Phytomelatonin-mediated epigenetic and RNA regulatory networks in plant abiotic stress resilience.

Abstract

Phytomelatonin has long been viewed as a pleiotropic stress signal that protects plants by scavenging reactive oxygen species (ROS), reinforcing antioxidant capacity, and coordinating hormonal responses. That view remains correct, but it is no longer sufficient. Recent work indicates that phytomelatonin also shapes the regulatory architecture that determines whether stress-responsive genes are accessible, whether transcripts are processed and translated efficiently, and whether stress-induced states can persist after the initial stimulus has disappeared. Here, we synthesize four emerging layers of phytomelatonin action: DNA methylation and histone modifications, noncoding RNA (ncRNA) networks, N6 methyladenosine (m6A) RNA methylation and stress memory with potential transgenerational effects. Rather than listing stress phenotypes, we emphasize regulatory logic. Phytomelatonin can buffer stress induced DNA methylation shifts, modulate histone acetylation and methylation marks, rewire microRNA (miRNA), long noncoding RNA (lncRNA) networks and counteract cadmium-induced m6A hypermethylation. Its involvement in circular RNA (circRNA) regulation remains a testable hypothesis. These layers are likely integrated through redox status, hormone crosstalk, RNA stability, chromatin accessibility and DNA repair. We propose that phytomelatonin functions as an epigenetic and epitranscriptomic trigger capable of converting transient stress perception into durable transcriptional competence. Finally, we outline how single-cell multi-omics, targeted epigenome editing, epitranscriptomic profiling and field-scale validation of priming strategies can transform this conceptual framework into testable mechanisms and crop-improvement strategies.