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At least 163 records · Page 9Linked to original sources
PubMed1981

Electron microscopic studies on cell-sized bilayer liposomes.

Cell-sized bilayer liposomes have been visualized directly in the electron microscope by a thin section method. Fixation in lanthanum nitrate plus potassium permanganate has made this visualization possible. Trilamellar images were seen in thin sections of the fixed liposomes; measurements made from microdensitometer tracings revealed a thickness (peak-to-peak distance) ranging from 25.3 to 55.3 A. The mean peak-to-peak distance of 35.6 +/- 8.2 A (+/- S.D.) was in good agreement with the value obtained by Robertson from typical myelin figures.

Liposomes↗
PubMed2003

Correlation between cell size and CD38 expression in chronic lymphocytic leukaemia.

Both CD38 expression and increased cell size are features of B-lymphocyte activation and have been implicated as adverse prognostic factors in B-cell chronic lymphocytic leukaemia (CLL). We therefore examined the relationship between these two variables by FACS analysis in 140 consecutive CLL patients. Using the mean forward-angle light scatter (FSC) as a measure of cell size, circulating B lymphocytes were found to be significantly larger in "CD38-positive" cases (those in which the antigen was expressed in at least 20% of the malignant cells) as compared with "CD38-negative" patients (p = 0.029). Furthermore, within individual cases B lymphocytes expressing CD38 were, on average, significantly larger than cells that did not express the antigen (p < 0.0001). Finally, when B lymphocytes of individual "CD38-positive" cases were arbitrarily divided into large and small subpopulations using their mean FSC as a cut-off, CD38 was found to be more frequently expressed on the larger cells (p < 0.0001). This strong positive correlation between CD38 expression and cell size implicates cell activation as a possible underlying determinant of both tumour-cell phenotype and clinical outcome in CLL.

ADP-ribosyl Cyclase↗
PubMed1977

Fat cell size and blood lactate in humans.

Twelve patients randomly selected as regards obesity were investigated. Morphological fat tissue parameters (size and number of adipose cells) were measured together with metabolic parameters in blood (K-value, fasting glucose, lactate, triglyceride, and free fatty acids). A high, positive correlation (0.86) between blood lactate and fat cell size was found. Also serum triglyceride and fat cell size showed a positive correlation (0.64). No correlations were found between fat cell number and the measured metabolic parameters.

Adipose Tissue↗
PubMed1980

Insulin binding and hexose transport in rat adipocytes. Relation to cell size.

Insulin binding, initial velocity of [14C]methylglucose transport, uptake of [14C]deoxyglucose and conversion of [U-14C]glucose to CO2, glyceride-glycerol and fatty acids were measured at 37 degrees C in adipocytes from rats of different weights (135-450 g) and therefore with different mean cell volumes (53-389 pl). Insulin binding per cell increased with increasing cell size and binding was 2.3 times higher in the largest cells than in the smallest cells with tracer alone. The difference was largely accounted for by an increase in the apparent affinity. Influx of methylglucose per cell increased with increasing cell size in the absence of insulin and remained constant as a function of cell size in its presence. The effect of insulin ranged from 11 fold in small cells to 3.5 fold in large cells. The rat of conversion of [U-14C]glucose to CO2 and lipids was about half of the rate of methylglucose transport under all conditions. In contrast, the uptake of deoxyglucose in insulin-stimulated cells decreased markedly with increasing cell size. Increasing cell size caused a small decrease in sensitivity which could be explained by a smaller amont of insulin bound per unit surface area. The results show that increasing cell size/animal weight causes changes in insulin binding which may explain changes in sensitivity. In addition, the hexose transport system is modified in a way which is not explained by changes in insulin binding. Finally, changes in deoxyglucose uptake with cell size do not parallel changes in methylglucose transport.

Adipose Tissue↗
PubMed2004

A dominant negative mutant of cyclin-dependent kinase A reduces endoreduplication but not cell size or gene expression in maize endosperm.

