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Article|27 Nov 2023|OPEN
A LlWRKY33-LlHSFA4-LlCAT2 module confers resistance to Botrytis cinerea in lily
Liping Ding1,2 ,† , Ze Wu1,2 ,† , Jun Xiang1,2 , Xing Cao3 and Sujuan Xu1,2 , Yinyi Zhang1,2 , Dehua Zhang1,2 , Nianjun Teng,1,2 ,
1Key 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
2Jiangsu Graduate Workstation of Nanjing Agricultural University and Nanjing Oriole Island Modern Agricultural Development Co., Ltd., Nanjing 210043, China
3College of Architecture, Yantai University, Yantai, 264005, China
*Corresponding author. E-mail:
Both authors contributed equally to the study.

Horticulture Research 11,
Article number: uhad254 (2024)
Views: 21

Received: 17 Jul 2023
Accepted: 14 Nov 2023
Published online: 27 Nov 2023


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.