Fig. 6: A model for myo-inositol regulation of ROS-induced PCD in apple.

In MdMIPS1/2-silenced lines, decreased MI biosynthesis induces SA accumulation by stimulating the accumulation of WS pectin. Enhanced SA signaling directly compromises POD, SOD, and anti-O₂⁻ activities, resulting in high ROS accumulation. Moreover, MI reduction also stimulates ET production and further induces ROS accumulation, possibly through SA-dependent and SA-independent pathways. Eventually, the accumulation of excess ROS directly leads to severe PCD and necrosis. In addition, metabolic influx of sorbitol causes additional oxidative stress and further accelerates necrosis around the leaf vein. G6P glucose-6-phosphate, Sor sorbitol, MI myo-inositol, and MI-1-P myo-inositol-1-phosphate. The solid and dashed lines refer to direct and indirect effects, respectively.