scholarly journals The effect of partial protein synthesis inhibition on cell proliferation in higher plants

1985 ◽  
Vol 76 (1) ◽  
pp. 97-104
Author(s):  
A. Cuadrado ◽  
M.H. Navarrete ◽  
J.L. Canovas
Keyword(s):  
Cell Cycle ◽  
Protein Synthesis ◽  
Steady State ◽  
Dna Synthesis ◽  
Higher Plants ◽  
Cell Mass ◽  
Small Cells ◽  
Average Cell ◽  
State Growth ◽  
S Period

Meristematic cells from Allium cepa L. roots can attain a steady state of growth in the presence of anisomycin at concentrations that effectively reduce the rate of protein synthesis. Under these conditions the lengths of cell cycle periods increase but not in the same proportion as the generation time (t). Mitosis is hardly affected and S period is slightly lengthened. G2 increases less in proportion to t, while G1 is extended much higher in proportion to t. Natural synchronous populations have been used to study cell cycle parameters during transition from the physiological steady state to the new one created by the presence of the drug. G2 was the same during transition as during steady-state growth. G1 was much shorter during transition. Average cell mass at division was reduced, and a negative correlation was observed between the length of G2 and the size of the cell at termination of DNA synthesis. We propose that in higher plants, G2 length is regulated by cell mass at completion of DNA synthesis (G2 being shorter in big cells than in small cells), though there is no cell size requirement for mitosis.

scholarly journals CHANGES IN THE DNA SYNTHESIS PATTERN OF PARAMECIUM WITH INCREASED CLONAL AGE AND INTERFISSION TIME

1974 ◽  
Vol 61 (3) ◽  
pp. 591-598 ◽  
Author(s):  
Joan Smith-Sonneborn ◽  
Michael Klass
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Unicellular Organism ◽  
Time Intervals ◽  
Synchronized Cells ◽  
Different Ages ◽  
Self Fertilization ◽  
Autoradiographic Analysis ◽  
S Period ◽  
First Time

The clonal age in paramecia refers to the total number of vegetative divisions a clone has undergone since its origin at autogamy (self-fertilization). As clonal age increases, the interfission time usually increases. The DNA synthesis pattern of cells of different ages was compared by autoradiographic analysis of the DNA synthesis of synchronized cells at various time intervals during the cell cycle (from one division to the next). The study showed that the G1 period (the lag in DNA synthesis post division) was constant, irrespective of interfission time or clonal age; but the duration of the DNA synthesis period increased with increased interfission time or clonal age. Therefore, we have shown for the first time that the G1 period is fixed, and the S period is increased in a eukaryotic unicellular organism as a function of interfission time and clonal age.

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.

CELLULAR GROWTH HORMONES, NUTRITION, AND TIME

PEDIATRICS ◽  
1968 ◽  
Vol 41 (1) ◽  
pp. 30-46
Author(s):  
Donald B. Cheek
Keyword(s):  
Growth Hormone ◽  
Body Composition ◽  
Body Weight ◽  
Protein Synthesis ◽  
Steady State ◽  
Cell Growth ◽  
Cell Mass ◽  
Cell Number ◽  
Fat Cells ◽  
Number Of Cells