Cells in maize (Zea mays) endosperm undergo multiple cycles of endoreduplication, with some attaining DNA contents as high as 96C and 192C. Genome amplification begins around 10 d after pollination, coincident with cell enlargement and the onset of starch and storage protein accumulation. Although the role of endoreduplication is unclear, it is thought to provide a mechanism that increases cell size and enhances gene expression. To investigate this process, we reduced endoreduplication in transgenic maize endosperm by ectopically expressing a gene encoding a dominant negative mutant form of cyclin-dependent kinase A. This gene was regulated by the 27-kD gamma-zein promoter, which restricted synthesis of the defective enzyme to the endoreduplication rather than the mitotic phase of endosperm development. Overexpression of a wild-type cyclin-dependent kinase A increased enzyme activity but had no effect on endoreduplication. By contrast, ectopic expression of the defective enzyme lowered kinase activity and reduced by half the mean C-value and total DNA content of endosperm nuclei. The lower level of endoreduplication did not affect cell size and only slightly reduced starch and storage protein accumulation. There was little difference in the level of endosperm gene expression with high and low levels of endoreduplication, suggesting that this process may not enhance transcription of genes associated with starch and storage protein synthesis.

Cell Cycle↗
PubMed1980

Development of basal lipolysis and fat cell size in the epididymal fat pad of normal rats.

The normal development of adipose tissue lipolysis as measured by glycerol release was studied in epididymal fat pads of fed and fasted Sprague-Dawley rats between 15 and 128 days of age and correlated with changes in fat cell size. At 15 and 17 days of age, when fat cell size was small, glycerol release per cell was highest and decreased steadily to adult levels by 73 days of age. Between 85 and 128 days of age as fat cell size continued to increase, glycerol release per cell began to rise. Therefore, glycerol release per cell inversely correlated with fat cell size during early development and directly correlated with fat cell size after 73 days of age. The response to fasting was variable in the younger rats but was established by the third postnatal week. The possible early reciprocal and later complementary roles of lipolytic activity and lipoprotein lipase activity in the "setting" and regulation of fat cell size during postnatal adipose tissue development is discussed.

Adipose Tissue↗
PubMed2004

Growth rate and cell size modulate the synthesis of, and requirement for, G1-phase cyclins at start.

In Saccharomyces cerevisiae, commitment to cell cycle progression occurs at Start. Progression past Start requires cell growth and protein synthesis, a minimum cell size, and G(1)-phase cyclins. We examined the relationships among these factors. Rapidly growing cells expressed, and required, dramatically more Cln protein than did slowly growing cells. To clarify the role of cell size, we expressed defined amounts of CLN mRNA in cells of different sizes. When Cln was expressed at nearly physiological levels, a critical threshold of Cln expression was required for cell cycle progression, and this critical threshold varied with both cell size and growth rate: as cells grew larger, they needed less CLN mRNA, but as cells grew faster, they needed more Cln protein. At least in part, large cells had a reduced requirement for CLN mRNA because large cells generated more Cln protein per unit of mRNA than did small cells. When Cln was overexpressed, it was capable of promoting Start rapidly, regardless of cell size or growth rate. In summary, the amount of Cln required for Start depends dramatically on both cell size and growth rate. Large cells generate more Cln1 or Cln2 protein for a given amount of CLN mRNA, suggesting the existence of a novel posttranscriptional size control mechanism.

Blotting, Western↗
PubMed2003

Conservation of mechanisms controlling entry into mitosis: budding yeast wee1 delays entry into mitosis and is required for cell size control.

