Ethylene‐MPK8‐ERF.C1‐PR module confers resistance against Botrytis cinerea in tomato fruit without compromising ripening

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Deng, Heng | Pei, Yangang | Xu, Xin | Du, Xiaofei | Xue, Qihan | Gao, Zhuo | Shu, Peng | Wu, Yi | Liu, Zhaoqiao | Jian, Yongfei | Wu, Mengbo | Wang, Yikui | Li, Zhengguo | Pirrello, Julien | Bouzayen, Mondher | Deng, Wei | Hong, Yiguo | Liu, Mingchun

Edité par CCSD ; Wiley -

International audience. The plant hormone ethylene plays a critical role in fruit defense against Botrytis cinerea attack, but the underlying mechanisms remain poorly understood. Here, we showed that ethylene response factor SlERF.C1 acts as a key regulator to trigger the ethylene‐mediated defense against B. cinerea in tomato fruits without compromising ripening. Knockout of SlERF.C1 increased fruit susceptibility to B. cinerea with no effect on ripening process, while overexpression enhanced resistance. RNA‐Seq, transactivation assays, EMSA and ChIP‐qPCR results indicated that SlERF.C1 activated the transcription of PR genes by binding to their promoters. Moreover, SlERF.C1 interacted with the mitogen‐activated protein kinase SlMPK8 which allowed SlMPK8 to phosphorylate SlERF.C1 at the Ser 174 residue and increases its transcriptional activity. Knocking out of SlMPK8 increased fruit susceptibility to B. cinerea , whereas overexpression enhanced resistance without affecting ripening. Furthermore, genetic crosses between SlMPK8‐KO and SlERF.C1 ‐OE lines reduced the resistance to B. cinerea attack in SlERF.C1 ‐OE fruits. In addition, B. cinerea infection induced ethylene production which in turn triggered SlMPK8 transcription and enhanced the phosphorylation of SlERF.C1. Overall, our findings reveal the regulatory mechanism of the ‘Ethylene‐MPK8‐ERF.C1‐PR’ module in resistance against B. cinerea and provide new insight into the manipulation of gray mold disease in fruits.

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