Natural variation in priming of basal resistance: from evolutionary origin to agricultural exploitation

Abstract

Biotic stress has a major impact on the process of natural selection in plants. As plants have evolved under variable environmental conditions, they have acquired a diverse spectrum of defensive strategies against pathogens and herbivores. Genetic variation in the expression of plant defence offers valuable insights into the evolution of these strategies. The 'zigzag' model, which describes an ongoing arms race between inducible plant defences and their suppression by pathogens, is now a commonly accepted model of plant defence evolution. This review explores additional strategies by which plants have evolved to cope with biotic stress under different selective circumstances. Apart from interactions with plant-beneficial micro-organisms that can antagonize pathogens directly, plants have the ability to prime their immune system in response to selected environmental signals. This defence priming offers disease protection that is effective against a broad spectrum of virulent pathogens, as long as the augmented defence reaction is expressed before the invading pathogen has the opportunity to suppress host defences. Furthermore, priming has been shown to be a cost-efficient defence strategy under relatively hostile environmental conditions. Accordingly, it is possible that selected plant varieties have evolved a constitutively primed immune system to adapt to levels of disease pressure. Here, we examine this hypothesis further by evaluating the evidence for natural variation in the responsiveness of basal defence mechanisms, and discuss how this genetic variation can be exploited in breeding programmes to provide sustainable crop protection against pests and diseases.

Next-Generation Systemic Acquired Resistance

“…Priming of defense is a beneficial defense strategy in hostile environments with relatively minor costs (van Hulten et al, 2006;Ahmad et al, 2010). Epigenetic regulation of priming would allow plants to protect their progeny against recurring biotic stress without permanent genetic fixation of the trait and its associated costs.…”

“…This priming results in a faster and stronger induction of defense mechanisms after pathogen attack (Conrath et al, 2006;Conrath, 2011). Although inducible defenses are often too weak to protect the host plant against disease by virulent pathogens, an augmented induction of these defenses can be highly effective, particularly when their expression precedes the delivery of susceptibility-inducing effectors by the invading pathogen (Ahmad et al, 2010).…”

The role of sugar signaling in plant defense responses against fungal pathogens

“…In this model the plant immune system is divided into four phases. Although numerous modifications are continually being made to the details of this model, it still provides a good basis to explain molecular events (Ahmad et al 2010;Zipfel and Robatzek 2010;Rampitsch and Bykova 2012;Chujo et al 2013 Known plant PRRs are modular proteins harboring an extracellular domain consisting of LRR (leucine-rich repeat) or lysin motifs (LysM). PTI relies on MAP kinase (MAPK) activation, production of reactive oxygen species (ROS), transcriptional reprogramming, hormone biosynthesis and deposition of callose, a high molecular weight b-(1,3)-glucan polymer in the cell wall.…”

Priming by Rhizobacterium Protects Tomato Plants from Biotrophic and Necrotrophic Pathogen Infections through Multiple Defense Mechanisms

“…Most plausible explanations for ISR are the rapid up regulation of the PTI or basal resistance sufficient for abrogation of the ETS. Both PAMPs and microbe (including PGPR)-associated molecular patterns (MAMPs) are perceived as slowly evolving secretomes, therefore, they should share a lot of cognate factors capable of inducing PTI or PTIlike resistance (Ahmad et al, 2010;Van Wees et al, 2008). A part of recent investigations have focused on elucidation of ISR factors from PGPR, plant proteins whose expression was altered by PGPR treatment, and pathogen PAMPs triggering PTI-induced basal resistance (Bittel and Robatzek, 2007;Kandasamy et al, 2009).…”