TY  - JOUR
AU  - Gou, Rongxin
AU  - Wang, Yi
AU  - Yang, Tuo
AU  - Zeng, Zhen
AU  - Wang, Di
AU  - Jiang, Yin
AU  - Zhang, Guojun
AU  - Chen, Defeng
AU  - Wei, Zunzheng
PY  - 2026
TI  - ZeEIL1—ZeERF113—ZeMC2 cascade enhances colored calla lily resistance to soft rot through the ethylene signaling pathway
JO  - Horticultural Plant Journal
SN  - 2095-9885
SP  - 1910
EP  - 1923
VL  - 12
IS  - 8
AB  - Soft rot caused by Pectobacterium carotovorum poses a major threat to the cultivation of colored calla lily (Zantedeschia elliottiana). This study identified ZeERF113 through transcriptome analysis and weighted gene coexpression network analysis (WGCNA), revealing its close association with the accumulation of 1-aminocyclopropane-1-carboxylate (ACC) in colored calla lily after soft rot infection. The overexpression of ZeERF113 in Nicotiana tabacum significantly increased resistance to the pathogen, as evidenced by reduced lesion size, lower malondialdehyde (MDA) content, and elevated levels of various antioxidant enzymes. In colored calla lily, transient overexpression of ZeERF113 enhanced resistance to P. carotovorum, whereas silencing ZeERF113 weakened this resistance. Through yeast one-hybrid (Y1H) assays, dual-luciferase reporter assays, electrophoretic mobility shift assays (EMSAs), and biolayer interferometry (BLI) assays, we confirmed that ZeERF113 binds to and activates the promoter of ZeMC2. Transient overexpression of ZeMC2 in colored calla lily significantly enhanced resistance to P. carotovorum, while silencing ZeMC2 compromised this resistance. This study further revealed that ZeEIL1 responds to ethylene (ETH) signaling and subsequently activates the expression of ZeERF113, as demonstrated by Y1H assays, dual-luciferase reporter assays, EMSAs, and BLI assays. This discovery highlights the critical role of the ETH-regulated ZeEIL1–ZeERF113–ZeMC2 cascade in enhancing resistance to soft rot in colored calla lily, providing new insights into its disease resistance mechanism.
UR  - https://doi.org/10.1016/j.hpj.2025.03.004
DO  - 10.1016/j.hpj.2025.03.004