BACKGROUND: In fission yeast, the Wee1 kinase delays entry into mitosis until a critical cell size has been reached; however, a similar role for Wee1-related kinases has not been reported in other organisms. SWE1, the budding yeast homolog of wee1, is thought to function in a morphogenesis checkpoint that delays entry into mitosis in response to defects in bud morphogenesis. RESULTS: In contrast to previous studies, we found that budding yeast swe1 Delta cells undergo premature entry into mitosis, leading to birth of abnormally small cells. Additional experiments suggest that conditions that activate the morphogenesis checkpoint may actually be activating a G2/M cell size checkpoint. For example, actin depolymerization is thought to activate the morphogenesis checkpoint by inhibiting bud morphogenesis. However, actin depolymerization also inhibits bud growth, suggesting that it could activate a cell size checkpoint. Consistent with this possibility, we found that actin depolymerization fails to induce a G2/M delay once daughter buds pass a critical size. Other conditions that activate the morphogenesis checkpoint block bud formation, which could also activate a size checkpoint if cell size at G2/M is monitored in the daughter bud. Previous work reported that Swe1 is degraded during G2, which was proposed to account for failure of large-budded cells to arrest in response to actin depolymerization. However, we found that Swe1 is present throughout G2 and undergoes hyperphosphorylation as cells enter mitosis, as found in other organisms. CONCLUSIONS: Our results suggest that the mechanisms known to coordinate entry into mitosis in other organisms have been conserved in budding yeast.

Blotting, Western↗
PubMed1979

Relationship between lipolysis, cyclic AMP, and fat-cell size in human adipose tissue during fasting and in diabetes mellitus.

The in vitro relationship between fat-cell size, glycerol release, and peak concentration of cyclic AMP was investigated in human adipose tissue obtained from 25 obese nondiabetic patients before and after a 7-day fast and from 23 patients with untreated diabetes mellitus. In the obese nondiabetic patients there was a linear correlation between fat-cell size and cyclic AMP concentration, and fat-cell size and the rate of lipolysis. This was found both in nonfasting and fasting nondiabetic patients. However, in diabetes mellitus, there was only a relationship between cell size and cyclic AMP concentration. The alpha-adrenergic and beta-adrenergic activity in human adipose tissue was assessed by comparing the effect of isoprenaline and noradrenaline on the cyclic AMP concentration. The activity of both receptors was found to be increased in fasting obese patients and in diabetics. In both conditions the alpha-adrenergic response to catecholamines predominated in small fat cells, whereas in large ones the beta response predominated. The results suggest that during fasting and in diabetes mellitus there is a correlation between fat-cell size and the responsiveness of the adrenergic receptors. Thus, catecholamines may be involved in regulating the fat-cell volume. The view is expressed that the abnormal catecholamine-induced lipolysis is solely due to changes at the level of the adrenergic receptors during fasting, whereas in diabetes mellitus the sequentional activation of lipolysis is disturbed at deeper sites as well.

Adipose Tissue↗
PubMed2002

Checking cell size in yeast.

To remain viable, cells have to coordinate cell growth with cell division. In yeast, this occurs at two control points: the boundaries between G1 and S phases, also known as Start, and between G2 and M phases. Theoretically, coordination can be achieved by independent regulation of growth and division, or by participation of surveillance mechanisms in which cell size feeds back into cell-cycle control. This article discusses recent advances in the identification of sizing mechanisms in budding and in fission yeast, and how these mechanisms integrate with environmental stimuli. A comparison of the G1-S and G2-M size-control modules in the two species reveals a degree of conservation higher than previously thought. This reinforces the notion that internal sizing could be a conserved feature of cell-cycle control throughout eukaryotes.

Cell Cycle↗
PubMed2004

Clinal variation in body and cell size in a widely distributed vertebrate ectotherm.

Bergmann's rule states that, among conspecific populations, individuals are larger in cooler than in warmer environments as a consequence of selection related to heat conservation. Many of the most comprehensive assessments of Bergmann's rule to date have examined clinal patterns in body size among species assemblages. Our study is a more direct test of Bergmann's rule because we examine the pattern within a single, widely distributed species. We examined geographic variation in body and cell size in the spotted turtle ( Clemmys guttata). Our analysis of 818 turtles collected from the entire range (45-28 degrees N), indicated that body size increased with latitude; however, the relationship was driven by a population of large turtles at the northern extreme of the species' range. When the northern population was removed from the analyses, Bergmann's rule was not supported, and the smallest turtles occurred near the central part of the species' distribution. Recent literature has suggested that latitudinal clines in body size may simply be a physiological byproduct of the effects of temperature on cell division, resulting in larger cells, and hence larger organisms, from cooler temperatures. Measurements of the diameter of skin cells did not support the hypothesis that cell size increases with latitude and decreases with temperature in the spotted turtle, nor was there a significant relationship between body size and cell size. Our study suggests that neither Bergmann's rule nor cell size variation sufficiently explain the body size cline observed in the spotted turtle. We hypothesize that patterns in body size are related to variation in female size at maturity and reproductive cycles.

