Nanopore direct RNA sequencing reveals the m⁵C methylomes of tomato fruits in response to Botrytis cinerea
Abstract
RNA methylation, particularly 5-methylcytosine (m5C) modification, has emerged as a pivotal regulatory layer governing plant development and stress responses. However, the role of m5C in mediating the resistance of tomato (Solanum lycopersicum) fruit to the fungal pathogen Botrytis cinerea remains unclear. In this study, we utilized Nanopore direct RNA sequencing to generate the transcriptome-wide m5C methylomes in B. cinerea-infected tomato fruits. Our results revealed that m5C sites are preferentially enriched in coding sequences (CDSs) and 3' untranslated regions (3' UTRs). Notably, B. cinerea infection induced site-specific m5C changes without altering the global modification level. Integrated omics analysis identified a transcriptome-wide negative correlation between m5C modification and gene expression. Importantly, a large number of ethylene signaling pathway and defense-related genes exhibited reduced m5C levels, accompanied by significantly increased transcript abundance, implying that m5C may act as a novel regulator of fruit's resistance to B. cinerea by coordinating hormone signaling and defense response pathways. Furthermore, the putative m5C demethylase gene SlALKBH1 and the reader protein gene SlALY4 were transcriptionally downregulated and upregulated by B. cinerea infection, respectively. Collectively, this study establishes the first comprehensive m5C methylomes of tomato fruits upon B. cinerea infection and provides new insights into RNA-based epigenetic regulation of hormone signaling during plant–pathogen interactions.
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BibTeX
@article{cai2026nanopore,
title = {{Nanopore direct RNA sequencing reveals the m⁵C methylomes of tomato fruits in response to Botrytis cinerea}},
author = {Xinyao Cai and Baowen Huang and Yulin Cheng and Jianghua Cai and Hua Cassan-Wang and Guozheng Qin and Ying Gao and Leilei Zhou},
journal = {Plant Hormones},
year = {2026},
month = may,
doi = {10.48130/ph-0026-0010},
url = {https://hal.science/hal-05758781v1},
note = {CC BY},
}
RIS
TY - JOUR
TI - Nanopore direct RNA sequencing reveals the m⁵C methylomes of tomato fruits in response to Botrytis cinerea
AU - Xinyao Cai
AU - Baowen Huang
AU - Yulin Cheng
AU - Jianghua Cai
AU - Hua Cassan-Wang
AU - Guozheng Qin
AU - Ying Gao
AU - Leilei Zhou
PY - 2026
DA - 2026/05/14
JO - Plant Hormones
DO - 10.48130/ph-0026-0010
UR - https://hal.science/hal-05758781v1
AB - RNA methylation, particularly 5-methylcytosine (m5C) modification, has emerged as a pivotal regulatory layer governing plant development and stress responses. However, the role of m5C in mediating the resistance of tomato (Solanum lycopersicum) fruit to the fungal pathogen Botrytis cinerea remains unclear. In this study, we utilized Nanopore direct RNA sequencing to generate the transcriptome-wide m5C methylomes in B. cinerea-infected tomato fruits. Our results revealed that m5C sites are preferentially enriched in coding sequences (CDSs) and 3' untranslated regions (3' UTRs). Notably, B. cinerea infection induced site-specific m5C changes without altering the global modification level. Integrated omics analysis identified a transcriptome-wide negative correlation between m5C modification and gene expression. Importantly, a large number of ethylene signaling pathway and defense-related genes exhibited reduced m5C levels, accompanied by significantly increased transcript abundance, implying that m5C may act as a novel regulator of fruit's resistance to B. cinerea by coordinating hormone signaling and defense response pathways. Furthermore, the putative m5C demethylase gene SlALKBH1 and the reader protein gene SlALY4 were transcriptionally downregulated and upregulated by B. cinerea infection, respectively. Collectively, this study establishes the first comprehensive m5C methylomes of tomato fruits upon B. cinerea infection and provides new insights into RNA-based epigenetic regulation of hormone signaling during plant–pathogen interactions.
SN - 3067-221X
SN - 3067-221X
ER -