Abstract
1.1 Background
Plants are continuously attacked by pathogens in their environments which contribute to global crop
losses (Cerda et al., 2017). Plants use innate immunity to protect themselves and fight against these
pathogens (Nürnberger et al., 2004). The primary defence response, for organisms that have overcome
the initial preformed barriers, is known as the microbe-associated molecular pattern (MAMP)-triggered
immunity (MTI) which is orchestrated by the recognition of pathogen-derived MAMPs through plant
pattern recognition receptors (PRRs) (Nürnberger et al., 2004; Zipfel, 2014; Ranf, 2018). This triggers rapid
defence responses including increased reactive oxygen species (ROS) production, the elevation of
cytosolic calcium ([Ca2+]
cyt), activation of calcium-dependent protein kinase (CDPK), strengthening of
callose deposition, activation of signal transduction events associated with mitogen-activated protein
kinases (MAPKs) and biosynthesis of pathogenesis-related (PR)-proteins (Jones and Dangl, 2006; van Loon
et al., 2006; Klemptner et al., 2014). Some pathogens have devised means of evading MTI, such as
secretion of effector molecules that interact with plant targets and cause diseases, a phenomenon termed
effector-triggered susceptibility (ETS) (Jones and Dangl, 2006; Boller, 2012). For example, Pseudomonas
syringae effector HopAO1 disrupts the ability of bulb-type (B-type) lectin S-domain (SD)-1 RLK,
lipooligosaccharide-specific reduced elicitation (LORE) to activate receptor-like cytoplasmic kinase (RLCK)
PBL34, leading to the impaired immune response (Luo et al., 2020). On the other hand, plants use
polymorphic nucleotide-binding site leucine-rich repeat (NBS-LRR) resistance (R) proteins that recognise
these pathogen-secreted effector molecules and trigger effector-triggered immunity (ETI) (Jones and
Dangl, 2006). This secondary immunity is a more intense defence response which is often associated with
the hypersensitive response (HR) or programmed cell death that protects plants against such pathogens
(Jones and Dangl, 2006; De Wit, 2007; Tang et al., 2017; Saijo et al., 2018)...