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Abstract Abiotic stress severely restricts plant growth, necessitating swift and, at times, heritable reprogramming of gene expression. To regulate chromatin states and fine-tune stress-responsive pathways, plants rely on four key epigenetic mechanisms: DNA methylation, histone modifications, small RNA-mediated silencing, and chromatin remodeling. Cytosine methylation in CG, CHG, and CHH contexts, mediated by Methyltransferase 1 ( MET1 ), Chromomethylase 3 ( CMT3 ), and Domains Rearranged Methyltransferase 2 ( DRM2 ), controls promoter accessibility, transposable-element activity, and stress-induced transcription at loci such as High-Affinity K⁺ Transporter 1 ( HKT1 ), Nine-cis-epoxycarotenoid dioxygenase 3 ( NCED3 ), and Chromatin Remodeling 12 ( CBF ). Histone acetylation and methylation are catalyzed by General Control Non-Repressed 5 ( GCN5 ), Arabidopsis Trithorax 1/SET Domain Group ( ATX/SDG ) methyltransferases, and reversed by Histone Deacetylase/HISTONE DEACETYLASE2C ( HDA6/19/HD2C ) or Jumonji-C Domain-Containing Protein ( JMJ ) demethylases. Small RNAs, produced via the RdDM pathway (Pol IV/V, RDR2, DCLs), direct non-CG methylation, enabling rapid and reversible modulation of transcription in ion transporters, ABA signaling genes, and stress-related transcription factors. Chromatin remodelers like Chromatin Remodeling 12 ( CHR12 ) and Pickle Chromatin Remodeler ( PKL ), alongside epitranscriptomic modifications, such as m 6 A and m 5 C (written by MTA/MTB and NSUN2 , and erased by ALKBH demethylases), further influence transcript stability, translation, and heat-responsive transposable-element activation. These interconnected processes also generate stress memory, marked by sustained H3K4me3, persistent CHH hypomethylation, and siRNA loss at transposable-element loci, enabling faster reactivation during recurrent stress or, in some cases, transgenerational inheritance. This review offers an integrated framework that links molecular epigenetic mechanisms with adaptive stress physiology and highlights emerging opportunities for epigenetic priming, targeted epigenome editing, and trait engineering to develop climate-resilient crops.