enriched with 1,3-β-glucan cell wall polymer callose), lignin biosynthesis, or
changes in cell wall proteins and pectic polysaccharide structures (Wydra and Beri
2006; Boller and Felix 2009; Zipfel 2009; Yu et al. 2017; Peng et al. 2018). The
characteristic cellular defense responses observed for virus-derived molecules
(nucleic acids, e.g., dsRNAs) are very similar to that for microbial elicitors, which
trigger PTI (for innate immunity) and RNA interference (RNAi) (for adaptive
immunity) (Nicaise 2014).
The recognition of HAEs and HAMPs by PRRs induces ion imbalances,
variations in membrane potential and Ca
2+
fluxes, and generation of ROS that
stimulate downstream signaling activities in plants (Maffei et al. 2007). Besides
inducing defense responses, plants can either directly dissuade the attacking insects
by producing volatile compounds from the lipoxygenase (LOX) and terpenoid
pathways or indirectly apprentice natural enemies of their invaders, both of which
are regulated by the interacting signaling pathways of jasmonic acid (JA) with
ethylene (ET), salicylic acid (SA), and abscisic acid (ABA) (Pichersky and
Gershenzon 2002; Van Oosten et al. 2008; Arimura et al. 2009; War et al. 2012;
Gouhier-Darimont et al. 2013). Further, plants have complex locally and systemically induced signaling pathways in response to phytophagous herbivore insects to
reduce the capacity of their digestion, which involve JA, systemin,
oligogalacturonides (OGAs), hydrogen peroxide, and expression of downstream
defense protein inhibitors (amylase inhibitors, lectins, chitinases, and polyphenol
oxidases) (Fürstenberg-Hägg et al. 2013).
Besides, the successful pathogens that have evolved by utilizing virulence effector molecules can subdue PTI signaling or preclude host detection (Pel and Pieterse
2013). Consequently, plants have evolved NB-LRR receptor protein complex that
activates plant defense mechanisms more effectively. This recognition forms the Rgene-mediated or vertical resistance, constituting the effector-triggered immunity
(ETI) for the second line of defense (Dodds and Rathjen 2010). Further, Tollinterleukin 1 receptor (TIR) domain (TNLs) and coiled-coil (CC) domain (CNLs)
subgroups of NB-LRR can functionally interact with various proteins for resistance
signaling (Griebel et al. 2014). These interactions among pathogen and host plants
have resulted in a variety of pathogen effectors and resistance genes, as a manifestation of gene-for-gene resistance, that activates hypersensitive responses (HR) with
programmed cell death (PCD) in infected cells and the surrounding plant parts, and
RNA silencing for antiviral defense (Soosaar et al. 2005; Huang et al. 2016).
10.4 Microbe-Induced Resistance Against Biotic Stress in Plants
Plants secrete around 5–21% of their total assimilated carbon in the form of low
(amino acids, organic acids, sugars, phenolics, and secondary metabolites) and high
(polysaccharides and proteins) molecular mass compounds into rhizosphere via
roots (Hernández et al. 2015). Chemotactically, these compounds attract and/or
repel a complex diverse mixture of microorganisms including beneficial as well as
harmful ones and cause their proliferation, establishment, and colonization on/in the
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changes in cell wall proteins and pectic polysaccharide structures (Wydra and Beri
2006; Boller and Felix 2009; Zipfel 2009; Yu et al. 2017; Peng et al. 2018). The
characteristic cellular defense responses observed for virus-derived molecules
(nucleic acids, e.g., dsRNAs) are very similar to that for microbial elicitors, which
trigger PTI (for innate immunity) and RNA interference (RNAi) (for adaptive
immunity) (Nicaise 2014).
The recognition of HAEs and HAMPs by PRRs induces ion imbalances,
variations in membrane potential and Ca
2+
fluxes, and generation of ROS that
stimulate downstream signaling activities in plants (Maffei et al. 2007). Besides
inducing defense responses, plants can either directly dissuade the attacking insects
by producing volatile compounds from the lipoxygenase (LOX) and terpenoid
pathways or indirectly apprentice natural enemies of their invaders, both of which
are regulated by the interacting signaling pathways of jasmonic acid (JA) with
ethylene (ET), salicylic acid (SA), and abscisic acid (ABA) (Pichersky and
Gershenzon 2002; Van Oosten et al. 2008; Arimura et al. 2009; War et al. 2012;
Gouhier-Darimont et al. 2013). Further, plants have complex locally and systemically induced signaling pathways in response to phytophagous herbivore insects to
reduce the capacity of their digestion, which involve JA, systemin,
oligogalacturonides (OGAs), hydrogen peroxide, and expression of downstream
defense protein inhibitors (amylase inhibitors, lectins, chitinases, and polyphenol
oxidases) (Fürstenberg-Hägg et al. 2013).
Besides, the successful pathogens that have evolved by utilizing virulence effector molecules can subdue PTI signaling or preclude host detection (Pel and Pieterse
2013). Consequently, plants have evolved NB-LRR receptor protein complex that
activates plant defense mechanisms more effectively. This recognition forms the Rgene-mediated or vertical resistance, constituting the effector-triggered immunity
(ETI) for the second line of defense (Dodds and Rathjen 2010). Further, Tollinterleukin 1 receptor (TIR) domain (TNLs) and coiled-coil (CC) domain (CNLs)
subgroups of NB-LRR can functionally interact with various proteins for resistance
signaling (Griebel et al. 2014). These interactions among pathogen and host plants
have resulted in a variety of pathogen effectors and resistance genes, as a manifestation of gene-for-gene resistance, that activates hypersensitive responses (HR) with
programmed cell death (PCD) in infected cells and the surrounding plant parts, and
RNA silencing for antiviral defense (Soosaar et al. 2005; Huang et al. 2016).
10.4 Microbe-Induced Resistance Against Biotic Stress in Plants
Plants secrete around 5–21% of their total assimilated carbon in the form of low
(amino acids, organic acids, sugars, phenolics, and secondary metabolites) and high
(polysaccharides and proteins) molecular mass compounds into rhizosphere via
roots (Hernández et al. 2015). Chemotactically, these compounds attract and/or
repel a complex diverse mixture of microorganisms including beneficial as well as
harmful ones and cause their proliferation, establishment, and colonization on/in the
302
L. Thomas and I. Singh