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The Arabidopsis HSP1 Mediates Chitin-induced Defense Response by Regulating CERK1 Protein Level

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  • 1. Renmin Hospital, Hubei University of Medicine, Shiyan 442000, China
    2. College of Life Science and Technology, Huazhong Agricultural University, Wuhan 430000, China
    3. Third Clinical College of Hubei University of Medicine, Shiyan 442000, China
    4. First Clinical College of Hubei University of Medicine, Shiyan 442000, China
    5. School of Basic Medicine, Hubei University of Medicine, Shiyan 442000, China

Received date: 2022-06-07

  Accepted date: 2022-11-15

  Online published: 2022-11-29

Abstract

Chitin, a major component of the fungal cell wall, is a kind of typical microbe associated molecular pattern (MAMP) that is recognized by two plasma membrane located LysM receptors, CERK1 and LYK5, and trigger immune response in plants. In this study, the intracellular kinase domain of CERK1 was cloned and used to screen the yeast cDNA library, and identify its interaction with HSP1. Using CRISPR-Cas-mediated gene editing technology, we knocked out the HSP1 gene in wild-type Arabidopsis thaliana Col-0 and obtained hsp1 v63 deletion mutant. We showed that the expression of downstream defense-related genes and the phosphorylation pathway of mitogen-activated protein kinase were inhibited in the hsp1 v63 deletion mutant compared to the wild type Col-0. We also showed that the protein level of CERK1 in hsp1 v63 mutants was lower than that in the Col-0, and that reduced CERK1 levels in this mutant were associated with the endoplasmic reticulum degradation system. These results indicate that HSP1 is a key gene in the chitin-induced defense response pathway, thus revealing the important roles of molecular chaperone in regulating receptor protein level and improvement in crop resistance.

Cite this article

Shi Junxing, Yan Yijia, Dong Ru, Tao Xuan, Sun Xiaolong, Huang Congcong . The Arabidopsis HSP1 Mediates Chitin-induced Defense Response by Regulating CERK1 Protein Level[J]. Chinese Bulletin of Botany, 2023 , 58(5) : 712 -719 . DOI: 10.11983/CBB22117

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