Cell size increased in tissues from transgenic mice overexpressing a cell surface growth-related and cancer-specific hydroquinone oxidase, tNOX, with protein disulfide-thiol interchange activity

2008 ◽  
Vol 105 (6) ◽  
pp. 1437-1442 ◽  
Author(s):  
Kader Yagiz ◽  
Paul W. Snyder ◽  
D. James Morré ◽  
Dorothy M. Morré
Keyword(s):  
Cell Surface ◽  
Transgenic Mice ◽  
Cell Size ◽  
Surface Growth ◽  
A Cell ◽  
Hydroquinone Oxidase ◽  
Protein Disulfide

scholarly journals Cdk1-dependent control of membrane-trafficking dynamics

2012 ◽  
Vol 23 (17) ◽  
pp. 3336-3347 ◽  
Author(s):  
Derek McCusker ◽  
Anne Royou ◽  
Christophe Velours ◽  
Douglas Kellogg
Keyword(s):  
Cell Growth ◽  
Cell Surface ◽  
Membrane Trafficking ◽  
Cell Cycle Progression ◽  
Secretory Pathway ◽  
Surface Growth ◽  
Growth Defect ◽  
Actin Depolymerization ◽  
Polarized Cell Growth ◽  
A Cell

Cyclin-dependent kinase 1 (Cdk1) is required for initiation and maintenance of polarized cell growth in budding yeast. Cdk1 activates Rho-family GTPases, which polarize the actin cytoskeleton for delivery of membrane to growth sites via the secretory pathway. Here we investigate whether Cdk1 plays additional roles in the initiation and maintenance of polarized cell growth. We find that inhibition of Cdk1 causes a cell surface growth defect that is as severe as that caused by actin depolymerization. However, unlike actin depolymerization, Cdk1 inhibition does not result in a massive accumulation of intracellular secretory vesicles or their cargoes. Analysis of post-Golgi vesicle dynamics after Cdk1 inhibition demonstrates that exocytic vesicles are rapidly mistargeted away from the growing bud, possibly to the endomembrane/vacuolar system. Inhibition of Cdk1 also causes defects in the organization of endocytic and exocytic zones at the site of growth. Cdk1 thus modulates membrane-trafficking dynamics, which is likely to play an important role in coordinating cell surface growth with cell cycle progression.

scholarly journals Localized secretion of acid phosphatase reflects the pattern of cell surface growth in saccharomyces cerevisiae

1980 ◽  
Vol 86 (1) ◽  
pp. 123-128 ◽  
Author(s):  
C Field ◽  
R Schekman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Acid Phosphatase ◽  
Cell Surface ◽  
Mating Type ◽  
Surface Growth ◽  
Parent Cell ◽  
Limited Growth ◽  
Yeast Cell Surface ◽  
Dividing Cells ◽  
A Cell

Secretion of cell wall-bound acid phosphatase by Saccharomyces cerevisiae occurs along a restricted portion of the cell surface. Acid phosphatase activity produced during derepressed synthesis on a phosphate-limited growth medium is detected with an enzyme-specific stain and is localized initially to the bud portion of a dividing cell. After two to three generations of phosphate-limited growth, most of the cells can be stained; if further phosphatase synthesis is repressed by growth in excess phosphate, dividing cells are produced in which the parent but not the bud can be stained. Budding growth is interrupted in α-mating-type cells by a pheromone (α-factor) secreted by the opposite mating type; cell surface growth continues in the presence of α-factor and produces a characteristic cell tip. When acid phosphatase synthesis is initiated during α-factor treatment, only the cell tip can br stained; when phosphate synthesis is repressed during α-factor treatment, the cell body but not the tip can be stained. A mixture of derepressed α cells and phosphatase-negative α cells form zygotes in which mainly one parent cell surface can be stained. The cell cycle mutant, cdc 24 (Hartwell, L.H. 1971. Exp. Cell Res. 69:265-276), fails to bud and, instead, expands symmetrically as a sphere at a nonpermissive temperature (37 degrees C). This mutant does not form a cell tip during α-factor treatment at 37 degrees C, and although acid phosphatade secretion occurs at this temperature, it is not localized. These results suggest that secretion reflects a polar mode of yeast cell- surface growth, and that this organization requires the cdc 24 gene product.

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.

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.

Emulsion flow which preparation excludes a presence of mechanical impurities

2012 ◽  
Vol 9 (2) ◽  
pp. 118-122
Author(s):  
A.A. Rakhimov
Keyword(s):  
Cell Size ◽  
First Case ◽  
A Cell ◽  
Emulsion Flow ◽  
Blocking Mechanism

Experiments were carried out with waterhydrocarbon emulsions with various emulsifiers in capillaries with a length of 2 cm, diameters of 40 and 100 µm. To eliminate the influence of mechanical impurities comparable in size with the diameter of the capillary in first case emulsion components were filtered through fine-meshed filters. In second case obtained that way emulsion was additionally filtered through a system consisting of 3 filters with a cell size of 30-40 microns. In a capillary of 100 µm such emulsion came in a blocked state. Additional filtration of the emulsion through the mesh filters have led to an increase in viscosity but in 100 µm capillaries the time until the blocking 2-3 times more than the original. Rheology of used emulsions is well described by the model of Ostwald-de Waale. It was determined that emulsion blocking mechanism is due to the presence of inclusions not emulsion viscosity.

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