文献类型： 外文期刊

作者： Deng, Heng ¹ ; Pei, Yangang ¹ ; Xu, Xin ³ ; Du, Xiaofei ¹ ; Xue, Qihan ¹ ; Gao, Zhuo ¹ ; Shu, Peng ¹ ; Wu, Yi ¹ ; Liu, Zhaoqiao ¹ ; Jian, Yongfei ³ ; Wu, Mengbo ¹ ; Wang, Yikui ⁴ ; Li, Zhengguo ³ ; Pirrello, Julien ⁵ ; Bouzayen, Mondher ⁵ ; Deng, Wei ³ ; Hong, Yiguo ⁶ ; Liu, Mingchun ¹ ;

作者机构： 1.Sichuan Univ, Coll Life Sci, Minist Educ, Key Lab Bioresource & Ecoenvironm, Chengdu 610065, Peoples R China

2.Southwest Univ Sci & Technol, Sch Life Sci & Engn, Mianyang 621010, Peoples R China

3.Chongqing Univ, Sch Life Sci, Key Lab Plant Hormones & Dev Regulat Chongqing, Chongqing 400044, Peoples R China

4.Guangxi Acad Agr Sci, Vegetable Res Inst, Nanning 530007, Peoples R China

5.Univ Toulouse, UPS, CNRS, UMR 5546,Lab Rech Sci Vegetales Genomique & Biotec, Toulouse, France

6.Univ Warwick, Sch Life Sci, Warwick CV4 7AL, England

7.Hangzhou Normal Univ, Coll Life & Environm Sci, Res Ctr Plant RNA Signaling, Hangzhou 311121, Peoples R China

关键词： Botrytis cinerea; ERF; MPK; phosphorylation; postharvest disease

期刊名称：NEW PHYTOLOGIST （ 影响因子：9.4； 五年影响因子：10.5 ）

ISSN： 0028-646X

年卷期： 2024 年 242 卷 2 期

页码：

收录情况： SCI

摘要： 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 Ser174 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.