From Perception to Activation: The Molecular-Genetic and Biochemical Landscape of Disease Resistance Signaling in Plants

Abstract

More than 60 years ago, H.H. Flor proposed the "Gene-for-Gene" hypothesis, which described the genetic relationship between host plants and pathogens. In the decades that followed Flor's seminal work, our understanding of the plant-pathogen interaction has evolved into a sophisticated model, detailing the molecular genetic and biochemical processes that control host-range, disease resistance signaling and susceptibility. The interaction between plants and microbes is an intimate exchange of signals that has evolved for millennia, resulting in the modification and adaptation of pathogen virulence strategies and host recognition elements. In total, plants have evolved mechanisms to combat the ever-changing landscape of biotic interactions bombarding their environment, while in parallel, plant pathogens have co-evolved mechanisms to sense and adapt to these changes. On average, the typical plant is susceptible to attack by dozens of microbial pathogens, yet in most cases, remains resistant to many of these challenges. The sum of research in our field has revealed that these interactions are regulated by multiple layers of intimately linked signaling networks. As an evolved model of Flor's initial observations, the current paradigm in host-pathogen interactions is that pathogen effector molecules, in large part, drive the recognition, activation and subsequent physiological responses in plants that give rise to resistance and susceptibility. In this Chapter, we will discuss our current understanding of the association between plants and microbial pathogens, detailing the pressures placed on both host and microbe to either maintain disease resistance, or induce susceptibility and disease. From recognition to transcriptional reprogramming, we will review current data and literature that has advanced the classical model of the Gene-for-Gene hypothesis to our current understanding of basal and effector triggered immunity.

The Plant Host Can Affect the Encapsidation of Brome Mosaic Virus (BMV) RNA: BMV Virions Are Surprisingly Heterogeneous

“…3–5 The outcome of the viral infection is due to the compatibility of the interactions between plant pathogen sensors and the pathogen molecules. 6 However, how the host can affect the physiochemical properties of the virions is not well characterized.…”

Salicylic Acid Biosynthesis and Metabolism

“…The majority of characterized plant R proteins belong to the nucleotide binding-leucine-rich repeat (NB-LRR) class, which can be subdivided into two categories depending on whether the N terminus contains a toll-interleukin-1 receptor (TIR) domain or a coiled-coil (CC) domain (Collier and Moffett, 2009;Lukasik and Takken, 2009;Knepper and Day, 2010). Genetic analyses initially suggested that CC-type R proteins generally signal defenses via NDR1 (for Nonspecific Disease Resistance 1, At3g20600), whereas TIR-type NB-LRR proteins usually use EDS1 (Aarts et al, 1998).…”

Arabidopsis NDR1 Is an Integrin-Like Protein with a Role in Fluid Loss and Plasma Membrane-Cell Wall Adhesion

“…To accomplish this, the activation of plant resistance signaling requires the utilization of numerous preformed defense responses, systemic and cell-to-cell signaling, and, in many cases, the initiation of gene-for-gene resistance (Knepper and Day, 2010). While examples of the activation and regulation of parallel processes have been described (van Wees et al, 2000), there are numerous instances in which bifurcation exists .…”