The Effect of a Temperature Gradient on the Early Development of the Frog

1928 ◽  
Vol 5 (4) ◽  
pp. 309-336
Author(s):  
I. L. DEAN ◽  
M. E. SHAW ◽  
M. A. TAZELAAR
Keyword(s):  
Cell Size ◽  
Small Cells ◽  
Tail Bud ◽  
Animal Cells ◽  
Differential Growth ◽  
Experimental Conditions ◽  
Animal Pole ◽  
Stage Of Development ◽  
Permanent Effect ◽  
Two Sides

1. Temperature gradients were passed through the developing frog's egg and embryos. These gradients were applied either (a) apico-basally, when they were either (i) adjuvant, or (ii) antagonistic to the egg's own main gradient; or (b) transversely to the egg's main axis--lateral gradients. 2. (a) By this means considerable modification of segmentation and of cell size was induced, and was especially marked in the mid-blastula. Adjuvant gradients accentuated the normal differences in cell size between the animal and vegetative poles. Antagonistic gradients produced a double gradient in cell size, the smallest cells being in the region of the equator, and animal cells, in extreme cases, larger than yolk cells. (b) Several cases of the non-formation or obliteration of the blastocoel were obtained by all methods of treatment. (c) Too high temperature with adjuvant gradient produced inhibition at the animal pole, the large retarded cells being very sharply marked off from the surrounding small cells. (d) Lateral gradients produced a great difference in cell size on the two sides of the eggy and, as in the cases of "inhibition," a sharp line of demarcation may appear between the large cells of the cooled side and the small cells of the heated side. (e) When two sets of exactly similar eggs were treated simultaneously in opposite ways, then those subjected to the adjuvant gradient were always, at the close of the experiment, at a more advanced stage of development than those subjected to an antagonistic gradient. Because of this the yolk cells of the "adjuvant" eggs were smaller than those of the "antagonistic" eggs, although the former were cooled and the latter heated. (f) There seems to be a slight permanent effect of the gradient applied during segmentation. Eggs treated with antagonistic gradient tend to develop into microcephalous tadpoles and vice versa. 3. (a) Antagonistic gradients during gastrulation cause a reduction of the gastrular angle. (For definition see Bellamy (1919).) (b) Antagonistic gradient causes the eggs to gastrulate sooner than adjuvant eggs under exactly similar experimental conditions. (c) In the neurula stage the differential effect of the gradient is seen in the inhibition of the head and dorsal region in those subjected to antagonistic gradient, and inhibition of tail and ventral region in those subjected to adjuvant gradient. (d) Whether this alteration of relative sizes of head and tail regions is maintained in later development has not yet been ascertained. (e) Eggs exposed to lateral gradients in all stages of gastrulation showed marked asymmetries, some of which were apparently regulated later, while others persisted till the death of the tadpole. 4. Side-to-side treatment in the tail bud stage caused the development of marked asymmetry as the result of differential growth of the two sides. As in the case of 3 (e) some tadpoles appeared to regulate back to normal, whereas others remained markedly asymmetrical till death.

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 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.

scholarly journals Cell size sensing in animal cells coordinates anabolic growth rates and cell cycle progression to maintain cell size uniformity

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Miriam Bracha Ginzberg ◽  
Nancy Chang ◽  
Heather D'Souza ◽  
Nish Patel ◽  
Ran Kafri ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Size ◽  
Growth Rates ◽  
Cell Cycle Progression ◽  
Cellular Growth ◽  
Small Cells ◽  
Live Cells ◽  
Control Mechanisms ◽  
Animal Cells ◽  
Size Uniformity

Cell size uniformity in healthy tissues suggests that control mechanisms might coordinate cell growth and division. We derived a method to assay whether cellular growth rates depend on cell size, by monitoring how variance in size changes as cells grow. Our data revealed that, twice during the cell cycle, growth rates are selectively increased in small cells and reduced in large cells, ensuring cell size uniformity. This regulation was also observed directly by monitoring nuclear growth in live cells. We also detected cell-size-dependent adjustments of G1 length, which further reduce variability. Combining our assays with chemical/genetic perturbations confirmed that cells employ two strategies, adjusting both cell cycle length and growth rate, to maintain the appropriate size. Additionally, although Rb signaling is not required for these regulatory behaviors, perturbing Cdk4 activity still influences cell size, suggesting that the Cdk4 pathway may play a role in designating the cell’s target size.

