As global arid conditions worsen and groundwater resources diminish, drought stress has emerged as a critical impediment to plant growth and development globally, notably causing declines in crop yields and even the extinction of certain cultivated species. Numerous studies on drought resistance have demonstrated that DNA methylation dynamically interacts with plant responses to drought stress by modulating gene expression and developmental processes. However, the precise mechanisms underlying these interactions remain elusive. This article consolidates the latest research on the role of DNA methylation in plant responses to drought stress across various species, focusing on methods of methylation detection, mechanisms of methylation pattern alteration (including DNA de novo methylation, DNA maintenance methylation, and DNA demethylation), and overall responses to drought conditions. While many studies have observed significant shifts in genome-wide or gene promoter methylation levels in drought-stressed plants, the identification of specific genes and pathways involved remains limited. This review aims to furnish a reference for detailed research into plant responses to drought stress through epigenetic approaches, striving to identify drought resistance genes regulated by DNA methylation, specific signaling pathways, and their molecular mechanisms of action.
Glutathione S-transferases (GSTs) play crucial roles in crop stress tolerance through protection against oxidative damage. In this study, we conducted genome-wide identification and expression analysis of the GST gene family in the autotetraploid potato cultivar Cooperative-88 (C88) using bioinformatic approaches. We identified 366 GST genes in the potato genome, which were classified into 10 subfamilies. Chromosomal mapping revealed that StGSTs were distributed across all 12 chromosomes, with 13 tandem duplication events observed in three subfamilies. Analysis of protein sequences identified 10 conserved motifs, with motif 1 potentially representing the GST domain. Analysis of cis-acting elements in the StGSTs promoter regions suggested their involvement in stress response pathways. RNA-seq analysis revealed that most StGSTs responded to both drought stress and DNA demethylation treatments. Quantitative PCR validation of 16 selected StGSTs identified four members that showed strong responses to both treatments, with distinct expression patterns between drought-tolerant (QS9) and drought-sensitive (ATL) varieties. Transient expression assays in tobacco demonstrated that these four StGSTs enhanced drought tolerance and may be regulated through DNA methylation pathways, though the precise mechanisms require further investigation. These findings provide a theoretical foundation for understanding the response and epigenetic regulation of potato GST genes under drought stress.
As the global arid climate intensifies and the groundwater becomes increasingly scarce, drought stress has become a major challenge to plant growth and development worldwide, especially causing yield reduction and extinction of cultivated crops. In a large number of drought resistance studies, DNA methylation has been found dynamically associated with response to drought stress in plants by regulating gene expression and developments in plants, but the specific mechanisms are not yet clear. In this article, the current advances of research have been summarized on DNA methylation response to drought stress in various plant species, in terms of methylation detection methods, mechanisms of pattern changes (DNA de novo methylation, DNA maintenance methylation, and DNA demethylation), and its response to drought stress. With Most of the studies showed significant changes in genome or gene promoter methylation levels in plants subjected to drought stress, but the identification of the genes and pathways involved is still in the minority. The aim is to provide references for in-depth research on the response of plants to drought stress through epigenetics, and to uncover drought resistance genes regulated by DNA methylation, specific signaling pathways, and molecular mechanisms of action.