Negative feedback of glycolysis and oxidative phosphorylation: Mechanisms of and reasons for it

Sokolov, Svyatoslav S.; Balakireva, Anastasia V.; Маркова, О. В.; Severin, Fedor F.

doi:10.1134/s0006297915050065

Cited by 18 publications

(13 citation statements)

References 39 publications

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“…On one hand, galactose did not suppress respi ration of gpm1 cells. On the other hand, we showed earli er that galactose inhibits growth of gpm1 strain on solid medium [1]. We confirmed that this result was not an arti fact of the growth on solid substrates.…”

Section: Resultssupporting

confidence: 80%

“…Eukaryotic cells tend to avoid simultaneous activa tion of glycolysis and oxidative phosphorylation (see [1] for review). The bioenergetics of actively proliferating cells is usually based on glycolysis and not on respiration [2 4].…”

mentioning

confidence: 99%

“…This mechanism is called the Crabtree effect [10]. The molec ular machinery of the Crabtree effect and the signals trig gering it are still unclear (see [1] and [11] for reviews).…”

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confidence: 99%

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Triosephosphates as intermediates of the Crabtree effect

Sokolov

Маркова

Nikolaeva

et al. 2017

Biochemistry Moscow

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An increase in glucose concentration in the medium rapidly decreases respiration rate in many cell types, including tumor cells. The molecular mechanism of this phenomenon, the Crabtree effect, is still unclear. It was shown earlier that adding the intermediate product of glycolysis fructose-1,6-bisphosphate to isolated mitochondria suppresses their respiration. To study possible roles of glycolytic intermediates in the Crabtree effect, we used a model organism, the yeast Saccharomyces cerevisiae. To have the option to rapidly increase intracellular concentrations of certain glycolytic intermediates, we used mutant cells with glycolysis blocked at different stages. We studied fast effects of glucose addition on the respiration rate in such cells. We found that addition of glucose affected cells with deleted phosphoglycerate mutase (strain gpm1-delta) more strongly than ones with inactivated aldolase or phosphofructokinase. In the case of preincubation of gpm1-delta cells with 2-deoxyglucose, which blocks glycolysis at the stage of 2-deoxyglucosephosphate formation, the effect of glucose addition was absent. This suggests that triosephosphates are intermediates of the Crabtree effect. Apart from this, the incubation of gpm1-delta cells in galactose-containing medium appeared to cause a large increase in their size. It was previously shown that galactose addition did not have any short-term effect on respiration rate of gpm1-delta cells and, at the same time, strongly suppressed their growth rate. Apparently, the influence of increasing triosephosphate concentration on yeast physiology is not limited to the activation of the Crabtree effect.

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Section: Resultssupporting

confidence: 80%

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confidence: 99%

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Triosephosphates as intermediates of the Crabtree effect

Sokolov

Маркова

Nikolaeva

et al. 2017

Biochemistry Moscow

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“…Thus, ATP production of the cells varies with environment changes of the cells [ 25 ]. ATP in the cells is produced mainly by the glycolysis and OXPHOS [ 26 , 27 ]. The proportion of the two varies with the environment in which the cells live.…”

Section: Discussionmentioning

confidence: 99%

Oxaloacetate Ameliorates Chemical Liver Injury via Oxidative Stress Reduction and Enhancement of Bioenergetic Fluxes

Kuang

Han

et al. 2018

IJMS

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Chemical injury is partly due to free radical lipid peroxidation, which can induce oxidative stress and produce a large number of reactive oxygen species (ROS). Oxaloacetic acid is an important intermediary in the tricarboxylic acid cycle (TCA cycle) and participates in metabolism and energy production. In our study, we found that oxaloacetate (OA) effectively alleviated liver injury which was induced by hydrogen peroxide (H2O2) in vitro and carbon tetrachloride (CCl4) in vivo. OA scavenged ROS, prevented oxidative damage and maintained the normal structure of mitochondria. We further confirmed that OA increased adenosine triphosphate (ATP) by promoting the TCA production cycle and oxidative phosphorylation (OXPHOS). Finally, OA inhibited the mitogen-activated protein kinase (MAPK) and apoptotic pathways by suppressing tumor necrosis factor-α (TNF-α). Our findings reveal a mechanism for OA ameliorating chemical liver injury and suggest a possible implementation for preventing the chemical liver injury.

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“…If something similar exists in higher organisms, than tightening of cell cycle arrest by retrograde signaling under stress conditions can inhibit growth of cells with non-functional mitochondria. As cancer cells typically rely on glycolysis and inhibit mitochondrial energy functions [ 44 ], such regulation could be a mechanism that suppresses proliferation of such unwanted cells in multicellular eukaryotes.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial retrograde signaling inhibits the survival during prolong S/G2 arrest inSaccharomyces cerevisiae

et al. 2015

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Cell senescence is dependent on the arrest in cell cycle. Here we studied the role of mitochondrial retrograde response signaling in yeast cell survival under a prolonged arrest. We have found that, unlike G1, long-term arrest in mitosis or S phase results in a loss of colony-forming abilities. Consistent with previous observations, loss of mitochondrial DNA significantly increased the survival of arrested cells. We found that this was because the loss increases the duration of G1 phase. Unexpectedly, retrograde signaling, which is typically triggered by a variety of mitochondrial dysfunctions, was found to be a negative regulator of the survival after the release from S-phase arrest induced by the telomere replication defect. Deletion of retrograde response genes decreased the arrest-induced death in such cells, whereas deletion of negative regulator of retrograde signaling MKS1 had the opposite effect. We provide evidence that these effects are due to alleviation of the strength of the S-phase arrest.

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Negative feedback of glycolysis and oxidative phosphorylation: Mechanisms of and reasons for it

Cited by 18 publications

References 39 publications

Triosephosphates as intermediates of the Crabtree effect

Triosephosphates as intermediates of the Crabtree effect

Oxaloacetate Ameliorates Chemical Liver Injury via Oxidative Stress Reduction and Enhancement of Bioenergetic Fluxes

Mitochondrial retrograde signaling inhibits the survival during prolong S/G2 arrest inSaccharomyces cerevisiae

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