THE RELATIONSHIP BETWEEN CELL SIZE, YIELD, AND SUCROSE CONCENTRATION OF THE SUGARBEET ROOT

1981 ◽  
Vol 61 (2) ◽  
pp. 447-453 ◽  
Author(s):  
DEVON L. DONEY ◽  
ROGER E. WYSE ◽  
J. CLAIR THEURER

Increased root yields of sugarbeet (Beta vulgaris L.) have generally been accompanied by decreases in sucrose percentage. Plant breeders have been unable to break this negative relationship. Cell size and cell number were measured microscopically from stained root cross sections. Two separate tests with genotypes typifying a wide range of genetic variation in sucrose percentage indicated an inverse relationship between sucrose percentage and cell size; i.e., high-sucrose genotypes had small cells and low-sucrose genotypes had large cells. In most cases, this relationship offers a reasonable explanation of the effects of nitrogen, polyploidy, ring number, ring density, and past selection methods on yield and sucrose percentage. Genetic differences in cell size and cell division rate were detected in young plants (3- to 4-wk-old seedlings).

2017 ◽  
Author(s):  
François Bertaux ◽  
Samuel Marguerat ◽  
Vahid Shahrezaei

AbstractThe cell division rate, size, and gene expression programmes change in response to external conditions. These global changes impact on average concentrations of biomolecule and their variability or noise. Gene expression is inherently stochastic, and noise levels of individual proteins depend on synthesis and degradation rates as well as on cell-cycle dynamics. We have modelled stochastic gene expression inside growing and dividing cells to study the effect of division rates on noise in mRNA and protein expression. We use assumptions and parameters relevant to Escherichia coli, for which abundant quantitative data are available. We find that coupling of transcription, but not translation rates to the rate of cell division can result in protein concentration and noise homeostasis across conditions. Interestingly, we find that the increased cell size at fast division rates, observed in E. coli d other unicellular organisms, buffers noise levels even for proteins with decreased expression at faster growth. We then investigate the functional importance of these regulations using gene regulatory networks that exhibit bi-stability and oscillations. We find that network topology affects robustness to changes in division rate in complex and unexpected ways. In particular, a simple model of persistence, based on global physiological feedback, predicts increased proportion of persistors cells at slow division rates. Altogether, our study reveals how cell size regulation in response to cell division rate could help controlling gene expression noise. It also highlights that understanding of circuits’ robustness across growth conditions is key for the effective design of synthetic biological systems.


2021 ◽  
Vol 134 (7) ◽  
Author(s):  
Asadullah ◽  
Sandeep Kumar ◽  
Neha Saxena ◽  
Madhurima Sarkar ◽  
Amlan Barai ◽  
...  

ABSTRACT Phenotypic heterogeneity is increasingly acknowledged to confer several advantages to cancer progression and drug resistance. Here, we probe the collective importance of heterogeneity in cell size and deformability in breast cancer invasion. A computational model of invasion of a heterogeneous cell aggregate predicts that combined heterogeneity in cell size and deformability enhances invasiveness of the whole population, with maximum invasiveness at intermediate cell-cell adhesion. We then show that small cells of varying deformability, a subpopulation predicted to be enriched at the invasive front, exhibit considerable overlap with the biophysical properties of cancer stem cells (CSCs). In MDA-MB-231 cells, these include CD44hi CD24− mesenchymal CSCs, which are small and soft, and CD44hi CD24+ hybrid CSCs, which exhibit a wide range of size and deformability. We validate our predictions by tracking the pattern of cell invasion from spheroids implanted in three-dimensional collagen gels, wherein we show temporal enrichment of CD44hi cells at the invasive front. Collectively, our results illustrate the advantages imparted by biophysical heterogeneity in enhancing cancer invasiveness. This article has an associated First Person interview with the first author of the paper.


2018 ◽  
Vol 5 (3) ◽  
pp. 172234 ◽  
Author(s):  
François Bertaux ◽  
Samuel Marguerat ◽  
Vahid Shahrezaei

The cell division rate, size and gene expression programmes change in response to external conditions. These global changes impact on average concentrations of biomolecule and their variability or noise. Gene expression is inherently stochastic, and noise levels of individual proteins depend on synthesis and degradation rates as well as on cell-cycle dynamics. We have modelled stochastic gene expression inside growing and dividing cells to study the effect of division rates on noise in mRNA and protein expression. We use assumptions and parameters relevant to Escherichia coli , for which abundant quantitative data are available. We find that coupling of transcription, but not translation rates to the rate of cell division can result in protein concentration and noise homeostasis across conditions. Interestingly, we find that the increased cell size at fast division rates, observed in E. coli and other unicellular organisms, buffers noise levels even for proteins with decreased expression at faster growth. We then investigate the functional importance of these regulations using gene regulatory networks that exhibit bi-stability and oscillations. We find that network topology affects robustness to changes in division rate in complex and unexpected ways. In particular, a simple model of persistence, based on global physiological feedback, predicts increased proportion of persister cells at slow division rates. Altogether, our study reveals how cell size regulation in response to cell division rate could help controlling gene expression noise. It also highlights that understanding circuits' robustness across growth conditions is key for the effective design of synthetic biological systems.


