Phytoplasma-infected Chinese cherry (Cerasus pseudocerasus L.) exhibits symptoms of phyllody and stiff fruit. To reveal the molecular mechanism of stiff fruit, the current study integrated transcriptome with metabolome. Results showed that the differentially expressed genes and the differentially accumulated metabolites were related to a high proportion of two aspects: pathogen resistance and signaling or regulatory functions, and the molecular mechanism of stiff fruit that were majorly induced by plant biotic stress response via phytohormones signal transduction, especially signal pathways of salicylic acid, auxin, and abscisic acid. Notably, there was a large overlap between phytoplasma stress response and drought stress response genes. Phytohormone content displayed significant difference that abscisic acid and salicylic acid content of phytoplasma-infected fruit were higher than that of healthy fruit, whereas zeatin, jasmonic acid, and IAA showed the opposite results. In addition, the expression of key candidate genes, including IAA4, IAA9, IAA14, IAA31, ARF5, ARF9, GH3.1, GH3.17, SAUR20, SAUR32, SAUR40, PR1a, PRB1, TGA10, SnRK2.3, and AHK2, was responsible for cherry stiff fruit. In conclusion, the current study contributed a foundation for understanding the molecular mechanism of cherry phyllody disease on stiff fruit, a better understanding of fruit development, and found the potential candidate genes involved in cherry stiff fruit, which could be used for further research in associated fields.
Armet, an aphid effector protein, induces pathogen resistance in plants by promoting the accumulation of salicylic acid
