Histone H3K4 Methylation Mediates Exogenous Arginine Suppression of Cold‐Induced Damage in Tea Plant

Cold stress severely restricts the geographical distribution and productivity of Camellia sinensis (tea plant). Although the plant cuticle wax serves as a critical barrier in resisting both biotic and abiotic stresses, its epigenetic regulation during cold stress remains poorly understood. Here, we show that exogenous arginine alleviates cold‐induced damage by increasing cuticle thickness, and enhancing the accumulation of very‐long‐chain fatty acids and alkanes. Transcriptome‐based weighted gene co‐expression network analysis identified CsKCS3 as a key regulator of wax biosynthesis. Virus‐induced gene silencing in tea plants and heterologous overexpression in Arabidopsis thaliana demonstrated that CsKCS3 positively regulates fatty acid biosynthesis and contributes to cold tolerance. Furthermore, the trimethylation of histone H3 at Lysine 4 (H3K4me3) is increased during arginine‐induced processes and enhances the expression of the CsSDG36 and CsKCS3 . Further, we identified that CsSDG36 encodes an H3K4 methyltransferase. Arginine treatment mitigated cold damage in CsSDG36 ‐silenced tea plants, which was associated with recovery of CsKCS3 expression. Mechanistically, CsSDG36 enhanced H3K4me3 enrichment at the promoter and exon regions of CsKCS3 , thereby activating CsKCS3 transcription. These findings reveal a CsSDG36‐H3K4me3‐ CsKCS3 regulatory module through which arginine promotes cuticular wax accumulation and cold tolerance in tea plants. These findings uncover a novel epigenetic circuitry in which exogenous arginine regulates chromatin remodeling to structurally fortify the epidermal lipid barrier, offering a vital conceptual framework for breeding climate‐resilient perennial crops.