HortScience ◽  
2005 ◽  
Vol 40 (4) ◽  
pp. 1008B-1008 ◽  
Author(s):  
James W. Olmstead ◽  
Amy F. Iezzoni ◽  
Matthew D. Whiting

Although maximizing fruit size is critical for profitable sweet cherry (Prunusavium L.) production, little is known about the cellular differences among and between cultivars that contribute to fruit size differences. A wide range of fruit size exists among sweet cherries, and, due to cultural and environmental differences, significant variation exists among genetically identical fruit from the same cultivar. To determine the relative contributions of flesh cell number and cell size to final fruit size in sweet cherry, equatorial sections of three cultivars with a wide range in final average fruit size [`New York 54' (NY54; 1.4 g fresh weight, 11.8 mm diameter), `Emperor Francis' (EF; 6.1 g, 21.0 mm), and `Selah' (12.8 g, 25.5 mm)] were created from mature fruit. Cells intersecting a transverse line were counted and average cell length was calculated. The average cell numbers were significantly different (P ≤ 0.05) between `NY54', `EF', and `Selah' (26.7, 47.4, and 83.2, respectively), indicating that flesh cell number is the major contributor to differences in fruit size between cultivars. Flesh cell numbers of `NY54', `EF', and `Selah' were similar at bloom and increased rapidly for a short duration after fertilization, suggesting a key developmental period for fruit size differences. To determine the contribution of cell number differences to variation in fruit size within a cultivar, fruit from `Bing' and `Regina' trees exhibiting a range of size due to cultural and environmental differences were measured. In both cases, average cell number was not significantly different (P = 0.9, P = 0.3, respectively), while average cell size was (P ≤ 0.05), further indicating fruit flesh cell number is a genetically controlled trait.


2020 ◽  
Vol 2020 (9) ◽  
Author(s):  
Antonio Costantini ◽  
Federico De Lillo ◽  
Fabio Maltoni ◽  
Luca Mantani ◽  
Olivier Mattelaer ◽  
...  

Abstract High-energy lepton colliders with a centre-of-mass energy in the multi-TeV range are currently considered among the most challenging and far-reaching future accelerator projects. Studies performed so far have mostly focused on the reach for new phenomena in lepton-antilepton annihilation channels. In this work we observe that starting from collider energies of a few TeV, electroweak (EW) vector boson fusion/scattering (VBF) at lepton colliders becomes the dominant production mode for all Standard Model processes relevant to studying the EW sector. In many cases we find that this also holds for new physics. We quantify the size and the growth of VBF cross sections with collider energy for a number of SM and new physics processes. By considering luminosity scenarios achievable at a muon collider, we conclude that such a machine would effectively be a “high-luminosity weak boson collider,” and subsequently offer a wide range of opportunities to precisely measure EW and Higgs couplings as well as discover new particles.


Diabetologia ◽  
2021 ◽  
Author(s):  
Hironobu Sasaki ◽  
Yoshifumi Saisho ◽  
Jun Inaishi ◽  
Yuusuke Watanabe ◽  
Tami Tsuchiya ◽  
...  

Abstract Aims/hypothesis Type 2 diabetes is characterised by reduced beta cell mass (BCM). However, it remains uncertain whether the reduction in BCM in type 2 diabetes is due to a decrease in size or number of beta cells. Our aim was to examine the impact of beta cell size and number on islet morphology in humans with and without type 2 diabetes. Methods Pancreas samples were obtained from 64 Japanese adults with (n = 26) and without (n = 38) type 2 diabetes who underwent pancreatectomy. Using pancreatic tissues stained for insulin, we estimated beta cell size based on beta cell diameter. Beta cell number was estimated from the product of fractional beta cell area and pancreas volume divided by beta cell size. The associations of beta cell size and number with islet morphology and metabolic status were examined. Results Both beta cell size (548.7 ± 58.5 vs 606.7 ± 65.0 μm3, p < 0.01) and number (5.10 × 108 ± 2.35 × 108 vs 8.16 × 108 ± 4.27 × 108, p < 0.01) were decreased in participants with type 2 diabetes compared with those without diabetes, with the relative reduction in beta cell number (37%) being greater than for beta cell size (10%). Beta cell number but not size was positively correlated with BCM in participants with and without type 2 diabetes (r = 0.97 and r = 0.98, both p < 0.01) and negatively correlated with HbA1c (r = −0.45, p < 0.01). Conclusions/interpretation Both beta cell size and number were reduced in participants with type 2 diabetes, with the relative reduction in beta cell number being greater. Decrease in beta cell number appears to be a major contributor to reduced BCM in type 2 diabetes. Graphical abstract


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