ◽  
E O'Brien ◽  
EC Gordon-Smith ◽  
JA Dormandy
Keyword(s):  
Mechanical Properties ◽  
Plasmodium Falciparum ◽  
Cell Surface ◽  
Surface Area ◽  
Volume Ratio ◽  
Great Difficulty ◽  
Cell Entry ◽  
Cell Surface Area ◽  
Entry Time ◽  
Main Factor

Abstract Although changes in the mechanical properties of infected red cells may contribute to the pathophysiology of malaria, such changes have not previously been described in detail. In this study, the physical properties of individual cells from both clinical and cultured samples infected with Plasmodium falciparum were tested using micropipette aspiration techniques. Cells containing ring forms took about 50% longer to enter 3 microns pipettes compared with nonparasitised cells, and there was a similar increase in the critical pressure required to induce cell entry. These abnormalities were similar in clinical and cultured samples. More mature cultured parasites (ie, trophozoites and schizonts containing pigment) caused much greater loss of deformability, with entry time and pressure increased four to sixfold. The decrease in deformability of the ring forms was attributable to a deficit in cell surface area/volume ratio (based on micropipette measurement of the surface area and volume of individual cells) and slight stiffening of the cell membrane (shear elastic modulus increased 13%, as measured by pipette aspiration of small membrane tongues). Measurement of the rate of cell shape recovery indicated that the membrane of parasitised cells was not more viscous. The main factor in the drastic loss of deformability of the trophozoites and schizonts was the presence of the large very resistant parasite itself. Otherwise, the cell surface area/volume deficit was slightly less and membrane rigidification slightly greater compared with ring forms. The above abnormalities should cause the trophozoites and schizonts to have great difficulty in traversing splenic or marrow sinuses and could contribute to microvascular occlusion and sequestration. On the other hand, the ring forms may be expected to circulate relatively unhindered.

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