**1. Introduction**

The disease triangle concept, introduced in the 1960s by George McNew to predict plant disease outcomes, shows the complex interactions among the environment, the host and the infectious (or abiotic) agent [1]. Plants, continuously challenged by numerous abiotic stresses, potential pests and pathogens, have evolved efficient strategies to perceive and respond to

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such threats. Plants lack specialized immune cells and their survival relies upon a highly sophisticated innate immune system, in which each plant cell responds autonomously [2–5]. The first line of defence is a basal resistance response called pattern-triggered immunity (PTI). It is induced by recognition of exogenous microbe or pathogen-associated molecular patterns (MAMPs or PAMPs) or endogenous molecules released on pathogen perception or pathogeninduced cell damage (damage-associated molecular patterns, DAMPs) via pattern-recognition receptors (PRRs) in the plasma membrane [4]. Successful pathogens overcome PTI by secreting effectors, hydrolytic enzymes or toxins, which suppress or interfere with host defence molecules [6]. In an evolutionary arms race, plants have evolved a robust defence response network termed effector-triggered immunity (ETI) to intercept pathogen effectors through intracellular receptors, such as nucleotide-binding site/leucine-rich repeat (NLR) proteins [5,7,8]. An intricate network of signalling pathways transduces these incoming signals into a diverse array of immune responses activating reactive oxygen species (ROS) generation, MAP kinases, Ca2+ signalling, the production of phytohormones and extensive transcriptional reprogramming [9].

In the past, comprehensive research has been dedicated to understanding plant physiolog‐ ical and molecular responses to individual abiotic and biotic stresses under controlled laboratory conditions. Recent studies of plant responses to concurrent abiotic and biotic stress conditions [10–16] have demonstrated that plants perceive and respond to com‐ bined stresses in a specific and unique manner. Moreover, the underlying signalling pathways are carefully modulated [14,17,18] and coordinated to ensure that plant growth and fitness are not significantly retarded [19].

Vascular wilt pathogens are soil-borne bacteria, fungi and oomycetes that employ various infection strategies to invade plant roots at different infection sites [20]. They subsequently advance inter- or intracellularly through the root cortex and enter the xylem vessels, where they proliferate and spread passively with xylem sap to aerial plant parts [21]. The character‐ istic wilt symptoms develop as a consequence of obstructed transportation of water and minerals, either due to the physical blockage of vessels by the pathogen or indirectly due to the activation of plant physical defence responses (e.g. formation of tyloses, accumulation of pectin-rich gels and gums) that confine the further spread of the pathogen [22]. In addition to wilting, other disease symptoms include vein clearing, leaf epinasty, chlorosis, vascular browning, stunting, necrosis and eventually plant death [21–24].

Primarily due to the specific lifestyle of vascular wilt pathogens, relatively little is known about their interactions with host plants and root-specific defence responses on molecular and biochemical levels compared to foliar pathogens. This chapter, therefore, summarizes the currently available molecular, cellular and systems biology data gathered from studies of signalling networks in model plants and crops challenged by bacterial or fungal pathogens and applies this general knowledge to advance understanding of vascular wilt pathogenesis and implement all these findings into the design of new strategies for the protection of crops and forest ecosystems.