For many years the study of growth has rested mainly on the application of anthropometric techniques and the measurement of height and weight. A few years ago Tanner9 correctly pointed out that studies on body composition were mainly related to body weight and, therefore, added little to the thinking. A more penetrating approach to the study of growth was recommended.2 The present approach,11 documented in part here, has been to apply biochemical and physiological techniques for the measurement of body cell mass, cell size, cell number and, to some extent, cell function. Body function and heat production as well as maturational age have been of concern. These studies have been made in the same children at tile same time. It is anticipated that inspection of these three dimensions of growth, size, function, and maturational age should help to elucidate problems related to growth retardation. In the clinic it is possible to predict cell-extracellular mass of children by applying equations based on relationships between body composition and height and weight. We began by presenting information on growth of muscle and the differences between the sexes with the progress of time and with respect to size and number of cells. Increments in growth rate of the male at adolescence were found. Such differences in cell growth must be related to some extent to the restrictive action of estrogens on cell multiplication in the female and to the stimulating action of androgens in the male. Growth hormone is an important hormone for the multiplication of cells, while insulin is of importance to protein synthesis. Both hormones are needed for growth. Thyroid hormone appears to play a secondary role but is important to protein synthesis especially in early postnatal life. The energy requirement for normal growth is only slightly above the basal state and the visceral cell mass is the most direct standard of reference for heat production. Restriction of nutrition can either retard growth in the size of cells, in the number of cells, or both. Current studies58 show that ingestion of protein and calories incite the secretion of growth hormone and insulin in specific patterns and at appropriate times. Growth hormone has been labelled the "feasting" hormone and insulin tile "feasting" hormone.59 Thus, the subtle relationship between nutrition and cell growth becomes apparent. Of concern is the possibility that overnutrition early in life may program excess secretion of hormones such as insulin or growth hormone. Overnutrition is a major problem in the affluent society, while conservative nutrition is compatible with longevity.6 Hirsch, et al.60 informs us that growth of adipose tissue is mainly by cell number increase–as we have seen for muscle. Again, a steady state of cell number is reached for fat cells. But, obese subjects have an excess of fat cells which do not disappear with time and diet. Such cells become increasingly insensitive to insulin as they enlarge.61 One might view the passing parade of life and growth and observe the relation of the intracellular phase to body weight from infancy to senility (Fig. 12). Here we see the upward increase of cell mass with respect to time and body weight increase. The adult data are taken from F. D. Moore.62 Clearly, with senility we can suspect that more and more of the body weight is extracellular or connective tissue and less and less of the weight is soft tissue or oxidizing protoplasm. Data on body potassium are even more remarkable in this demonstration.11 It is difficult to say with Browning: Grow old along with me! The best is yet to be.... Nevertheless, it is possible that with increased information and research the understanding of these stages of cell growth will be achieved and, no doubt, the departure from the steady state of cell population which occurs at the autumn of our existence– when cancer, and cardiovascular disease supervene–will be understood.63 However, the problems of aging can only be exposed after the physiology of growth is understood.

Regulation of G2 by cell size contributes to maintaining cell size variability within certain limits in higher plants

1987 ◽  
Vol 87 (5) ◽  
pp. 635-641
Author(s):  
M.H. Navarrete ◽  
A. Cuadrado ◽  
M. Escalera ◽  
J.L. Canovas
Keyword(s):  
Steady State ◽  
Dna Replication ◽  
Dna Synthesis ◽  
Surface Area ◽  
Cell Size ◽  
Coefficient Of Variation ◽  
Higher Plants ◽  
Cell Populations ◽  
Cell Area ◽  
Size Variability

The variability of (1) surface area projection (size) at which cells terminate DNA replication, (2) the area at which they initiate mitosis, (3) the area at which they divide, (4) the duration of G2, and (5) the duration of G2 plus mitosis (in fact, prophase + metaphase + anaphase) has been estimated in steady-state cell populations of Allium cepa root meristems. The coefficient of variation of cell area at termination of DNA synthesis was found to be 14% while the coefficient of variation of cell area at mitosis initiation was 13%. As there is also a substantial variability of G2 (the coefficient of variation was estimated to be 38%), the combination of these data indicates that cell size regulation of G2 contributes to maintaining cell size variability (and therefore DNA concentration) within certain limits. Mitosis also varies but less than G2 (the coefficient of variation of G2 + mitosis was found to be 31%). As the coefficient of variation of cell area at division (14%) is hardly larger than the coefficient of variation of cell area at initiation of mitosis, it can be suggested that coordination between cell size and mitosis duration helps to avoid a significant increase in the variability of cell size at the end of the division cycle.

scholarly journals Insulin and TSH promote growth in size of PC Cl3 rat thyroid cells, possibly via a pathway different from DNA synthesis: comparison with FRTL-5 cells

1999 ◽  
pp. 94-103 ◽  
Author(s):  
T Kimura ◽  
JE Dumont ◽  
A Fusco ◽  
J Golstein
Keyword(s):  
Protein Synthesis ◽  
Dna Replication ◽  
Dna Synthesis ◽  
Cell Lines ◽  
Insulin Action ◽  
Cell Mass ◽  
Thyroid Cell ◽  
Thyroid Cells ◽  
Rat Thyroid ◽  
Stimulation Of

