RPW8.1 enhances the ethylene-signaling pathway to feedback-attenuate its mediated cell death and disease resistance inArabidopsis

TheArabidopsis RESISTANCE TO POWDERY MILDEW 8.1(RPW8.1) activates confined cell death and defense against different pathogens. However, the underlying regulatory mechanisms still remain elusive. Here, we show that RPW8.1 activates ethylene signaling that, in turn, negatively regulatesRPW8.1expression. RPW8.1 binds and stabilizes 1-aminocyclopropane-1-carboxylate oxidase 4 (ACO4), which may in part explain increased ethylene production and signaling inRPW8.1-expressing plants. In return, ACO4 and other key components of ethylene signaling negatively regulate RPW8.1-mediated cell death and disease resistance via suppressingRPW8.1expression. Loss of function inACO4,EIN2,EIN3 EIL1,ERF6,ERF016orORA59increases RPW8.1-mediated cell death and defense response. By contrast, overexpression ofEIN3abolishes or significantly compromises RPW8.1-mediated cell death and disease resistance. Furthermore,ERF6,ERF016andORA59appear to act as trans-repressors ofRPW8.1, withOAR59being able to directly bind to theRPW8.1promoter. Taken together, our results have revealed a feedback regulatory circuit connectingRPW8.1and the ethylene-signaling pathway, in whichRPW8.1enhances ethylene signaling, and the latter, in return, negatively regulates RPW8.1-mediated cell death and defense response via suppressingRPW8.1expression to attenuate its defense activity.

Automated summary

The study reveals a feedback regulatory circuit between RPW8.1 and the ethylene-signaling pathway, where RPW8.1 enhances ethylene signaling which in turn negatively regulates RPW8.1-mediated cell death and defense response. Key components of ethylene signaling like ACO4, EIN2, EIN3, EIL1, ERF6, ERF016, and ORA59 act as negative regulators of RPW8.1, suppressing its expression and defense activity.