FIGURE 10.
The hypothesized P5C-Pro cycle and its hyperactivity during uncoupled P5C oxidation. In response to abiotic stresses, Pro is gradually accumulated by increased synthesis and suppressed oxidation. Once the stress is relieved, ProDH-FAD complex oxidizes Pro to P5C while transferring electrons to the mtETC. P5C further oxidation to Glu and then to α ketoglutarate (αKG) is coupled to NAD(P)H formation. When Pro is supplied in excess and ProDH transcription and activity are induced, P5CDH activity does not keep up with ProDH activity, and Pro oxidation becomes uncoupled. Under such conditions, the rate of P5C generation in the mitochondria exceeds its further oxidation to Glu. P5C excess is transported to the cytosol and reduced by P5CR to Pro that is transported to the mitochondria. This P5C-Pro intensive cycling elevates the flow of electrons through ProDH-FAD to the mtETC and to O2, leading to concomitant generation of ROS. In the p5cdh mutant, the intensive operation of this cycle enhances ROS generation and their spreading to the nuclei and very likely induces programmed cell death (PCD). ETC, electron transfer chain; UQ, ubiquinone.