Ethylene promotes singlet oxygen-mediated disease development in Arabidopsis infected by fungus Alternaria alternata

• Necrotrophic Alternaria alternata induces EX1-dependent ETRGs expression in Arabidopsis • ET contributes to 1 O 2 -responsive gene expression • High levels of ET enhance JARGs expression and JA accumulation • ET promotes 1 O 2 -mediated disease development through JA pathway via A. alternata infection The pathogenic fungus Alternaria alternata induces chloroplast-derived singlet oxygen ( 1 O 2 ) production and activates EXECUTER (EX)1-dependent 1 O 2 signaling in Arabidopsis through tenuazonic acid (TeA), its key virulence factor leading to plant death. This 1 O 2 is known to trigger the biosynthesis and signaling of various defense hormones. TeA rapidly upregulates nuclear genes involved in jasmonic acid (JA) synthesis and signaling, and EX1-mediated reverse signaling appears to be a critical link for establishing a signaling cascade from 1 O 2 to JA. Although JA and ethylene (ET) are known to synergistically regulate plant defense responses against necrotrophic pathogens, the precise role of ET in A. alternata -induced disease development in Arabidopsis remains unclear, and relatively little research has examined potential cross-talk between ET and ¹O 2 signaling. Our investigations revealed that A. alternata infection significantly enhances the expression of ET response genes (ETRGs) and that EX1EX2 inactivation leads to a significant reduction in ETRGs expression levels. Through the exogenous application of both an ET precursor (1-aminocyclopropane-1-carboxylic acid) and ET inhibitor (silver thiosulfate), we corroborated that ET contributes to the expression of 1 O 2 -responsive genes (SORGs) and the progression of disease. This suggests that ET signaling interacts with EX1-dependent 1 O 2 signaling thereby promoting 1 O 2 -induced cell death. Concurrently, we observed that inactivation of EIN2 and ERF6 results in reduced levels of JA synthesis gene expression and JA production, and that the AOC3 mutation reduces the expression levels of A. alternata -induced ETRGs. The findings collectively demonstrate that ET promotes the expression of JA-responsive genes (JARGs) and JA production, which, in turn, exacerbates the sensitivity of Arabidopsis to A. alternata .