scholarly journals Yeast cells under glucose-limitation environment need increased response cost for osmostress defense

2021 ◽  
Author(s):  
Chunxiong Luo ◽  
Wenting Shen ◽  
Ziqing Gao ◽  
Kaiyue Chen ◽  
Qi Ouyang
Keyword(s):  
Cell Growth ◽  
Environmental Changes ◽  
Yeast Cells ◽  
Protein Accumulation ◽  
Response Cost ◽  
Glucose Limitation ◽  
Dynamic Expression ◽  
Normal Glucose ◽  
Low Glucose ◽  
Glucose Condition

Cells always make responses to environmental changes, involving dynamic expression of tens to hundreds of proteins. This response system may demand substantial cost and thus affect cell growth. Here, we studied the cell's responses to osmostress under glucose-limitation environments. Through analyzed thirteen osmotic-downstream proteins and two related transcription factors, we found that the cells required stronger responses under low glucose concentrations than normal glucose condition after being stimulated by osmostress, even the cell growth rate was unchanged in these two constant conditions. We proposed and verified that under a glucose-limitation environment, the glycolysis intermediates were limited (defense reserve saving), which caused that cells needed more glycerol production enzymes to adapt to the osmostress. Further experiments proved that this 'defense reserve-saving' strategy required cells to spend more response cost when facing stress, which on the other hand, enhanced the fitness for the coming environment variations via protein accumulation reserve.

scholarly journals Low Glucose Mediated Fluconazole Tolerance in Cryptococcus neoformans

2021 ◽  
Vol 7 (6) ◽  
pp. 489
Author(s):  
Somanon Bhattacharya ◽  
Natalia Kronbauer Oliveira ◽  
Anne G. Savitt ◽  
Vanessa K. A. Silva ◽  
Rachel B. Krausert ◽  
...  
Keyword(s):  
Cryptococcus Neoformans ◽  
Mitochondrial Function ◽  
Efflux Pump ◽  
Nile Red ◽  
Fold Increase ◽  
Growth Conditions ◽  
Chromosome 1 ◽  
Normal Glucose ◽  
Low Glucose ◽  
Synthetic Media

Chronic meningoencephalitis is caused by Cryptococcus neoformans and is treated in many parts of the world with fluconazole (FLC) monotherapy, which is associated with treatment failure and poor outcome. In the host, C. neoformans propagates predominantly under low glucose growth conditions. We investigated whether low glucose, mimicked by growing in synthetic media (SM) with 0.05% glucose (SMlowglu), affects FLC-resistance. A > 4-fold increase in FLC tolerance was observed in seven C. neoformans strains when minimum inhibitory concentration (MIC) was determined in SMlowglu compared to MIC in SM with normal (2%) glucose (SMnlglu). In SMlowglu, C. neoformans cells exhibited upregulation of efflux pump genes AFR1 (8.7-fold) and AFR2 (2.5-fold), as well as decreased accumulation (2.6-fold) of Nile Red, an efflux pump substrate. Elevated intracellular ATP levels (3.2-fold and 3.4-fold), as well as decreased mitochondrial reactive oxygen species levels (12.8-fold and 17-fold), were found in the presence and absence of FLC, indicating that low glucose altered mitochondrial function. Fluorescence microscopy revealed that mitochondria of C. neoformans grown in SMlowglu were fragmented, whereas normal glucose promoted a reticular network of mitochondria. Although mitochondrial membrane potential (MMP) was not markedly affected in SMlowglu, it significantly decreased in the presence of FLC (12.5-fold) in SMnlglu, but remained stable in SMlowglu-growing C. neoformans cells. Our data demonstrate that increased FLC tolerance in low glucose-growing C. neoformans is the result of increased efflux pump activities and altered mitochondrial function, which is more preserved in SMlowglu. This mechanism of resistance is different from FLC heteroresistance, which is associated with aneuploidy of chromosome 1 (Chr1).

scholarly journals Is there any Effect of Blood Glucose Level on Finger Biting?

