Ihave mutant cells that make no pfk2enzyme. i measure rates of oxygen consumption in these mutant cells and compare them to wild type cells.

The correct answer is that mutant cells will exhibit diminished oxygen consumption; decreased glycolysis results in decreased Kreb's cycle and electron transport chain.

The PFK2 enzyme catalyzes the generation of F26BP, this binds with the allosteric site of PFK-1 and increases the affinity of PFK-1 with F6P and also decreases the affinity of allosteric inhibitors citrate and ATP to PFK-1. Thus, PFK-1 will combine with F6P at a greater rate.

This ultimately results in more glycolysis, thus, more ETC and more consumption of O2. If there is no PFK2, then there will be a reduction in glycolysis, TCA, ETC, and consumption of oxygen.

The PFK2 is an enzyme accountable for monitoring the rates of gluconeogenesis and glycolysis in the human body. In the absence of glycolysis, there will be a reduction in TCA, ETC, and consumption of O2.

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