**6. Defence mechanism of rice against blast infection**

Rice employs a twolayered innate immune system to defend itself against blast invasion. PAMP-triggered immunity (PTI) forms the first layer of immunity, and is boosted after PAMP recognition by membrane-associated PRR on the host cell membrane [172]. Chitin well-known type of PAMP capable of activating plant immune responses. Chitin from *M. oryzae* is recognized by rice transmembrane LysM receptor-like proteins (LysM-RLPs), including two lysin motif-containing proteins, OsLYP4 and OsLYP6, and a chitin elicitor binding protein (CEBiP). When defending against *M. oryzae*, rice forms a receptor complex called LysM-RLPsOsCERK1. Two rice Receptor like kinases (RLKs), Flagellin Sensing 2 (OsFLS2) and BRI1-Associated receptor Kinase 1 (OsBAK1), are also involved in PTI. To achieve successful infection, virulent *M. oryzae* isolates have evolved a strategy to secrete effectors into the rice cell for subverting PTI, leading to effector-triggered susceptibility (ETS).To combat a blast fungus capable of subverting PTI, rice deploys nucleotide-binding site leucine-rich repeat (NLR) proteins to recognize the effectors named avirulence (AVR) proteins. Several AVR proteins have been cloned, including AVR-Pita, AVR-Pi9, and Avr-Pizt [173, 174]. Recognition of AVR by NLR promotes strong immune responses referred to as effector-triggered immunity (ETI), which arms rice with a second layer of protection in case of disabled PTI [172]. Defence regulators (DR) genes can activate various signaling pathways, such as MAPK cascades and the ubiquitination-mediated pathway, as well as hormonal signaling (**Figure 3**). Upon activation by extracellular stimuli, MAPKs transmit signals from the cell membrane to the nucleus, acting in defense against *M. oryzae* [172]. Transcription factors (TFs) are also involved in defense against infection by *M. oryzae*. of particular interest are broad-spectrum resistance Digu 1 (bsr-d1) and Ideal Plant Architecture 1 (IPA1). Lesion-mimic mutant (LMM) genes are the main DR genes capable of activating immune responses such as ROS bursts. Lesionmimic mutants, including spl30-1, spl33, spl35, lmm24 and spl-D usually show increased disease resistance [172]. Several other DR genes can confer similar blast resistance by initiating ROS bursts. For example, SPL11 cell-Death Suppressor 2 (SDS2) is a ubiquitination substrate of SPL11 (an E3 ubiquitin ligase comprising an armadillo repeat domain and a U-box domain). SDS2 interacts with OsRLCK118/176 and phosphorylates OsRbohB, and then induces a ROS burst, resulting in increased resistance to *M. oryzae* [172]. Hormones are another class of regulators involved in rice blast defense response. Suppressor of Salicylic acid Insensitivity-2 (OsSSI2), OsSec3a (a principal subunit of the exocyst complex in rice), OsAAA-ATPase 1 all mediate resistance by modulating salicylic acid (SA) signaling [175]. JA-resistant 1 (OsJAR1) and JAresponsive MYB (OsJAMyb) are associated with jasmonic acid (JA) signaling, and determine rice blast disease resistance. In the early stage of infection by pathogens, rice accumulates antimicrobial compounds as a defense response. For example, cyanide contributes to rice resistance by restricting fungal growth [176]. Bayogenin 3-O-cellobioside confers cultivar-nonspecific defense against the rice blast fungus [177]. Diterpenoids are a major group of antimicrobial phytoalexins in rice, and their

#### **Figure 3.**

*Rice innate immunity signalling pathways triggered by M. oryzae. (1) On the rice cell membrane (2) Upon chitin perception, the LysM-RLP-OsCERK1 complex also elicits the OsRacGEF1-dependent pathway. (3) The rice blast fungus secretes effectors, such as Chitinase 1 (MoChia1) and Secreted a LysM protein 1 (Slp 1), into the rice cell to subvert PTI, resulting in the emergence of effector-triggered susceptibility (ETS). (4) Alternatively, secreted effectors called avirulence (AVR) proteins are recognized by rice nucleotide-binding site leucine-rich repeat (NLR) proteins, leading to a particularly strong immune response referred to as effectortriggered immunity (ETI). (5) The integrated decoy model (6) Pit employs its CC domain to bind to OsSPK1 for activating OsRac1 and induction of cell death. (7) In ETI, OsRac1 is required for Pb1, Pid3-mediated blast resistance. (8) NLR proteins mediate defense response by direct interaction with transcription factors [172].*

role in rice disease resistance has been indicated by functional analysis of a diterpenoid gene cluster (DGC7) located on rice chromosome 7 [178]. Excessive or deficient supply of nutrients, such as nitrogen, phosphate, potassium, and silica, affects stress response and can potentially influence rice disease resistance. For instance, nitrogen partially breaks down rice blast resistance triggered by the Pi1 gene. Potassium is also associated with rice blast resistance. For example, *M. oryzae* can disrupt rice immune response by regulating host K+ channels. Silicon nutrition can mitigate various biotic stresses [172]. On one hand, silicon acts as a physical barrier against plant disease. On the other hand, silicon boosts the plant's defense by functioning as a biological inducer. Silicon-induced defense response and cell silicification of leaves both contribute to rice blast disease resistance. In *M. oryzae*-infected rice plants, silicon-enhanced blast disease resistance is also associated with an increase in photochemical efficiency and adjustment of mineral nutrient absorption.

#### **7. Strategies for breeding blast resistance in Rice**

Although few cultural practices such as nutrient and water management, planting time, spacing, and application of fungicides are employed in managing blast disease, it has not been possible for the farming community to effectively and efficiently offset the blast disease [179]. This is mainly because of the complex etiology of the pathogen *M. oryzae* that includes infection of almost all parts of the rice plant, at all stages starting from seedling stage to maturity. Hence, breeding

#### *Rice Blast Disease in India: Present Status and Future Challenges DOI: http://dx.doi.org/10.5772/intechopen.98847*

for durable resistance and resistant cultivars has been a proven ecologically viable and crucial option for addressing the infection by rice blast fungus [155, 180, 181]. Breeding for blast resistance in rice can be broadly categorized into four classes, including conventional breeding methods, marker-dependent breeding methods, breeding approaches requiring genetic transformation, and genome editing.
