Recognition and repair of damaged tissue are an integral part of life. The failure of cells and tissues to appropriately respond to damage can lead to severe dysfunction and disease. Therefore, it is essential that we understand the molecular pathways of wound recognition and response. In this review, we aim to provide a broad overview of the molecular mechanisms underlying the fate of damaged cells and damage recognition in plants. Damaged cells release the so-called damage associated molecular patterns to warn the surrounding tissue. Local signaling through calcium (Ca2+), reactive oxygen species (ROS), and hormones, such as jasmonic acid, activates defense gene expression and local reinforcement of cell walls to seal off the wound and prevent evaporation and pathogen colonization. Depending on the severity of damage, Ca2+, ROS, and electrical signals can also spread throughout the plant to elicit a systemic defense response. Special emphasis is placed on the spatiotemporal dimension in order to obtain a mechanistic understanding of wound signaling in plants.

The inhibitory effect of extracellular DNA (exDNA) on the growth of conspecific individuals was demonstrated in different kingdoms. In plants, the inhibition has been observed on root growth and seed germination, demonstrating its role in plant–soil negative feedback. Several hypotheses have been proposed to explain the early response to exDNA and the inhibitory effect of conspecific exDNA. We here contribute with a whole-plant transcriptome profiling in the model species Arabidopsis thaliana exposed to extracellular self- (conspecific) and nonself- (heterologous) DNA. The results highlight that cells distinguish self- from nonself-DNA. Moreover, confocal microscopy analyses reveal that nonself-DNA enters root tissues and cells, while self-DNA remains outside. Specifically, exposure to self-DNA limits cell permeability, affecting chloroplast functioning and reactive oxygen species (ROS) production, eventually causing cell cycle arrest, consistently with macroscopic observations of root apex necrosis, increased root hair density and leaf chlorosis. In contrast, nonself-DNA enters the cells triggering the activation of a hypersensitive response and evolving into systemic acquired resistance. Complex and different cascades of events emerge from exposure to extracellular self- or nonself-DNA and are discussed in the context of Damage- and Pathogen-Associated Molecular Patterns (DAMP and PAMP, respectively) responses.

Damage-associated molecular patterns (DAMPs) have been studied recently to understand plant self–nonself recognition in response to attack by biotic and abiotic stresses. Extracellular DNA has emerged as a possible DAMP. As a DAMP DNA seems to function depending on the phylogenetic scale and has been tested in a few plant species. This study aimed to evaluate the possible role of self DNA (sDNA) as a DAMP by analysing changes in CpG DNA methylation and defence-related responses in lettuce (Lactuca sativa L.) as a model plant. sDNA and nonself DNA (nsDNA) from Capsicum chinense Murray (both species belong to the same clade, Asterids) stimulated aberrant seed germination and root growth in lettuce seedlings. Similar resultswere obtained with nsDNA obtained from Acaciella angustissima (Mill.) Britton & Rose plants (belonging to the clade Rosids I), although at significantly higher concentrations. Moreover, in most cases, this behaviour was correlated with hypomethylation of CpG DNA as well as defence responses measured as altered gene expression associated with oxidative burst and production of secondary metabolites (phenylpropanoids) related to coping with stress conditions. Our results suggested that extracellular and fragmented DNA has a role as a DAMP depending on phylogenetic closeness in plants as lettuce, inducing epigenetic, genetic and biochemical changes within the plant. The importance of our results is that, for the first time, they demonstrate that sDNA acts as a DAMP in plants, changing CpG DNA methylation levels as well as increasing the production of secondary metabolites associated with defence responses to stress.

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