Role of salicylic acid in alleviating the inhibition of root elongation by suppressing ethylene emission in rice under Al toxicity conditions

Salicylic acid (SA) is the phytohormone responsible for the regulation of growth and response to environmental stress in plants. In the present study, the application of 1 mu M SA significantly enhanced the SA content in rice roots and improved their growth when affected by Al toxicity by concomitantly decreasing the Al content of the root apex. The addition of SA significantly inhibited the synthesis of pectin and hemicellulose, suppressed the activity of pectin methylesterase (PME), and decreased the cell wall Al content. The expression of OsSTAR1 (sensitive to Al rhizotoxicity) and OsSTAR2 was induced by SA to mask the Al-binding sites in the cell walls. The expression of OsALS1 (Al sensitive) was also stimulated by SA, which improved the transport of cytoplasmic Al into the vacuoles. In rice affected by Al toxicity, SA significantly increased the activity of catalase and peroxidase and reduced the H2O2 content and malondialdehyde content. The expression of OsACS1 (ACC synthase) and OsACO1 (ACC oxidase) was inhibited by SA and thus inhibited ethylene emission. The addition of ethylene precursor 1-aminocylopropane-1-carboxylic acid (ACC) along with SA under Al toxicity conditions aggravated the inhibition of root elongation, accompanied by an increased Al content in the root apex and cell walls, increased pectin content, and rendered PME activity greater than with single Al treatment. However, the addition of aminoethoxyvinylglycine (AVG, inhibitor of the ACC synthase) along with SA under Al toxicity conditions showed the opposite effect, indicating that SA inhibited ethylene emission, thus reducing the Al deposition on cell walls.