Dynamic N6‐methyladenosine RNA modification regulates peanut resistance to bacterial wilt

Author:

Zhao Kai1ORCID,Li Zhongfeng1,Ke Yunzhuo2,Ren Rui1,Cao Zenghui1,Li Zhan1,Wang Kuopeng1,Wang Xiaoxuan1,Wang Jinzhi1,Ma Qian1,Cao Di1,Zhao Kunkun1,Li Yaoyao1,Hu Sasa1,Qiu Ding1ORCID,Gong Fangping1ORCID,Ma Xingli1,Zhang Xingguo1,Fan Guoqiang3,Liang Zhe2ORCID,Yin Dongmei1ORCID

Affiliation:

1. College of Agronomy & Peanut Functional Genome and Molecular Breeding Engineering Henan Agricultural University Zhengzhou 450046 China

2. Biotechnology Research Institute Chinese Academy of Agricultural Sciences Beijing 100081 China

3. College of Forestry Henan Agricultural University Zhengzhou 450046 China

Abstract

Summary N6‐methyladenosine (m6A) is the most abundant mRNA modification in eukaryotes and is an important regulator of gene expression as well as many other critical biological processes. However, the characteristics and functions of m6A in peanut (Arachis hypogea L.) resistance to bacterial wilt (BW) remain unknown. Here, we analyzed the dynamic of m6A during infection of resistant (H108) and susceptible (H107) peanut accessions with Ralstonia solanacearum (R. solanacearum), the causative agent of BW. Throughout the transcriptome, we identified ‘URUAY’ as a highly conserved motif for m6A in peanut. The majority of differential m6A located within the 3′ untranslated region (UTR) of the transcript, with fewer in the exons. Integrative analysis of RNA‐Seq and m6A methylomes suggests the correlation between m6A and gene expression in peanut R. solanacearum infection, and functional analysis reveals that m6A‐associated genes were related to plant‐pathogen interaction. Our experimental analysis suggests that AhALKBH15 is an m6A demethylase in peanut, leading to decreased m6A levels and upregulation of the resistance gene AhCQ2G6Y. The upregulation of AhCQ2G6Y expression appears to promote BW resistance in the H108 accession.

Funder

Innovation Scientists and Technicians Troop Construction Projects of Henan Province

National Natural Science Foundation of China

Publisher

Wiley

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