Multi-omics analysis of the role of muskmelon mitochondria in Si-induced resistance mechanisms.

Abstract

Post-harvest senescence and fungal infection, particularly Pink Mold Rot caused by Trichothecium roseum , significantly compromise the storage quality and economic value of muskmelon ( Cucumis melo cv. Yujinxiang). While Silicon (Si) application is recognized as an effective strategy for enhancing post-harvest disease resistance, the molecular mechanisms driving this resistance-specifically the interplay between DNA methylation, transcriptional regulation, and mitochondrial function-remain largely uncharacterized. This study employed an integrated multi-omics approach, combining Whole-Genome Bisulfite Sequencing (WGBS), RNA sequencing (RNA- seq ), and physiological assays, to elucidate the regulatory networks induced by Si treatment in T. roseum-inoculated muskmelons. Physiologically, Si treatment significantly alleviated oxidative stress and maintained mitochondrial energy status, evidenced by elevated ATP levels and increased Ca 2+ -ATPase activity compared to untreated controls. At the epigenomic level, we identified a distinct, context-specific enhancement of DNA methylation induced by Si. Notably, the CG context within the upstream 2 kilobases (up2k) regions exhibited the most significant response to treatment, surpassing changes in CHG and CHH contexts. Integrative analysis of the methylome and transcriptome revealed that this observed promoter hypermethylation correlates with the fine-tuning of gene expression related to energy metabolism and defense. Rather than simple repression, this epigenetic modification appears to stabilize transcriptional responses, potentially preventing the metabolic energy drain associated with hyper-immune responses or delaying the activation of senescence-associated genes. These findings establish a novel mechanistic link between epigenetic modification, and cellular energy metabolism. Ultimately, this research provides a theoretical basis for the utilization of Si as a post-harvest treatment to extend the shelf life of muskmelons by reinforcing mitochondrial function via epigenetic regulation.