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Dynamic N 6 -methyladenosine RNA modification regulates peanut resistance to bacterial wilt

N -methyladenosine (m A) 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 m A in peanut (Arachis hypogea L.) resistance to bacterial wilt (BW) remai...

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Bibliographic Details
Published in:The New phytologist 2024-04, Vol.242 (1), p.231-246
Main Authors: Zhao, Kai, Li, Zhongfeng, Ke, Yunzhuo, Ren, Rui, Cao, Zenghui, Li, Zhan, Wang, Kuopeng, Wang, Xiaoxuan, Wang, Jinzhi, Ma, Qian, Cao, Di, Zhao, Kunkun, Li, Yaoyao, Hu, Sasa, Qiu, Ding, Gong, Fangping, Ma, Xingli, Zhang, Xingguo, Fan, Guoqiang, Liang, Zhe, Yin, Dongmei
Format: Article
Language:English
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Summary:N -methyladenosine (m A) 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 m A in peanut (Arachis hypogea L.) resistance to bacterial wilt (BW) remain unknown. Here, we analyzed the dynamic of m A 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 m A in peanut. The majority of differential m A located within the 3' untranslated region (UTR) of the transcript, with fewer in the exons. Integrative analysis of RNA-Seq and m A methylomes suggests the correlation between m A and gene expression in peanut R. solanacearum infection, and functional analysis reveals that m A-associated genes were related to plant-pathogen interaction. Our experimental analysis suggests that AhALKBH15 is an m A demethylase in peanut, leading to decreased m A levels and upregulation of the resistance gene AhCQ2G6Y. The upregulation of AhCQ2G6Y expression appears to promote BW resistance in the H108 accession.
ISSN:0028-646X
1469-8137
DOI:10.1111/nph.19568