A LlWRKY33-LlHSFA4-LlCAT2 module confers resistance to Botrytis cinerea in lily

Liping Ding; Ze Wu; Jun Xiang; Xing Cao; Sujuan Xu; Yinyi Zhang; Dehua Zhang; Nianjun Teng

doi:10.1093/hr/uhad254

A LlWRKY33-LlHSFA4-LlCAT2 module confers resistance to Botrytis cinerea in lily

Hortic Res. 2023 Nov 27;11(1):uhad254. doi: 10.1093/hr/uhad254. eCollection 2024 Jan.

Authors

Liping Ding^{1

2}, Ze Wu^{1

2}, Jun Xiang^{1

2}, Xing Cao³, Sujuan Xu^{1

2}, Yinyi Zhang^{1

2}, Dehua Zhang^{1

2}, Nianjun Teng^{1

2}

Affiliations

¹ Key Laboratory of Landscaping, Ministry of Agriculture and Rural Affairs, Key Laboratory of Biology of Ornamental Plants in East China, National Forestry and Grassland Administration, College of Horticulture, Nanjing Agricultural University, Nanjing 210095, China.
² Jiangsu Graduate Workstation of Nanjing Agricultural University and Nanjing Oriole Island Modern Agricultural Development Co., Ltd., Nanjing 210043, China.
³ College of Architecture, Yantai University, Yantai, 264005, China.

Abstract

Gray mold caused by Botrytis cinerea is one of the major threats in lily production. However, limited information is available about the underlying defense mechanism against B. cinerea in lily. Here, we characterized a nuclear-localized class A heat stress transcription factor (HSF)-LlHSFA4 from lily (Lilium longiflorum), which positively regulated the response to B. cinerea infection. LlHSFA4 transcript and its promoter activity were increased by B. cinerea infection in lily, indicating its involvement in the response to B. cinerea. Virus-induced gene silencing (VIGS) of LlHSFA4 impaired the resistance of lily to B. cinerea. Consistent with its role in lily, overexpression of LlHSFA4 in Arabidopsis (Arabidopsis thaliana) enhanced the resistance of transgenic Arabidopsis to B. cinerea infection. Further analysis showed that LlWRKY33 directly activated LlHSFA4 expression. We also found that both LlHSFA4 and LlWRKY33 positively regulated plant response to B. cinerea through reducing cell death and H₂O₂ accumulation and activating the expression of the reactive oxygen species (ROS) scavenging enzyme gene LlCAT2 (Catalase 2) by binding its prompter, which might contribute to reducing H₂O₂ accumulation in the infected area. Taken together, our data suggested that there may be a LlWRKY33-LlHSFA4-LlCAT2 regulatory module which confers B. cinerea resistance via reducing cell death and the ROS accumulation.