Myo-inositol mediates reactive oxygen species-induced programmed cell death via salicylic acid-dependent and ethylene-dependent pathways in apple

Abstract

As a versatile compound, <i>myo</i>-inositol plays vital roles in plant biochemistry and physiology. We previously showed that exogenous application of <i>myo</i>-inositol had a positive role in salinity tolerance in <i>Malus hupehensis</i> Rehd. In this study, we used <i>MdMIPS</i> (the rate-limiting gene of <i>myo</i>-inositol biosynthesis) transgenic apple lines to gain new insights into the physiological role of <i>myo</i>-inositol in apple. Decreasing <i>myo</i>-inositol biosynthesis in apple lines by RNA silencing of <i>MdMIPS1/2</i> led to extensive programmed cell death, which manifested as necrosis of both the leaves and roots and, ultimately, plant death. Necrosis was directly caused by the excessive accumulation of reactive oxygen species, which may be closely associated with the cell wall polysaccharide-mediated increase in salicylic acid and a compromised antioxidant system, and this process was enhanced by an increase in ethylene production. In addition, a high accumulation of sorbitol promoted necrosis. This synergetic interplay between salicylic acid and ethylene was further supported by the fact that increased <i>myo</i>-inositol accumulation significantly delayed leaf senescence in <i>MdMIPS1</i>-overexpressing apple lines. Taken together, our results indicated that apple <i>myo</i>-inositol regulates reactive oxygen species-induced programmed cell death through salicylic acid-dependent and ethylene-dependent pathways.