12.3.5 Callose Deposition
Callose is a β-1,3 glucan polymer with a high molecular weight that strengthens
plant cell walls (Luna et al. 2011). Callose deposits in a timely manner at the site of
infections, forming a prominent physical barrier against pathogen attacks. Various
PAMPs or DAMPs, including flg22, elf18, chitin, PGN (peptidoglycan), and OG
(oligogalacturonide), induce callose deposits in plant roots, cotyledons, and leaves
(Luna et al. 2011). Callose deposition seems to be regulated at multiple levels and
requires the activity of multiple proteins. For instance, function loss of RBOHD, a
key enzyme involved in apoplastic ROS formation, results in compromised flg22and OG-induced callose deposits (Clay et al. 2009).
12.4 ETI in Rice–M. oryzae Interaction
ETI signaling events have been well characterized by the gene-for-gene concept
where identification of a pathogen secreted Avr protein by the R-gene product of the
plants results in the activation of defense responses and culminating into resistance
(Stotz et al. 2014). However, a growing body of evidence suggests that direct
interaction between R-gene and Avr gene products is relatively rare and the recognition of an Avr protein by corresponding R-gene product is major because of the
indirect interactions between these two, employing one or more additional
components (Jia et al. 2000).
12.4.1 Effector Suppression of PTI
Bacterial and fungal pathogens suppress plant immunity through the secretion of
numerous effector proteins that either hinders the plant defense signaling or increase
their susceptibility. The number and types of effector proteins secreted by the
pathogens determine their virulence level and host range. For instance, XOO1488
targets RLCK185 to suppress the OsCERK1-mediated defense (Yamaguchi et al.
2013). Moreover, when host LysM immune receptor proteins detect fungal-derived
chitin to activate immunity, fungi employ LysM effectors to prevent the recognition
of chitin by host immune receptors. Slp1 (secreted LysM protein 1), such one
secreted protein with two LysM domains in M. oryzae, prevents chitin recognition
by CEBiP via direct binding to chitin oligosaccharides released from the fungal cell
wall (Mentlak et al. 2012).
12.4.2 R-Genes and Avr Effectors
To date, more than 100 rice R-genes conferring rice blast resistance have been
identified, of which 23 were cloned, while a total of 13 Avr effector genes have
been cloned from M. oryzae (Sharma et al. 2012). Five cloned rice R-gene and
372
N. Khatri et al.
Callose is a β-1,3 glucan polymer with a high molecular weight that strengthens
plant cell walls (Luna et al. 2011). Callose deposits in a timely manner at the site of
infections, forming a prominent physical barrier against pathogen attacks. Various
PAMPs or DAMPs, including flg22, elf18, chitin, PGN (peptidoglycan), and OG
(oligogalacturonide), induce callose deposits in plant roots, cotyledons, and leaves
(Luna et al. 2011). Callose deposition seems to be regulated at multiple levels and
requires the activity of multiple proteins. For instance, function loss of RBOHD, a
key enzyme involved in apoplastic ROS formation, results in compromised flg22and OG-induced callose deposits (Clay et al. 2009).
12.4 ETI in Rice–M. oryzae Interaction
ETI signaling events have been well characterized by the gene-for-gene concept
where identification of a pathogen secreted Avr protein by the R-gene product of the
plants results in the activation of defense responses and culminating into resistance
(Stotz et al. 2014). However, a growing body of evidence suggests that direct
interaction between R-gene and Avr gene products is relatively rare and the recognition of an Avr protein by corresponding R-gene product is major because of the
indirect interactions between these two, employing one or more additional
components (Jia et al. 2000).
12.4.1 Effector Suppression of PTI
Bacterial and fungal pathogens suppress plant immunity through the secretion of
numerous effector proteins that either hinders the plant defense signaling or increase
their susceptibility. The number and types of effector proteins secreted by the
pathogens determine their virulence level and host range. For instance, XOO1488
targets RLCK185 to suppress the OsCERK1-mediated defense (Yamaguchi et al.
2013). Moreover, when host LysM immune receptor proteins detect fungal-derived
chitin to activate immunity, fungi employ LysM effectors to prevent the recognition
of chitin by host immune receptors. Slp1 (secreted LysM protein 1), such one
secreted protein with two LysM domains in M. oryzae, prevents chitin recognition
by CEBiP via direct binding to chitin oligosaccharides released from the fungal cell
wall (Mentlak et al. 2012).
12.4.2 R-Genes and Avr Effectors
To date, more than 100 rice R-genes conferring rice blast resistance have been
identified, of which 23 were cloned, while a total of 13 Avr effector genes have
been cloned from M. oryzae (Sharma et al. 2012). Five cloned rice R-gene and
372
N. Khatri et al.