J Integr Plant Biol ›› 2022, Vol. 64 ›› Issue (10): 1979-1993.DOI: 10.1111/jipb.13339

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  • 收稿日期:2022-04-20 接受日期:2022-08-03 出版日期:2022-10-01 发布日期:2022-10-20

The lncRNA39896–miR166b–HDZs module affects tomato resistance to Phytophthora infestans

Yuhui Hong1, Yuanyuan Zhang1,2, Jun Cui1,3, Jun Meng4, Yinhua Chen5, Chengwei Zhang6, Jinxiao Yang6* and Yushi Luan1*   

  1. 1 School of Bioengineering, Dalian University of Technology, Dalian 116024, China
    2 State Key Laboratory of Rice Biology, China National Rice Research Institute, Hangzhou 311400, China
    3 College of Life Science, Hunan Normal University, Changsha 410081, China
    4 School of Computer Science and Technology, Dalian University of Technology, Dalian 116024, China
    5 Hainan Key Laboratory for Sustainable Utilization of Tropical Bioresource, College of Tropical Crops, Hainan University, Haikou 570228, China
    6 Beijing Key Laboratory of Maize DNA Fingerprinting and Molecular Breeding, Beijing Academy of Agriculture & Forestry Sciences, Beijing 100000, China

    *Correspondences: Jinxiao Yang (yangjinxiao@maizedna.org); Yushi Luan (ysluan@dlut.edu.cn, Dr. Luan is fully responsible for the distributions of all materials associated with this article)
  • Received:2022-04-20 Accepted:2022-08-03 Online:2022-10-01 Published:2022-10-20

Abstract: The yield and quality of tomatoes (Solanum lycopersicum) is seriously affected by Phytophthora infestans. The long non-coding RNA (lncRNA) Sl-lncRNA39896 is induced after P. infestans infection and was previously predicted to act as an endogenous target mimic (eTM) for the microRNA Sl-miR166b, which function in stress responses. Here, we further examined the role of Sl-lncRNA39896 and Sl-miR166b in tomato resistance to P. infestans. Sl-miR166b levels were higher in Sl-lncRNA39896-knockout mutants than in wild-type plants, and the mutants displayed enhanced resistance to P. infestans. A six-point mutation in the region of Sl-lncRNA39896 that binds to Sl-miR166b disabled the interaction, suggesting that Sl-lncRNA39896 acts as an eTM for Sl-miR166b. Overexpressing Sl-miR166b yielded a similar phenotype to that produced by Sl-lncRNA39896-knockout, whereas silencing of Sl-miR166b impaired resistance. We verified that Sl-miR166b cleaved transcripts of its target class III homeodomain-leucine zipper genes SlHDZ34 and SlHDZ45. Silencing of SlHDZ34/45 decreased pathogen accumulation in plants infected with P. infestans. Additionally, jasmonic acid and ethylene contents were elevated following infection in the plants with enhanced resistance. Sl-lncRNA39896 is the first known lncRNA to negatively regulate resistance to P. infestans in tomato. We propose a novel mechanism in which the lncRNA39896–miR166b–HDZ module modulates resistance to P. infestans.

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