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

2010 ◽  
Vol 27 (1) ◽  
pp. 181-190 ◽  
Author(s):  
Marie-Françoise Clincke ◽  
Emmanuel Guedon ◽  
Frances T. Yen ◽  
Virginie Ogier ◽  
Olivier Roitel ◽  
...  


2018 ◽  
Author(s):  
Robin Green ◽  
Sonal ◽  
Lin Wang ◽  
Samuel F.M. Hart ◽  
Wenyun Lu ◽  
...  

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.



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 ◽  
...  

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.



2011 ◽  
Vol 5 (S8) ◽  
Author(s):  
Noëlia Sanchez ◽  
Nga Lao ◽  
Clair Gallagher ◽  
Martin Clynes ◽  
Niall Barron


Author(s):  
Ying Zhang ◽  
Wei Wang ◽  
Yubing Xie ◽  
Weiting Yu ◽  
Guojun Lv ◽  
...  
Keyword(s):  




2021 ◽  
Author(s):  
Chunxiong Luo ◽  
Wenting Shen ◽  
Ziqing Gao ◽  
Kaiyue Chen ◽  
Qi Ouyang

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.



Author(s):  
Maria J. De Jesus ◽  
M. Bourgeois ◽  
G. Baumgartner ◽  
P. Tromba ◽  
Martin Jordan ◽  
...  


2008 ◽  
Vol 99 (15) ◽  
pp. 7143-7151 ◽  
Author(s):  
G. Chabanon ◽  
L. Alves da Costa ◽  
B. Farges ◽  
C. Harscoat ◽  
S. Chenu ◽  
...  


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