Animals↗
PubMed2003

Heterotrimeric G proteins regulate daughter cell size asymmetry in Drosophila neuroblast divisions.

Cell division often generates unequally sized daughter cells by off-center cleavages, which are due to either displacement of mitotic spindles or their asymmetry. Drosophila neuroblasts predominantly use the latter mechanism to divide into a large apical neuroblast and a small basal ganglion mother cell (GMC), where the neural fate determinants segregate. Apically localized components regulate both the spindle asymmetry and the localization of the determinants. Here, we show that asymmetric spindle formation depends on signaling mediated by the G beta subunit of heterotrimeric G proteins. G beta 13F distributes throughout the neuroblast cortex. Its lack induces a large symmetric spindle and causes division into nearly equal-sized cells with normal segregation of the determinants. In contrast, elevated G beta 13F activity generates a small spindle, suggesting that this factor suppresses spindle development. Depletion of the apical components also results in the formation of a small symmetric spindle at metaphase. Therefore, the apical components and G beta 13F affect the mitotic spindle shape oppositely. We propose that differential activation of G beta signaling biases spindle development within neuroblasts and thereby causes asymmetric spindles. Furthermore, the multiple equal cleavages of G beta mutant neuroblasts accompany neural defects; this finding suggests indispensable roles of eccentric division in assuring the stem cell properties of neuroblasts.

Animals↗
PubMed2004

Cell size and water permeability as determining factors for cell viability after freezing at different cooling rates.

This work studied the viabilities of five types of cells (two yeast cells, Saccharomyces cerevisiae CBS 1171 and Candida utilis; two bacterial strains, Escherichia coli and Lactobacillus plantarum; and one human leukemia K562 cell) as a function of cooling rate during freezing. The range of investigated cooling rates extended from 5 to 30,000 degrees C/min. Cell viability was classified into three ranges: (i) high viability for low cooling rates (5 to 180 degrees C/min), which allow cell water outflow to occur completely and do not allow any intracellular crystallization; (ii) low viability for rapid cooling rates (180 to 5,000 degrees C/min), which allow the heat flow to prevail over water outflow (in this case, cell water crystallization would occur as water was flowing out of the cell); (iii) high viability for very high cooling rates (>5,000 degrees C/min), which allow the heat flow to be very rapid and induce intracellular crystallization and/or vitrification before any water outflow from the cell. Finally, an assumption relating cell death to the cell water crystallization as water is flowing out of the cell is made. In addition, this general cell behavior is different for each type of cell and seems to be moderated by the cell size, the water permeability properties, and the presence of a cell wall.

Candida↗
PubMed1985

The distributions of cell size and generation time in a model of the cell cycle incorporating size control and random transitions.

A deterministic/probabilistic model of the cell division cycle is analysed mathematically and compared to experimental data and to other models of the cell cycle. The model posits a random-exiting phase of the cell cycle and a minimum-size requirement for entry into the random-exiting phase. By design, the model predicts exponential "beta-curves", which are characteristic of sister cell generation times. We show that the model predicts "alpha-curves" with exponential tails and hyperbolic-sine-like shoulders, and that these curves fit observed generation-time data excellently. We also calculate correlation coefficients for sister cells and for mother-daughter pairs. These correlation coefficients are more negative than is generally observed, which is characteristic of all size-control models and is generally attributed to some unknown positive correlation in growth rates of related cells. Next we compare theoretical size distributions with observed distributions, and we calculate the dependence of average cell mass on specific growth rate and show that this dependence agrees with a well-known relation in bacteria. In the discussion we argue that unequal division is probably not the source of stochastic fluctuations in deterministic size-control models, transition-probability models with no feedback from cell size cannot account for the rapidity with which the new, stable size distribution is established after perturbation, and Kubitschek's rate-normal model is not consistent with exponential beta-curves.