Joint regulation of growth and division timing drives size homeostasis in proliferating animal cells

2017 ◽  
Author(s):  
Abhyudai Singh ◽  
Cesar A. Vargas-Garcia ◽  
Mikael Björklund
Keyword(s):  
Growth Rate ◽  
Cell Size ◽  
Cellular Proliferation ◽  
Animal Cell ◽  
Size Control ◽  
Small Cells ◽  
Mitochondrial Activity ◽  
Optimal Size ◽  
Animal Cells ◽  
Activity Increase

AbstractHow organisms maintain cell size homeostasis is a long-standing problem that remains unresolved, especially in multicellular organisms. Recent experiments in diverse animal cell types demonstrate that within a cell population the extent of growth and cellular proliferation (i.e., fitness) is low for small and large cells, but high at intermediate sizes. Here we use mathematical models to explore size-control strategies that drive such a non-monotonic fitness profile resulting in an optimal cell size. Our analysis reveals that if cell size grows exponentially or linearly over time, then fitness always varies monotonically with size irrespective of how timing of division is regulated. Furthermore, if the cell divides upon attaining a critical size (as in the Sizer or size-checkpoint model), then fitness always increases with size irrespective of how growth rate is regulated. These results show that while several size control models can maintain cell size homeostasis, they fail to predict the optimal cell size, and hence unable to explain why cells prefer a certain size. Interestingly, fitness maximization at an optimal size requires two key ingredients: 1) The growth rate decreases with increasing size for large enough cells; and 2) The cell size at the time of division is a function of the newborn size. The latter condition is consistent with the Adder paradigm for division control (division is triggered upon adding a fixed size from birth), or a Sizer-Adder combination. Consistent with theory, Jurkat T cell growth rates, as measured via oxygen consumption or mitochondrial activity, increase with size for small cells, but decrease with size for large cells. In summary, regulation of both growth and cell division timing is critical for size control in animal cells, and this joint-regulation leads to an optimal size where cellular fitness is maximized.Address inquires to A. Singh, E-mail: [email protected].

scholarly journals Size uniformity of animal cells is actively maintained by a p38 MAPK-dependent regulation of G1-length

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Shixuan Liu ◽  
Miriam Bracha Ginzberg ◽  
Nish Patel ◽  
Marc Hild ◽  
Bosco Leung ◽  
...  
Keyword(s):  
Cell Size ◽  
P38 Mapk ◽  
Large Scale ◽  
Cell Cycle Progression ◽  
Molecular Mechanisms ◽  
Mapk Pathway ◽  
Small Cells ◽  
Animal Cells ◽  
Size Uniformity ◽  
Size Heterogeneity

Animal 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.

scholarly journals Cell size sensing in animal cells coordinates anabolic growth rates with cell cycle progression to maintain uniformity of cell size

2017 ◽  
Author(s):  
Miriam B. Ginzberg ◽  
Nancy Chang ◽  
Ran Kafri ◽  
Marc W. Kirschner
Keyword(s):  
Cell Cycle ◽  
Growth Rate ◽  
Cell Size ◽  
Growth Rates ◽  
Cell Cycle Progression ◽  
Time Lapse ◽  
Small Cells ◽  
Live Cells ◽  
Control Mechanisms ◽  
Animal Cells

AbstractThe uniformity of cell size in healthy tissues suggests that control mechanisms might coordinate cell growth and division. We derived a method to assay whether growth rates of individual cells depend on cell size, by combining time-lapse microscopy and immunofluorescence to monitor how variance in cell size changes as cells grow. This analysis revealed two periods in the cell cycle when cell size variance decreases in a manner incompatible with unregulated growth, suggesting that cells sense their own size and adjust their growth rate to correct aberrations. Monitoring nuclear growth in live cells confirmed that these decreases in variance reflect a process that selectively inhibits the growth of large cells while accelerating growth of small cells. We also detected cell-size-dependent adjustments of G1 length, which further reduce variability. Combining our assays with chemical and genetic perturbations confirmed that cells employ two strategies, adjusting both cell cycle length and growth rate, to maintain the appropriate 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.

Sialoconjugates and development of the tail bud

Development ◽  
1990 ◽  
Vol 108 (3) ◽  
pp. 479-489
Author(s):  
C.M. Griffith ◽  
M.J. Wiley
Keyword(s):  
Sialic Acid ◽  
Lectin Histochemistry ◽  
Limulus Polyphemus ◽  
Chick Embryos ◽  
Developmental Sequence ◽  
Tail Bud ◽  
Bud Development ◽  
Stage Of Development ◽  
Higher Doses ◽  
Axial Development

