Plant Responses to Biotic Stress: Old Memories Matter

Abstract

Plants are fascinating organisms present in most ecosystems and a model system for studying different facets of ecological interactions on Earth. In the environment, plants constantly encounter a multitude of abiotic and biotic stresses. The zero-avoidance phenomena make them more resilient to such environmental odds. Plants combat biotic stress or pathogenic ingression through a complex orchestration of intracellular signalling cascades. The plant-microbe interaction primarily relies on acquired immune response due to the absence of any specialised immunogenic cells for adaptive immune response. The generation of immune memory is mainly carried out by T cells as part of the humoral immune response in animals. Recently, prodigious advancements in our understanding of epigenetic regulations in plants invoke the "plant memory" theory afresh. Current innovations in cutting-edge genomic tools have revealed stress-associated genomic alterations and strengthened the idea of transgenerational memory in plants. In plants, stress signalling events are transferred as genomic imprints in successive generations, even without any stress. Such immunogenic priming of plants against biotic stresses is crucial for their eco-evolutionary success. However, there is limited literature capturing the current knowledge of the transgenerational memory of plants boosting biotic stress responses. In this context, the present review focuses on the general concept of memory in plants, recent advancements in this field and comprehensive implications in biotic stress tolerance with future perspectives.

Keywords: abiotic stress; biotic interaction; epigenetic modification; histone; priming; stress memory; transgenerational immune priming.

Figure 1

Schematic representation of plant immune response against pathogens. (A) Representation of the classical “zig-zag” model of the plant immunity. Pathogen-associated molecular patterns (PAMPs)/microbe-associated molecular patterns (MAMPs), when interacting with cognate host receptors (PRRs), instigate the first line of defence response called PAMP-triggered immunity (PTI). Pathogens then produce specific effector molecules or toxins that subside the PTI to the basal level, called effector-triggered susceptibility (ETS; I). Plants possess the “R” gene that produces antitoxins or inhibitors of toxins produced by the pathogens, and a second line of defence response is initiated, called effector-triggered immunity (ETI). Some pathogens can produce modified effectors to re-establish the ETS (II). This arms race continues, until one wins. (B). Graphical representation of the amplitude of the immune response in plants. The PTI induces sharp induction over the basal resistance response, but the amplitude of the ETI supersedes all, as it is the most specific against pathogens among all.

Figure 2

Illustration depicting the mechanistic basis of the establishment of immune memory in plants. Pathogen recognition by receptor-like kinases (RLKs), receptor-like proteins (RLPs) and intracellular NOD-like receptors (NLRs) leads to complex defence signalling and transcriptome reprogramming that induces epigenetic marks on the genome. These marks may be temporary or permanent, depending on the magnitude and frequency of the particular stress. Priming through SA and establishing SAR is a customary event for plant memory against biotic pathogens. In many cases, such biotic stress memories are transgenerational. TMD, transmembrane domain; HDM, histone demethylase; HMT, histone methyltransferase; HDAC, histone deacetylase; HAT, histone acetyltransferase; RBOH, respiratory burst oxidase; ROS, reactive oxygen species; CC/TIR, coiled-coil/toll-interleukin receptor; NBD, nucleotide-binding domain; TF, transcription factor; SA, salicylic acid; SAR, systemic acquired resistance.