(HAEs) comprising of herbivore-associated molecular patterns (HAMPs) and herbivore effectors during plant–insect interaction (Santamaria et al. 2013). Apart from
this, plants also as a consequence of infection or injury release some chemicals,
called as danger- or damage-associated molecular patterns (DAMPs) (Yu et al.
2017). Some commonly reported PAMPs/MAMPs are bacterial flagellin and elongation factor Tu (EF-Tu), fungal chitin, yeast mannans, and Oomycete xylanase and
heptaglucan (Dodds and Rathjen 2010; Newman et al. 2013). HAMPs are present in
oral secretions released by chewing insects containing proteins, fatty acid-amino
acid conjugates (FACs), sulfur-containing fatty acids, plant-derived degradation
products of ATP synthase and cell walls generated following insect herbivory, and
insect egg ovipositional fluids (Wu and Baldwin 2009; Foyer et al. 2015). Similarly,
plant derived chemicals such as proteins (AtPEPs, PIPs, and HMGB3),
oligogalacturonides and extracellular ATP may act as DAMPs (Yu et al. 2017).
Plants detect various elicitors with the help of certain receptors. PAMPs/MAMPs are
recognized by plasma membrane bound extracellular receptors, called as pattern
recognition receptors (PRRs), of either receptor-like kinase or receptor-like protein
families (Nurnberger and Kemmerling 2009). The structure of PRRs contain an
extracellular ligand-specific domain and a transmembrane domain. Examples of
extracellular domains include leucine-rich repeats (LRRs) that help in peptide ligand
perception and signaling, lysine motifs (LysMs) that help in GlcNAc containing
ligand perception and signaling, and lectin motifs that help in lipopolysaccharide
perception (Couto and Zipfel 2016; Yu et al. 2017). Similarly, HAMPs and DAMPs
are also recognized by PRRs (Heil et al. 2012; Santamaria et al. 2013).
In contrast to PAMPs/MAMPs, effectors are recognized intracellularly by resistance (R) proteins, encoded by R genes that directly or indirectly recognize specific
virulence effectors (Avr proteins) from pathogens or pests (Cui et al. 2015). Most R
proteins contain specific domains, namely, a variable N-terminal effector, a
conserved central Nucleotide Binding Site (NBS), and a C-terminal Leucine-Rich
Repeat (LRR). With other accessory proteins, the R proteins form a nucleotidebinding-leucine rich repeat (NB-LRR) receptor protein complex that can recognize
many specific pathogen effector molecules (Meyers et al. 2003; Dodds and Rathjen
2010).
10.3.2 Overcoming Biotic Stress
Subsequent to recognition of PAMPs/MAMPs and effectors, plants develop PAMPtriggered immunity (PTI) and effector-triggered immunity (ETI), respectively (Peng
et al. 2018). These defense mechanisms induce a cascade of somewhat overlapping
events that include rapid ion fluxes across the plasma membrane, oxidative bursts
with generation of reactive oxygen species (ROS), activation of mitogen-activated
protein kinases (MAPKs) and calcium-dependent protein kinases (CDPKs),
localized induction of defense-related genes or pathogen cell wall/cell membrane
lysing enzymes/peptides (e.g., chitinases, glucanases, and defensins), production of
antimicrobial phytoalexins, plant cell wall modifications (e.g., deposition of papillae,
10 Microbe-Mediated Biotic Stress Signaling and Resistance Mechanisms in Plants
301
this, plants also as a consequence of infection or injury release some chemicals,
called as danger- or damage-associated molecular patterns (DAMPs) (Yu et al.
2017). Some commonly reported PAMPs/MAMPs are bacterial flagellin and elongation factor Tu (EF-Tu), fungal chitin, yeast mannans, and Oomycete xylanase and
heptaglucan (Dodds and Rathjen 2010; Newman et al. 2013). HAMPs are present in
oral secretions released by chewing insects containing proteins, fatty acid-amino
acid conjugates (FACs), sulfur-containing fatty acids, plant-derived degradation
products of ATP synthase and cell walls generated following insect herbivory, and
insect egg ovipositional fluids (Wu and Baldwin 2009; Foyer et al. 2015). Similarly,
plant derived chemicals such as proteins (AtPEPs, PIPs, and HMGB3),
oligogalacturonides and extracellular ATP may act as DAMPs (Yu et al. 2017).
Plants detect various elicitors with the help of certain receptors. PAMPs/MAMPs are
recognized by plasma membrane bound extracellular receptors, called as pattern
recognition receptors (PRRs), of either receptor-like kinase or receptor-like protein
families (Nurnberger and Kemmerling 2009). The structure of PRRs contain an
extracellular ligand-specific domain and a transmembrane domain. Examples of
extracellular domains include leucine-rich repeats (LRRs) that help in peptide ligand
perception and signaling, lysine motifs (LysMs) that help in GlcNAc containing
ligand perception and signaling, and lectin motifs that help in lipopolysaccharide
perception (Couto and Zipfel 2016; Yu et al. 2017). Similarly, HAMPs and DAMPs
are also recognized by PRRs (Heil et al. 2012; Santamaria et al. 2013).
In contrast to PAMPs/MAMPs, effectors are recognized intracellularly by resistance (R) proteins, encoded by R genes that directly or indirectly recognize specific
virulence effectors (Avr proteins) from pathogens or pests (Cui et al. 2015). Most R
proteins contain specific domains, namely, a variable N-terminal effector, a
conserved central Nucleotide Binding Site (NBS), and a C-terminal Leucine-Rich
Repeat (LRR). With other accessory proteins, the R proteins form a nucleotidebinding-leucine rich repeat (NB-LRR) receptor protein complex that can recognize
many specific pathogen effector molecules (Meyers et al. 2003; Dodds and Rathjen
2010).
10.3.2 Overcoming Biotic Stress
Subsequent to recognition of PAMPs/MAMPs and effectors, plants develop PAMPtriggered immunity (PTI) and effector-triggered immunity (ETI), respectively (Peng
et al. 2018). These defense mechanisms induce a cascade of somewhat overlapping
events that include rapid ion fluxes across the plasma membrane, oxidative bursts
with generation of reactive oxygen species (ROS), activation of mitogen-activated
protein kinases (MAPKs) and calcium-dependent protein kinases (CDPKs),
localized induction of defense-related genes or pathogen cell wall/cell membrane
lysing enzymes/peptides (e.g., chitinases, glucanases, and defensins), production of
antimicrobial phytoalexins, plant cell wall modifications (e.g., deposition of papillae,
10 Microbe-Mediated Biotic Stress Signaling and Resistance Mechanisms in Plants
301