Keywords
PAMP-triggered immunity · Effector-triggered immunity (ETI) · Cellular and
physiological responses · MAPK cascade · Biotic stress
12.1 Introduction
Rice is one of the most cultivated staple crops across the globe with an annual
production of approximately 480 million tons worldwide (Skorbiansky 2018).
However, similar to the other crops, rice productivity is constrained by various
factors including biotic and abiotic stresses (Wang et al. 2019). Among the biotic
stresses, rice blast disease, caused by a hemibiotrophic pathogen, Magnaporthe
oryzae is the most devastating rice disease limiting up to 30% of the global rice
productivity (Meng et al. 2019b). Because food security has become a global issue in
recent years, especially for staple crops such as rice, efforts have been put in the past
few decades to control this deadly disease of rice. The development and cultivation
of resistant crop plants is the most effective and environmental-friendly approach for
disease control (Liu et al. 2013).
During the course of evolution, plants have developed a two-layered immune
system to fight against the invading pathogens (Gupta et al. 2015a). During plant–
pathogen interaction, both the organisms secrete various small proteins and other
small molecules including lipids, nucleic acids, and carbohydrates in the host
apoplast, where these proteins interact with each other (Jones and Dangl 2006).
This interaction among the pathogen and host-derived proteins determines the
outcome of their relationship. While pathogen-derived proteins facilitate the pathogenicity for infecting the plants, host-derived proteins are involved in the recognition
of these proteins to activate the defense signaling (Liu et al. 2014). During incompatible interactions, the molecular signatures in the pathogen-derived molecules,
termed as pathogen-associated molecular patterns (PAMPs), are recognized by
plants plasma membrane-localized pattern recognition receptors (PRRs) to activate
the first line of defense, termed as PAMP-triggered immunity (PTI) (Jones and
Dangl 2006). PTI responses are not host specific and are relatively weak and
function to restrict the pathogen colonization (Miller et al. 2017). To overcome the
PTI, pathogens secrete effector proteins directly inside the host cells, which are
recognized by the intracellular receptors of the plants to activate the second line of
defense which is known as effector-triggered immunity (ETI). As these pathogen
secreted proteins trigger the ETI responses in plants upon recognition by the
intracellular receptors, these effectors are termed as avirulence (Avr) proteins
(Stotz et al. 2014). Intracellular receptors of the plants are the products of resistance
(R)-genes and are associated with the well-known gene-for-gene hypothesis, to
directly or indirectly recognize cytosolic pathogen effectors to activate the ETI
(Jones and Dangl 2006). ETI responses are host specific and are more rapid and
robust than PTI. ETI responses often culminate into the hypersensitive response at
the site of infection (Gupta et al. 2015a).
364
N. Khatri et al.
PAMP-triggered immunity · Effector-triggered immunity (ETI) · Cellular and
physiological responses · MAPK cascade · Biotic stress
12.1 Introduction
Rice is one of the most cultivated staple crops across the globe with an annual
production of approximately 480 million tons worldwide (Skorbiansky 2018).
However, similar to the other crops, rice productivity is constrained by various
factors including biotic and abiotic stresses (Wang et al. 2019). Among the biotic
stresses, rice blast disease, caused by a hemibiotrophic pathogen, Magnaporthe
oryzae is the most devastating rice disease limiting up to 30% of the global rice
productivity (Meng et al. 2019b). Because food security has become a global issue in
recent years, especially for staple crops such as rice, efforts have been put in the past
few decades to control this deadly disease of rice. The development and cultivation
of resistant crop plants is the most effective and environmental-friendly approach for
disease control (Liu et al. 2013).
During the course of evolution, plants have developed a two-layered immune
system to fight against the invading pathogens (Gupta et al. 2015a). During plant–
pathogen interaction, both the organisms secrete various small proteins and other
small molecules including lipids, nucleic acids, and carbohydrates in the host
apoplast, where these proteins interact with each other (Jones and Dangl 2006).
This interaction among the pathogen and host-derived proteins determines the
outcome of their relationship. While pathogen-derived proteins facilitate the pathogenicity for infecting the plants, host-derived proteins are involved in the recognition
of these proteins to activate the defense signaling (Liu et al. 2014). During incompatible interactions, the molecular signatures in the pathogen-derived molecules,
termed as pathogen-associated molecular patterns (PAMPs), are recognized by
plants plasma membrane-localized pattern recognition receptors (PRRs) to activate
the first line of defense, termed as PAMP-triggered immunity (PTI) (Jones and
Dangl 2006). PTI responses are not host specific and are relatively weak and
function to restrict the pathogen colonization (Miller et al. 2017). To overcome the
PTI, pathogens secrete effector proteins directly inside the host cells, which are
recognized by the intracellular receptors of the plants to activate the second line of
defense which is known as effector-triggered immunity (ETI). As these pathogen
secreted proteins trigger the ETI responses in plants upon recognition by the
intracellular receptors, these effectors are termed as avirulence (Avr) proteins
(Stotz et al. 2014). Intracellular receptors of the plants are the products of resistance
(R)-genes and are associated with the well-known gene-for-gene hypothesis, to
directly or indirectly recognize cytosolic pathogen effectors to activate the ETI
(Jones and Dangl 2006). ETI responses are host specific and are more rapid and
robust than PTI. ETI responses often culminate into the hypersensitive response at
the site of infection (Gupta et al. 2015a).
364
N. Khatri et al.