Control of respiration similar to that seen in mitochondria of higher plants and animals was found in the phosphate-deficient cells of
Brevibacterium ammoniagenes when phosphate is supplied, and was named "Pi-effect."
The phosphate-deficient cells of this organism can incorporate phosphate at a great rate whereas the phosphate-sufficient ones can take it up only slightly. Accompanying the phosphate incorporation, marked stimulation of the rate of respiration is observed and after exhaustion of phosphate the rate returns to the initial low level. This stimulation by phosphate can be repeated many times until cellular phosphate pool is filled to the maximum extent.
The "Pi-effect" is independent of the phosphate transport as a counterion in cation transport, phosphate-requiring enzyme systems, substrate level phosphorylation in glycolytic pathway, and the energy-requiring synthesis of macromolecules.
The "Pi-effect" is distributed widely in gram-negative enteric bacteria.
The relationship between the "Pi-effect" and phosphorylating respiration in this organism is discussed.
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