In the rat thyroid cell lines PC Cl3, FRTL- 5 and WRT, proliferation is mainly regulated by insulin or IGF, and TSH. However, the mechanism regulating cell mass doubling prior to division is still unknown. Our laboratory has shown that in dog thyroid cells insulin promotes growth in size while TSH in the presence of insulin triggers DNA replication. In the absence of insulin, TSH has no effect on cell growth. In this report we investigated insulin action on both cell mass and DNA synthesis and its modulation by TSH and insulin in PC Cl3 and FRTL-5 cells. In PC Cl3 cells, insulin activated not only DNA synthesis but also protein synthesis and accumulation. Although TSH potentiated the stimulation of DNA synthesis induced by insulin, enhancement of protein synthesis by both agents was additive. All TSH effects were reproduced by forskolin. Similar effects were also obtained in FRTL-5 cells. This suggests that insulin and TSH, via cAMP, modulate both growth in size and DNA replication in these cell lines. Lovastatin, which blocks 3-hydroxy-3-methylglutaryl coenzyme A reductase, decreased the induction of DNA synthesis, but not of protein synthesis induced by insulin or TSH in PC Cl3 cells. In FRTL-5 cells, lovastatin reduced protein and DNA synthesis stimulated by insulin but not TSH-induced protein synthesis. Taking these data together, we propose that insulin and/or TSH both modulate cell mass doubling and DNA synthesis in these cell lines, presumably via different pathways, and that there are at least two pathways which regulate growth in size in FRTL-5 thyroid cells: one triggered by insulin, which is lovastatin sensitive, and the other activated by TSH, which is not sensitive to lovastatin.

scholarly journals Cell cycle-dependent expression of thymidylate synthase in Saccharomyces cerevisiae.

1984 ◽  
Vol 4 (12) ◽  
pp. 2858-2864 ◽  
Author(s):  
R K Storms ◽  
R W Ord ◽  
M T Greenwood ◽  
B Mirdamadi ◽  
F K Chu ◽  
...  
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Dna Synthesis ◽  
Thymidylate Synthase ◽  
S Phase ◽  
Mrna Levels ◽  
Activity Profile ◽  
S Period ◽  
Cycle Dependent ◽  
Specific Mrna

Synchronous populations of Saccharomyces cerevisiae cells, generated by two independent methods, have been used to show that thymidylate synthase, in contrast to the vast majority of cellular proteins thus far examined, fluctuates periodically during the S. cerevisiae cell cycle. The enzyme, as assayed by two different methods, accumulated during S period and peaked in mid to late S phase, and then its level dropped. These observations suggest that both periodic synthesis and the instability of the enzyme contribute to the activity profile seen during the cell cycle. Accumulation of thymidylate synthase is determined at the level of its transcript, with synthase-specific mRNA levels increasing at least 10-fold to peak near the beginning of S period and then falling dramatically to basal levels after the onset of DNA synthesis. This mRNA peak coincided with the time during the cell cycle when thymidylate synthase levels were increasing maximally and immediately preceded the peak of DNA synthesis, for which the enzyme provides precursor dTMP.

Control of thymidine kinase mRNA during the cell cycle

1987 ◽  
Vol 7 (8) ◽  
pp. 2925-2932
Author(s):  
D L Coppock ◽  
A B Pardee
Keyword(s):  
Cell Cycle ◽  
Protein Synthesis ◽  
Dna Synthesis ◽  
Thymidine Kinase ◽  
Gene Transcription ◽  
Half Life ◽  
Mammalian Cells ◽  
Mrna Degradation ◽  
S Phase ◽  
3T3 Cells

To investigate the mechanism which controls the onset of DNA synthesis, we examined the regulation of thymidine kinase (TK) and its mRNA in the cell cycle. TK activity provides a useful marker for the onset of the S phase in mammalian cells. The present analysis of regulation of TK mRNA in BALB/c 3T3 cells showed that (i) the increase in TK activity depended on the availability of TK mRNA, (ii) the level of TK mRNA between G0 and S increased more than 20-fold, (iii) the rate of run-on TK transcription increased at most 2- to 4-fold between the G0 and S phases, (iv) the half-life of TK mRNA was greater than 8 to 12 h in the S and M phases and decreased as cells entered quiescence, (v) the TK mRNA increase was fully blocked by inhibition of protein synthesis by only 60%, (vi) this inhibition was completely effective for up to about 10 h following serum addition and progressively much less effective when the drugs were added later. These results suggest that the appearance of TK mRNA at the beginning of the S phase in serum-stimulated 3T3 cells is controlled not only by the rate of gene transcription but importantly also by the decreased rate of mRNA degradation. Similar mechanisms may be involved in regulation of the onset of DNA synthesis and the increase in TK mRNA since both are controlled in a manner consistent with a requirement for a labile protein.

