Which molecule serves as a feedback signal to glycolysis by inhibiting PFK-1 when biosynthetic intermediates are abundant?

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Multiple Choice

Which molecule serves as a feedback signal to glycolysis by inhibiting PFK-1 when biosynthetic intermediates are abundant?

Glycolysis is tuned by allosteric regulators of phosphofructokinase-1 to match the cell’s needs for energy versus biosynthesis. When biosynthetic intermediates are abundant, citrate builds up because it’s an intermediate that links the TCA cycle to fatty acid, nucleotide, and other biosyntheses. Citrate in the cytosol signals that there are plenty of carbon skeletons and energy, so glycolysis should slow down to divert glucose toward biosynthetic pathways rather than toward immediate energy production. Citrate achieves this by binding to PFK-1 and inhibiting its activity, reducing the conversion of fructose-6-phosphate to fructose-1,6-bisphosphate and thereby downregulating the glycolytic flux. In contrast, fructose-2,6-bisphosphate acts to activate PFK-1 when biosynthesis is needed, and ATP or NADH reflect energy or redox state rather than signaling biosynthetic abundance; they can inhibit or modulate PFK-1 under different conditions, but citrate specifically serves as the signal indicating that biosynthetic intermediates are plentiful and glycolysis should be dialed back.

Glycolysis is tuned by allosteric regulators of phosphofructokinase-1 to match the cell’s needs for energy versus biosynthesis. When biosynthetic intermediates are abundant, citrate builds up because it’s an intermediate that links the TCA cycle to fatty acid, nucleotide, and other biosyntheses. Citrate in the cytosol signals that there are plenty of carbon skeletons and energy, so glycolysis should slow down to divert glucose toward biosynthetic pathways rather than toward immediate energy production. Citrate achieves this by binding to PFK-1 and inhibiting its activity, reducing the conversion of fructose-6-phosphate to fructose-1,6-bisphosphate and thereby downregulating the glycolytic flux.

In contrast, fructose-2,6-bisphosphate acts to activate PFK-1 when biosynthesis is needed, and ATP or NADH reflect energy or redox state rather than signaling biosynthetic abundance; they can inhibit or modulate PFK-1 under different conditions, but citrate specifically serves as the signal indicating that biosynthetic intermediates are plentiful and glycolysis should be dialed back.

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