Strategies for regulating the central pathways in carbohydrate metabolism vary among different cells in one organism and among organisms. Slight changes in the regulation of enzymes in central metabolism can effectively re-route metabolite traffic through these pathways, just like a small mutation in PFK-1 can convert a healthy cell into a cancerous one. For instance, Gillaspera mold uses an alternative strategy for regulation the TCA and glycolysis. Gillaspera contains a unique isocitrate dehydrogenase that has an allosteric site for citrate. High citrate inhibits isocitrate dehydrogenase in this organism. Gillaspera also lacks a citrate binding site on PFK-1, so this variant of the enzyme is not affected by citrate concentrations at all. Gillaspera lacks the enzymes ethanol dehydrogenase and lactate dehydrogenase and no carbons are lost in its unique fermentation product. Would high glucose in these organisms lead to production of carbon dioxide from glucose catabolism? Why do you say this?
Strategies for regulating the central pathways in carbohydrate
For instance, Gillaspera mold uses an alternative strategy for regulation the TCA and glycolysis.
Gillaspera contains a unique isocitrate dehydrogenase that has an allosteric site for citrate. High citrate inhibits isocitrate dehydrogenase in this organism.
Gillaspera also lacks a citrate binding site on PFK-1, so this variant of the enzyme is not affected by citrate concentrations at all.
Gillaspera lacks the enzymes ethanol dehydrogenase and lactate dehydrogenase and no carbons are lost in its unique fermentation product.
Would high glucose in these organisms lead to production of carbon dioxide from glucose catabolism? Why do you say this?
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