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Genome-Wide Profiling of DNA Methylome and Transcriptome Reveals Epigenetic Regulation of Potato Response to DON Stress.

ABSTRACT: Potato is an important food crop that occupies lesser area but has greater production than rice and wheat. However, potato production is affected by numerous biotic and abiotic stresses, among which Fusarium dry rot is a disease that has significant effect on potato production, storage, and processing. However, the role of DNA methylation in regulating potato response to Fusarium toxin deoxynivalenol (DON) stress is still not fully understood. In this study, we performed DNA methylome and transcriptome analyses of potato tubers treated with five concentrations of DON. The global DNA methylation levels in potato tubers treated with different concentrations of DON showed significant changes relative to those in the control. In particular, the 20 ng/ml treatment showed the largest decrease in all three contexts of methylation levels, especially CHH contexts in transposon regions. The differentially methylated region (DMR)-associated differentially expressed genes (DEGs) were significantly enriched in resistance-related metabolic pathways, indicating that DNA methylation plays an essential role in potato response to DON stress. Furthermore, we examined lesions on potato tubers infested with Fusarium after treatment. Furthermore, the potato tubers treated with 5 and 35 ng/ml DON had lesions of significantly smaller diameters than those of the control, indicating that DON stress may induce resistance. We speculate that this may be related to epigenetic memory created after DNA methylation changes. The detailed DNA methylome and transcriptome profiles suggest that DNA methylation plays a vital role in potato disease resistance and has great potential for enhancing potato dry rot resistance.

SUBMITTER: Shi Y

PROVIDER: S-EPMC9260311 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundAtherosclerotic plaque vulnerability is a key feature of atheroprogression and precipitating acute cardiovascular events. Although the pivotal role of epigenetic regulation in atherosclerotic plaque destabilization is being recognized, the DNA methylation profile and its potential role in driving the progression and destabilization of atherosclerotic cardiovascular disease remains largely unknown. We conducted a genome-wide analysis to identify differentially methylated genes in vulnerable and non-vulnerable atherosclerotic lesions to understand more about pathogenesis.ResultsWe compared genome-wide DNA methylation profiling between carotid artery plaques of patients with clinically symptomatic (recent stroke or transient ischemic attack) and asymptomatic disease (no recent stroke) using Infinium Methylation BeadChip arrays, which revealed 90,368 differentially methylated sites (FDR < 0.05, |delta beta|> 0.03) corresponding to 14,657 annotated genes. Among these genomic sites, 30% were located at the promoter regions and 14% in the CpG islands, according to genomic loci and genomic proximity to the CpG islands, respectively. Moreover, 67% displayed hypomethylation in symptomatic plaques, and the differentially hypomethylated genes were found to be involved in various aspects of inflammation. Subsequently, we focus on CpG islands and revealed 14,596 differentially methylated sites (|delta beta|> 0.1) located at the promoter regions of 7048 genes. Integrated analysis of methylation and gene expression profiles identified that 107 genes were hypomethylated in symptomatic plaques and showed elevated expression levels in both advanced plaques and ruptured plaques. The imprinted gene PLA2G7, which encodes lipoprotein-associated phospholipase A2 (Lp-PLA2), was one of the top hypomethylated genes with an increased expression upon inflammation. Further, the hypomethylated CpG site at the promoter region of PLA2G7 was identified as cg11874627, demethylation of which led to increased binding of Sp3 and expression of Lp-PLA2 through bisulfate sequencing, chromatin immunoprecipitation assay and enzyme-linked immunosorbent assay. These effects were further enhanced by deacetylase.ConclusionExtensive DNA methylation modifications serve as a new and critical layer of biological regulation that contributes to atheroprogression and destabilization via inflammatory processes. Revelation of this hitherto unknown epigenetic regulatory mechanism could rejuvenate the prospects of Lp-PLA2 as a therapeutic target to stabilize the atherosclerotic plaque and reduce clinical sequelae.

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Genome-Wide Profiling of DNA Methylome and Transcriptome Reveals Epigenetic Regulation of Potato Response to DON Stress.

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