A CONSTANS-like transcriptional co-activator couples ethylene signaling to jasmonate biosynthesis and is targeted by a fungal effector.

Abstract

Ethylene and jasmonate synergistically regulate immunity against necrotrophic pathogens, but how ethylene signaling promotes jasmonate biosynthesis remains unclear. Here, we show that the apple CONSTANS-like (COL) protein MdCOL4 functions as a transcriptional co-activator that couples ethylene signaling to jasmonate biosynthesis during disease resistance. The ethylene-responsive transcription factor MdERF098 directly activates the jasmonate biosynthetic genes MdOPR2 and MdOPR3. MdCOL4 physically associates with MdERF098 and enhances its DNA-binding activity, thereby promoting MdOPR2/3 transcription, jasmonate accumulation, and resistance to apple Valsa canker, a destructive trunk disease caused by Valsa mali, a necrotrophic fungal pathogen. We further identify a fungal effector from V. mali, Vm11039, that translocates into the host nucleus and binds MdCOL4 with higher affinity than MdERF098, competitively disrupting the MdCOL4-MdERF098 complex. This interference attenuates jasmonate biosynthesis and promotes pathogen infection. Together, our findings uncover a transcriptional co-activation mechanism that couples ethylene signaling to jasmonate biosynthesis and establish transcriptional co-activator complexes as vulnerable regulatory hubs targeted by pathogen effectors to suppress hormone-mediated immunity, thereby providing a potential target for engineering resistance against necrotrophic diseases.

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