Unveiling the role of epigenetics in leaf senescence: a comparative study to identify different epigenetic regulations of senescence types in barley leaves

Developmental leaf senescence (DLS) is an irreversible process followed by cell death. Dark-induced leaf senescence (DILS) is a reversible process that allows adaptations to changing environmental conditions. As a result of exposure to adverse environmental changes, plants have developed mechanisms that enable them to survive. One of these is the redirection of metabolism into the senescence pathway. The plant seeks to optimise resource allocation. Our research aims to demonstrate how epigenetic machinery regulates leaf senescence, including its irreversibility. In silico analyses allowed the complex identification and characterisation of 117 genes involved in epigenetic processes in barley. These genes include those responsible for DNA methylation, post-translational histone modifications, and ATP-dependent chromatin remodelling complexes. We then performed RNAseq analysis after DILS and DLS to evaluate their expression in senescence-dependent leaf metabolism. Principal component analysis revealed that evaluated gene expression in developmental senescence was similar to controls, while induced senescence displayed a distinct profile. Western blot experiments revealed that senescence engages senescence-specific histone modification. During DILS and DLS, the methylation of histone proteins H3K4me3 and H3K9me2 increased. H3K9ac acetylation levels significantly decreased during DILS and remained unchanged during DLS. The study identified different epigenetic regulations of senescence types in barley leaves. These findings are valuable for exploring epigenetic regulation of senescence-related molecular mechanisms, particularly in response to premature, induced leaf senescence. Based on the results, we suggest the presence of an epigenetically regulated molecular switch between cell survival and cell death in DILS, highlighting an epigenetically driven cell survival metabolic response.