The transcriptional landscape of Populus pattern/effector‐triggered immunity and how PagWRKY18 involved in it

Author:

Chen Sisi123,Tan Shuxian123,Jin Zhelun123,Wu Jiadong123,Zhao Yiyang123,Xu Weijie123,Liu Sijia123,Li Yue123,Huang Huahong4,Bao Fei123,Xie Jianbo123ORCID

Affiliation:

1. State Key Laboratory of Tree Genetics and Breeding, College of Biological Sciences and Technology Beijing Forestry University Beijing China

2. National Engineering Research Center of Tree Breeding and Ecological Restoration, College of Biological Sciences and Technology Beijing Forestry University Beijing China

3. The Tree and Ornamental Plant Breeding and Biotechnology Laboratory of National Forestry and Grassland Administration Beijing Forestry University Beijing China

4. State Key Laboratory of Subtropical Silviculture Zhejiang A&F University Hangzhou Lin'an China

Abstract

AbstractPlants trigger a robust immune response by activating massive transcriptome reprogramming through crosstalk between PTI and ETI. However, how PTI and ETI contribute to the quantitative or/and qualitative output of immunity and how they work together when both are being activated were unclear. In this study, we performed a comprehensive overview of pathogen‐triggered transcriptomic reprogramming by analyzing temporal changes in the transcriptome up to 144 h after Colletotrichum gloeosporioides inoculated in Populus. Moreover, we constructed a hierarchical gene regulatory network of PagWRKY18 and its potential target genes to explore the underlying regulatory mechanisms of PagWRKY18 that are not yet clear. Interestingly, we confirmed that PagWRKY18 protein can directly bind the W‐box elements in the promoter of a transmembrane leucine‐rich repeat receptor‐like kinase, PagSOBIR1 gene, to trigger PTI. At the same time, PagWRKY18 functions in disease tolerance by modulation of ROS homeostasis and induction of cell death via directly targeting PagGSTU7 and PagPR4 respectively. Furthermore, PagPR4 can interact with PagWRKY18 to inhibit the expression of PagPR4 genes, forming a negative feedback loop. Taken together, these results suggest that PagWRKY18 may be involved in regulating crosstalk between PTI and ETI to activate a robust immune response and maintain intracellular homeostasis.

Publisher

Wiley

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