Using lectin histochemistry, we have previously shown that there are alterations in the distribution of glycoconjugates in the tail bud of chick embryos that parallel the developmental sequence of the caudal axis. If glycoconjugates or the cells bearing them play a role in caudal axial development, then, restriction of their availability by binding with lectins would be expected to produce abnormalities of caudal development. In the present study, we treated embryos at various stages of tail bud development by microinjection with a variety of lectins. Administration of WGA by sub-blastodermal injection resulted in high incidences of secondary neural tube and notochordal abnormalities in lectin-treated embryos. The incidence of malformations was dependent upon both the dose of WGA received and the stage of development at the time of treatment. Using an anti-WGA antibody, we have also shown binding of the lectin in regions where defects were found. The lectin WGA binds to the sialic acid residues of glycoconjugates and to N-acetylglucosamine. Treatment of embryos with Limulus polyphemus lectin (LPL), which also binds to sialic acid, produced results similar to those of WGA. Treatments using lectins with other sugar-binding specificities, including succinylated WGA (with N-acetylglucosamine specificity only) produced defects that differed from those produced by WGA and LPL, and only with the administration of much higher doses. The results suggest that glycoconjugates in general and sialoconjugates in particular, or the cells carrying them, may have a role in caudal axial development.

Changes in protein during development of Triturus embryos

Development ◽  
1973 ◽  
Vol 30 (3) ◽  
pp. 647-659
Author(s):  
Hiroshi Imoh ◽  
Tsutomu Minamidani
Keyword(s):  
Protein Synthesis ◽  
Protein Content ◽  
Sodium Carbonate ◽  
Dna Content ◽  
Total Protein ◽  
Soluble Protein ◽  
Nuclear Protein ◽  
Polyacrylamide Gel Electrophoresis ◽  
Tail Bud ◽  
Stage Of Development

The present paper reports basic data on DNA content, protein content, and protein synthesis in Triturus pyrrhogaster embryos during development from cleavage to the hatching stage. Except for measurements of DNA and total protein contents, embryos were labeled with sodium carbonate-14C for 10 h and fractionated into embryonic cell components, i.e. cytoplasmic mass, yolk and pigment granules, and nuclei, in a discontinuous density gradient of sucrose. The protein content and the radioactivity incorporated into protein were measured in each fraction. Those fractions combining protein soluble in buffer at pH 8·3 and in 0·25 N-HCl were further studied with polyacrylamide gel electrophoresis. In the newt embryo, four stages of active DNA increase were observed when cultured at constant temperature; they were gastrula, neurula, late tail-bud, and before-hatching stages. Total protein per embryo decreased from 3 to 2 mg during the development studied. The content of cytoplasmic soluble protein per embryo was low and constant throughout development. Synthesis of the fraction was observed at the earliest stage of development studied though the rate was not high and specific activity of the soluble protein increased during development. Qualitative changes in the newly synthesized protein were observed. With the yolk fraction, synthesis of protein, other than from probable contamination with the cytoplasmic fraction, was not detected and a detailed description was omitted. Changes were observed at two stages of development in the synthesis of nuclear protein soluble in buffer at pH 8·3, the first at gastrulation and the second at late tail-bud stage. The change at gastrulation seemed to be the start of syntheses of the nuclear soluble proteins, while quantitative enhancement rather than qualitative change was noticed at late tail-bud stage. Most of the nuclear protein soluble in 0·25 N-HCI was histone. The histone content increased in accordance with increase in the DNA content and the rate of DNA accumulation was accompanied by proportionate incorporation of radioactivity into histone. Among histone fractions, unique behaviour of the very lysine-rich histone was observed. The availability of [14C]sodium carbonate in rough estimations of protein synthesis in embryos and significance of the data obtained have been discussed.

scholarly journals Functional gap junctions are not required for muscle gene activation by induction in Xenopus embryos.

1987 ◽  
Vol 104 (3) ◽  
pp. 557-564 ◽  
Author(s):  
A Warner ◽  
J B Gurdon
Keyword(s):  
Gap Junctions ◽  
Gap Junction ◽  
Close Contact ◽  
Gene Activation ◽  
Gene Probe ◽  
Animal Cells ◽  
Animal Pole ◽  
Junction Protein ◽  
Pole Cells ◽  
Muscle Gene

Muscle gene expression is known to be induced in animal pole cells of a Xenopus blastula after 2-3 h of close contact with vegetal pole cells. We tested whether this induction requires functional gap junctions between vegetal and animal portions of an animal-vegetal conjugate. Muscle gene transcription was assayed with a muscle-specific actin gene probe and the presence or absence of communication through gap junctions was determined electrophysiologically. Antibodies to gap junction protein were shown to block gap junction communication for the whole of the induction time, but did not prevent successful induction of muscle gene activation. The outcome was the same whether communication between inducing vegetal cells and responding animal cells was blocked by introducing antibodies into vegetal cells alone or into animal cells alone. We conclude that gap junctions are not required for this example of embryonic induction.

Sign in / Sign up

Export Citation Format

Share Document