Loss of ACO4 in petunia improves abiotic stress tolerance by reducing the deleterious effects of stress-induced ethylene.

To investigate the role of ethylene (ET) in abiotic stress tolerance in petunia cv. 'Mirage Rose', petunia plants in which the ET biosynthesis gene 1-aminocyclopropane-1-carboxylic acid oxidase 4 (ACO4) was knocked out (phaco4 mutants) and wild-type (WT) plants were exposed to heat and drought conditions. Loss of function of ACO4 significantly delayed leaf senescence and chlorosis under heat and drought stress by maintaining the SPAD values and the relative water content, indicating a greater stress tolerance of phaco4 mutants than that of WT plants. This tolerance was related to the lower ET and reactive oxygen species levels in the mutants than in WT plants. Furthermore, the stress-induced expression of genes related to ET signal transduction, antioxidant and proline activities, heat response, and biosynthesis of abscisic acid was higher in the mutants than in WT plants, indicating a greater stress tolerance in the former than in the latter. These results demonstrate the deleterious effects of stress-induced ET on plant growth and provide a better physiological and molecular understanding of the role of stress ET in the abiotic stress response of petunia. Because the loss of function of ACO4 in petunia improved stress tolerance, we suggest that ACO4 plays a vital role in stress-induced leaf senescence and acts as a negative regulator of abiotic stress tolerance.