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Hira Naeem Qureshi
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Glucose Level ◽  
High Glucose ◽  
Normal Glucose ◽  
Normal Glucose Level ◽  
Low Glucose ◽  
Glucose Meter ◽  
High Glucose Level

To interact glucose level of blood with finger biting was the goal of present research. 130 subjects took part in present research, where their glucose level of blood calculated. The normal glucose level in blood is in between 100 to 140mg/dl. The hyperglycemia is known as high glucose level while hypoglycemia is known as low glucose level. The biting of fingers in the mouth with teeth is known as finger biting. It also refer as onychophagia. There were 130 students take part in this research and they measured their sugar level by using glucose meter. Then they correlate the glucose level with finger biting. It was concluded from the present study that glucose level of blood has no impact on finger biting.

scholarly journals Autotoxin-mediated voluntary triage in starved yeast community

2020 ◽  
Author(s):  
Arisa H. Oda ◽  
Miki Tamura ◽  
Kunihiko Kaneko ◽  
Kunihiro Ohta ◽  
Tetsuhiro S. Hatakeyama
Keyword(s):  
Environmental Changes ◽  
Yeast Cells ◽  
Glucose Starvation ◽  
Uniform Stress ◽  
Universal System ◽  
Stressful Environment ◽  
Yeast Community ◽  
Unicellular Organisms ◽  
Multicellular Organisms ◽  
Cell Community

When organisms face crises, such as starvation, every individual should adapt to environmental changes (1, 2), or the community alters their behaviour (3–5). Because a stressful environment reduces the carrying capacity (6), the population size of unicellular organisms shrinks in such conditions (7, 8). However, the uniform stress response of the cell community may lead to overall extinction or severely damage their entire fitness. How microbial communities accommodate this dilemma remains poorly understood. Here, we demonstrate an elaborate strategy of the yeast community against glucose starvation, named the voluntary triage. During starvation, yeast cells release some autotoxins, such as leucic acid and L-2keto-3methylvalerate, which can even kill the cells producing them. Although it may look like mass suicide at first glance, cells use epigenetic “tags” to adapt to the autotoxin inheritably. If non-tagged latecomers, regardless of whether they are closely related, try to invade the habitat, autotoxins kill them and inhibit their growth, but the tagged cells can selectively survive. Phylogenetically distant fission and budding yeast (9) share this strategy using the same autotoxins, which implies that the universal system of voluntary triage may be relevant to the major evolutional transition from unicellular to multicellular organisms (10).

scholarly journals Metabolic excretion associated with nutrient-growth dysregulation promotes the rapid evolution of an overt metabolic defect

2018 ◽  
Author(s):  
Robin Green ◽  
Sonal ◽  
Lin Wang ◽  
Samuel F.M. Hart ◽  
Wenyun Lu ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Growth ◽  
Slow Growth ◽  
Rapid Evolution ◽  
Auxotrophic Mutant ◽  
Ecological Interactions ◽  
Glucose Limitation ◽  
Metabolic Defects ◽  
Fitness Advantage ◽  
Selection Of

AbstractIn eukaryotes, conserved mechanisms ensure that cell growth is coordinated with nutrient availability. Overactive growth during nutrient limitation (“nutrient-growth dysregulation”) can lead to rapid cell death. Here, we demonstrate that cells can adapt to nutrient-growth dysregulation by evolving major metabolic defects. Specifically, when yeast lysine auxotrophic mutant lys- encountered lysine limitation, an evolutionarily novel stress, cells suffered nutrient-growth dysregulation. A sub-population repeatedly evolved to lose the ability to synthesize organosulfurs (lys-orgS-). Organosulfurs, mainly glutathione and glutathione conjugates, were released by lys- cells during lysine limitation when growth was dysregulated, but not during glucose limitation when growth was regulated. Limiting organosulfurs conferred a frequency-dependent fitness advantage to lys-orgS- by eliciting a proper slow growth program including autophagy. Thus, nutrient-growth dysregulation is associated with rapid organosulfur release, which enables the selection of organosulfur auxotrophy to better tune cell growth to the metabolic environment. We speculate that evolutionarily novel stresses can trigger atypical release of certain metabolites, setting the stage for the evolution of new ecological interactions.

