Ultrastructural aspect of size dependent regulation of surface pattern of complex ciliary organelle in a protozoan ciliate

Development ◽  
1980 ◽  
Vol 59 (1) ◽  
pp. 355-375
Author(s):  
Julita Bąkowska ◽  
Maria Jerka-Dziadosz
Keyword(s):  
Pattern Formation ◽  
Cell Size ◽  
Small Cells ◽  
Surface Pattern ◽  
Ventral Part ◽  
Normal Cells ◽  
Ultrastructural Aspect ◽  
Size Dependent

A regulation is shown for size and number of the elements of complex ciliary structures forming the oral apparatus (OA) of a ciliate Paraurostyla weissei. Morphometric investigations were performed on oral ciliature of normal and size-reduced cells. Those constituents of the OA which exist as single structures, such as the inner and outer preoral membranelles, are not eliminated. Both shorten and the outer membranelle becomes narrower. Within the adornal zone of membranelles in size-reduced cells some frontal and ventral membranelles become eliminated, whereas the respective ratio of these types remains size invariant. In each individual adoral zone of membranelles there are membranelles of different length specificially located along the ventral part. Membranelles from small cells are significantly smaller than those of normal cells. The number of kinetosomes is reduced in all four rows constructing an adoral membranelle. The analysis showed that regardless of cell size, the number of kinetosomes in the two inner rows of a membranelle is linearly and proportionately related. Regulation of the size of all components of the oral ciliature in P. weissei occurs at the time when the primordia of oral ciliature are formed. The results are discussed in relation to recent ideas about pattern formation and size dependent regulation of the number and size of pattern elements.

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 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 Cell size–dependent regulation of Wee1 localization by Cdr2 cortical nodes

2018 ◽  
Vol 217 (5) ◽  
pp. 1589-1599 ◽  
Author(s):  
Corey A.H. Allard ◽  
Hannah E. Opalko ◽  
Ko-Wei Liu ◽  
Uche Medoh ◽  
James B. Moseley
Keyword(s):  
Cell Growth ◽  
Cell Size ◽  
Total Internal Reflection ◽  
Kinase Activity ◽  
Size Control ◽  
Small Cells ◽  
Mitotic Entry ◽  
Size Dependent ◽  
N Terminus ◽  
Biochemical Fractionation

Cell 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 total internal reflection fluorescence microscopy videos, 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 caused in part by 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.

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 Histocytology of Lymphoid Tumors in the Dog, Cat and Cow

1981 ◽  
Vol 18 (4) ◽  
pp. 494-512 ◽  
Author(s):  
V. E. Valli ◽  
B. J. Mcsherry ◽  
B. M. Dunham ◽  
R. M. Jacobs ◽  
J. H. Lumsden
Keyword(s):  
Retrospective Study ◽  
Cell Size ◽  
Cell Tumor ◽  
Small Cells ◽  
Age At Death ◽  
Biological Behaviour ◽  
Tumor Types

In a retrospective study of lymphomas in animals, tumors in 72 dogs, 81 cats and 90 cows were classified on the basis of cell size (small, medium and large), nuclear cleavage (follicular center cells), and histologic architecture (nodular or diffuse). Each subtype was classified by age of animal at death, number of metastases, breed, and sex. As in man, nodular cleaved tumors are rare in animals, the cow having the most varied tumor types. There was one cleaved-cell tumor in 72 lymphomas in dogs, 23 of 81 in cats, and 33 of 90 in cows. There were six nodular tumors of 72 in dogs, two of 81 in cats, and eight of 90 in cows. Fifteen of 16 nodular lymphomas had noncleaved cells and twelve had small or predominantly small cells. Cats with nodular lymphomas were older at death than cats with diffuse lymphomas. Nodularity was not associated with greater age at death in dogs and cows. Animals with cleaved-cell lymphomas were older at death than those with noncleaved tumors; this difference was highly significant in cows. The number of metastases was greater with nodular tumors in all three species, and was equal in cleaved and noncleaved tumors. The biological behaviour of lymphoid tumors in animals is similar to those in man when the same criteria of classification are used.

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.

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