Epigenetic Control of Defense Signaling and Priming in Plants

Abstract

Immune recognition of pathogen-associated molecular patterns or effectors leads to defense activation at the pathogen challenged sites. This is followed by systemic defense activation at distant non-challenged sites, termed systemic acquired resistance (SAR). These inducible defenses are accompanied by extensive transcriptional reprogramming of defense-related genes. SAR is associated with priming, in which a subset of these genes is kept at a poised state to facilitate subsequent transcriptional regulation. Transgenerational inheritance of defense-related priming in plants indicates the stability of such primed states. Recent studies have revealed the importance and dynamic engagement of epigenetic mechanisms, such as DNA methylation and histone modifications that are closely linked to chromatin reconfiguration, in plant adaptation to different biotic stresses. Herein we review current knowledge regarding the biological significance and underlying mechanisms of epigenetic control for immune responses in plants. We also argue for the importance of host transposable elements as critical regulators of interactions in the evolutionary "arms race" between plants and pathogens.

Keywords: DNA methylation; defense priming; epigenetic control; histone modification; plant immunity; plant-microbe interactions; transposable elements.

FIGURE 1

A general model of epigenetic regulation of defense-related genes. Hypomethylation of regions flanking both ends of defense-related genes enhances their expression during pathogen challenges. Filled lollipops indicate transposable elements (TEs) or repetitive elements that may be methylated or de-methylated.

FIGURE 2

Bivalent phenomena hypothesis in plant defense priming. (A) An interplay of opposing histone modification marks in enhancer and promoter regions modulate the expression status of defense-related genes. Polycomb-group (PcG) and Trithorax (TrxG) proteins may assemble with interacting proteins, such as transcription factors (TFs). (B) Opposing histone marks on the same lysine-site (K-site) act as a switch to modulate the expression status of defense-related genes.