Effects of glucose on hypoxic vasoconstriction in isolated ferret lungs

1991 ◽  
Vol 70 (1) ◽  
pp. 439-446 ◽  
Author(s):  
C. M. Wiener ◽  
J. T. Sylvester
Keyword(s):  
High Glucose ◽  
Early Phase ◽  
Continuous Measurement ◽  
Late Phase ◽  
Vascular Response ◽  
Vasomotor Responses ◽  
Hypoxic Vasoconstriction ◽  
Normal Glucose ◽  
Low Glucose ◽  
Pulmonary Arterial

To characterize the effects of glucose on the pulmonary vascular response to anoxia and hypoxia, isolated ferret lungs were ventilated with 28% O2 and 5% CO2 and perfused at constant flow (100 ml.kg-1.min-1). Perfusate glucose concentrations were allowed to fall spontaneously to less than 1 mM (low glucose) or were controlled at 5–6 mM (normal glucose) or 12–17 mM (high glucose). At 60, 120, and 180 min of perfusion, the inspired O2 tension (PIO2) was reduced to 0, 10, or 30 Torr for 30 min, and vasomotor responses were quantified by continuous measurement of pulmonary arterial pressure. At PIO2 of 0 Torr, the response consisted of an early phase of transient intense vasoconstriction and a late phase of sustained slight vasoconstriction. High glucose markedly potentiated the magnitude of late-phase vasoconstriction with each successive anoxic exposure. This effect was not reproduced in normal glucose lungs and was not caused by a change in perfusate osmolarity, an action on blood cells, or an altered ability of pulmonary vascular smooth muscle to contract. At PIO2 of 10 Torr, high glucose not only potentiated late-phase vasoconstriction but also slowed the onset of early-phase vasoconstriction. At PIO2 of 30 Torr, high glucose had no effect on vasomotor responses, which were characterized by a slowly developing sustained vasoconstriction. Our results suggest that the vascular response of isolated ferret lungs to severe hypoxia consisted of separate early and late phases of vasoconstriction. This biphasic response may have resulted from two distinct vasoconstrictor mechanisms or from modulation of a single vasoconstrictor mechanism by a secondary vasodilator influence.(ABSTRACT TRUNCATED AT 250 WORDS)

Modelling yeast cell growth using stochastic branching processes

1981 ◽  
Vol 18 (04) ◽  
pp. 799-808 ◽  
Author(s):  
P. J. Green
Keyword(s):  
Cell Growth ◽  
Branching Process ◽  
Deterministic Model ◽  
Branching Processes ◽  
Yeast Cells ◽  
Fixed Duration ◽  
Full Generality ◽  
Asymmetric Growth ◽  
Special Case ◽  
Natural Way

This paper aims to demonstrate that the general Crump–Mode–Jagers branching process may be used in a natural way to model the asymmetric growth of budding yeast cells. The models obtained are generalisations of the deterministic model proposed by Hartwell and Unger (1977): all the results that are derived in that paper may be obtained using branching-process methods, but such methods also apply when account is taken of the biologically obvious fact that the various phases of the cell growth are of random rather than fixed duration. In their full generality, branching processes involve more parameters than can be estimated by experiment, but we present below a special case in which this problem is not likely to arise. A recent paper, Lord and Wheals (1980), discusses more of the biological background than is appropriate here. In the present paper, we show how certain statistical procedures for our model may be developed.