Bacteria↗
PubMedDate not supplied

Some physical parameters controlling cell size during the evolution of the procaryons.

Possible factors controlling cell size during the evolution of unicellular organisms have been examined. It has been shown that considerations of osmotic and membrane pressure eqilibria will predict minimal cell sizes which are in good agreement with those found in present day microorganisms. It has also been shown that the possibility of random proton 'noise' would not be a limiting factor for even the smallest organisms or structures. Maximum cell size would be governed by the requirements of diffusion and transport within the cell.

Bacteria↗
PubMed1979

Adipose cell size in spontaneously hypertensive rats (SHR).

The size of adipose cells in spontaneously hypertensive rats (SHR) and normotensive controls has been evaluated at 4, 8 and 26 weeks of age. Age-matched groups showed significant differences only in 8-week-old rats, but this can be explained by the lower body weight of SHR. In both groups of animals fat cell size varies with body weight (r = 0.965 in SHR and r = 0.863 in normotensive rats) independent of the stage of hypertension. The regression lines are not significantly different. Thus, no evidence of enlarged adipocytes in SHR has been obtained.

Adipose Tissue↗
PubMed1976

Adipose tissue cell size and lipolysis in the rat: response to exercise intensity and food restriction.

This experiment was designed to determine if the adaptive increase in adipose tissue epinephrine-stimulated lipolysis (ESL) observed in exercise trained rats is related to decreased adipocyte size or a direct response to exercise. Two levels of treadmill exercise and three levels of food restriction were imposed on male rats over a 12 week experimental period to create a distribution of adipose tissue cell sizes. Epinephrine-stimulated lipolysis was subsequently measured in the isolated adipocytes from rats trained at two different exercise levels and in untrained rats fed either ad libitum or 16%, 27%, or 35% dietary restriction. Energy restriction was effective in reducing body weight and to some extent epididymal fat pad weight; however, adipocyte size and number were not significantly affected. Exercise in both groups of trained rats was effective in reducing adipocyte size; however, cell size did not differ between training groups. The group receiving the greatest amount of daily exercise had significantly greater ESL indicating that the adaptive increase in lipolytic potential seen in adipose tissue of exercise trained rats is a true metabolic adaptation not secondary to reduced cell size.

Adipose Tissue↗
PubMed1993

Both isoforms of protein phosphatase Z are essential for the maintenance of cell size and integrity in Saccharomyces cerevisiae in response to osmotic stress.

The sequences of two genes encoding the protein-serine/threonine-phosphatases PPZ1 and PPZ2 from Saccharomyces cerevisiae have been determined. The molecular masses of PPZ1 and PPZ2 are 77.5 and 78.5 kDa, respectively, and each protein consists of two distinct domains. The C-terminal half of each molecule is 93% identical in PPZ1 and PPZ2, and comprises the protein-phosphatase catalytic domain, while the N-terminal halves, which are rich in serine and asparagine (PPZ1) or serine and arginine (PPZ2), are only 43% identical. Both N-termini start with the amino acids Met-Gly-Asn, suggesting that after removal of the initiating methionine, the N-terminal glycine of the mature protein is myristoylated. Disruption of the gene encoding either PPZ1 or PPZ2 leads to an increase in cell size and cell lysis, the latter being more pronounced in cells disrupted in PPZ1. Haploid cells carrying a double disruption of PPZ1 and PPZ2 genes also show a marked increase in cell size and cell lysis, which can be significantly reduced by the addition of 1 M sorbitol to the growth medium. These results suggest that PPZ1 and PPZ2 play a role in regulating osmotic stability.

Alleles↗