Cell cycle regulation of mouse H3 histone mRNA metabolism

1984 ◽  
Vol 4 (1) ◽  
pp. 123-132
Author(s):  
R B Alterman ◽  
S Ganguly ◽  
D H Schulze ◽  
W F Marzluff ◽  
C L Schildkraut ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Steady State ◽  
Dna Synthesis ◽  
In Vitro Transcription ◽  
S Phase ◽  
Gene Probe ◽  
Histone Mrna ◽  
Mrna Content

The mechanisms responsible for the periodic accumulation and decay of histone mRNA in the mammalian cell cycle were investigated in mouse erythroleukemia cells, using a cloned mouse H3 histone gene probe that hybridizes with most or all H3 transcripts. Exponentially growing cells were fractionated into cell cycle-specific stages by centrifugal elutriation, a method for purifying cells at each stage of the cycle without the use of treatments that arrest growth. Measurements of H3 histone mRNA content throughout the cell cycle show that the mRNA accumulates gradually during S phase, achieving its highest value in mid-S phase when DNA synthesis is maximal. The mRNA content then decreases as cells approach G2. These results demonstrate that the periodic synthesis of histones during S phase is due to changes in the steady-state level of histone mRNA. They are consistent with the conventional view in which histone synthesis is regulated coordinately with DNA synthesis in the cell cycle. The periodic accumulation and decay of H3 histone mRNA appear to be controlled primarily by changes in the rate of appearance of newly synthesized mRNA in the cytoplasm, determined by pulse-labeling whole cells with [3H]uridine. Measurements of H3 mRNA turnover by pulse-chase experiments with cells in S and G2 did not provide evidence for changes in the cytoplasmic stability of the mRNA during the period of its decay in late S and G2. Furthermore, transcription measurements carried out by brief pulse-labeling in vivo and by in vitro transcription in isolated nuclei indicate that the rate of H3 gene transcription changes to a much smaller extent than the steady-state levels of the mRNA or the appearance of newly synthesized mRNA in the cytoplasm. The results suggest that post-transcriptional processes make an important contribution to the periodic accumulation and decay of histone mRNA and that these processes may operate within the nucleus.

Comparative Analysis of the Kinetics of DNA Synthesis after Exposure during Different Phases of the Cell Cycle S Period

2013 ◽  
Vol 156 (2) ◽  
pp. 260-265 ◽  
Author(s):  
I. P. Shabalkin ◽  
E. Yu. Grigor’eva ◽  
P. I. Shabalkin ◽  
M. V. Gudkova ◽  
A. S. Yagubov
Keyword(s):  
Cell Cycle ◽  
Comparative Analysis ◽  
Dna Synthesis ◽  
S Period ◽  
Kinetics Of

scholarly journals ANALYSIS OF THE SCHEDULE OF DNA REPLICATION IN HEAT-SYNCHRONIZED TETRAHYMENA

1973 ◽  
Vol 59 (1) ◽  
pp. 1-11 ◽  
Author(s):  
William R. Jeffery ◽  
Joseph Frankel ◽  
Lawrence E. de Bault ◽  
Leslie M. Jenkins
Keyword(s):  
Cell Cycle ◽  
High Temperature ◽  
Dna Replication ◽  
Heat Shock ◽  
Dna Synthesis ◽  
Shock Treatment ◽  
Heat Shock Treatment ◽  
Dividing Cells ◽  
S Period ◽  
Selection Of

The temporal schedule of DNA replication in heat-synchronized Tetrahymena was studied by autoradiographic and cytofluorometric methods. It was shown that some cells, which were synchronized by selection of individual dividing cells or by temporary thymidine starvation, incorporated [3H]thymidine into macronuclei in a periodic fashion during the heat-shock treatment. It was concluded that supernumerary S periods occurred while cell division was blocked by high temperature. The proportion of cells which initiated supernumerary S periods was found to be dependent on the duration of the heat-shock treatment and on the cell cycle stage when the first heat shock was applied. Cytofluorometric measurements of Feulgen-stained macronuclei during the heat-shock treatment indicated that the DNA complement of these cells was substantially increased and probably duplicated during the course of each S period. Estimates of DNA content also suggested that the rate of DNA synthesis progressively declined during long heat-shock treatments. These results indicate that the mechanism which brings about heat-induced division synchrony is not an interruption of the process of DNA replication. Further experiments were concerned with the regulation of DNA synthesis during the first synchronized division cycle. It was shown that participation in DNA synthesis at this time increased as more cells were able to conclude the terminal S period during the preceding heat-shock treatment. It is suggested that a discrete period of time is necessary after the completion of DNA synthesis before another round of DNA synthesis can be initiated.

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