Dependence on glucose limitation of thepCO2 influences on CHO cell growth, metabolism and IgG production

2007 ◽  
Vol 97 (6) ◽  
pp. 1479-1488 ◽  
Author(s):  
Shinya Takuma ◽  
Chikashi Hirashima ◽  
James M. Piret
Keyword(s):  
Cell Growth ◽  
Cho Cell ◽  
Glucose Limitation ◽  
Growth Metabolism

scholarly journals Compartmentalized nodes control mitotic entry signaling in fission yeast

2013 ◽  
Vol 24 (12) ◽  
pp. 1872-1881 ◽  
Author(s):  
Lin Deng ◽  
James B. Moseley
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Fission Yeast ◽  
Cell Polarity ◽  
Cell Cycle Progression ◽  
Interaction Network ◽  
Yeast Cells ◽  
Cell Cortex ◽  
Cycle Progression ◽  
Mitotic Entry

Cell cycle progression is coupled to cell growth, but the mechanisms that generate growth-dependent cell cycle progression remain unclear. Fission yeast cells enter into mitosis at a defined size due to the conserved cell cycle kinases Cdr1 and Cdr2, which localize to a set of cortical nodes in the cell middle. Cdr2 is regulated by the cell polarity kinase Pom1, suggesting that interactions between cell polarity proteins and the Cdr1-Cdr2 module might underlie the coordination of cell growth and division. To identify the molecular connections between Cdr1/2 and cell polarity, we performed a comprehensive pairwise yeast two-hybrid screen. From the resulting interaction network, we found that the protein Skb1 interacted with both Cdr1 and the Cdr1 inhibitory target Wee1. Skb1 inhibited mitotic entry through negative regulation of Cdr1 and localized to both the cytoplasm and a novel set of cortical nodes. Skb1 nodes were distinct structures from Cdr1/2 nodes, and artificial targeting of Skb1 to Cdr1/2 nodes delayed entry into mitosis. We propose that the formation of distinct node structures in the cell cortex controls signaling pathways to link cell growth and division.

scholarly journals Growth Factors Can Influence Cell Growth and Survival through Effects on Glucose Metabolism

2001 ◽  
Vol 21 (17) ◽  
pp. 5899-5912 ◽  
Author(s):  
Matthew G. Vander Heiden ◽  
David R. Plas ◽  
Jeffrey C. Rathmell ◽  
Casey J. Fox ◽  
Marian H. Harris ◽  
...  
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Cell Growth ◽  
Glucose Uptake ◽  
Fixed Dose ◽  
Glucose Limitation ◽  
Growth And Survival ◽  
Glucose Levels ◽  
Dependent Cell ◽  
High Concentrations

ABSTRACT Cells from multicellular organisms are dependent upon exogenous signals for survival, growth, and proliferation. The relationship among these three processes was examined using an interleukin-3 (IL-3)-dependent cell line. No fixed dose of IL-3 determined the threshold below which cells underwent apoptosis. Instead, increasing growth factor concentrations resulted in progressive shortening of the G1 phase of the cell cycle and more rapid proliferative expansion. Increased growth factor concentrations also resulted in proportional increases in glycolytic rates. Paradoxically, cells growing in high concentrations of growth factor had an increased susceptibility to cell death upon growth factor withdrawal. This susceptibility correlated with the magnitude of the change in the glycolytic rate following growth factor withdrawal. To investigate whether changes in the availability of glycolytic products influence mitochondrion-initiated apoptosis, we artificially limited glycolysis by manipulating the glucose levels in the medium. Like growth factor withdrawal, glucose limitation resulted in Bax translocation, a decrease in mitochondrial membrane potential, and cytochromec redistribution to the cytosol. In contrast, increasing cell autonomous glucose uptake by overexpression of Glut1 significantly delayed apoptosis following growth factor withdrawal. These data suggest that a primary function of growth factors is to regulate glucose uptake and metabolism and thus maintain mitochondrial homeostasis and enable anabolic pathways required for cell growth. Consistent with this hypothesis, expression of the three genes involved in glucose uptake and glycolytic commitment, those for Glut1, hexokinase 2, and phosphofructokinase 1, was found to rapidly decline to nearly undetectable levels following growth factor withdrawal.

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