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Review
. 2022 May 30;8(6):584.
doi: 10.3390/jof8060584.

Understanding the Dynamics of Blast Resistance in Rice- Magnaporthe oryzae Interactions

Basavantraya N Devanna  1 , Priyanka Jain  2 , Amolkumar U Solanke  2 , Alok Das  3 , Shallu Thakur  3 , Pankaj K Singh  2 , Mandeep Kumari  2 , Himanshu Dubey  2 , Rajdeep Jaswal  4 , Deepak Pawar  5 , Ritu Kapoor  4 , Jyoti Singh  2 , Kirti Arora  2 , Banita Kumari Saklani  2 , Chandrappa AnilKumar  1 , Sheshu Madhav Maganti  6 , Humira Sonah  4 , Rupesh Deshmukh  4 , Rajeev Rathour  7 , Tilak Raj Sharma  8
Affiliations
Review

Understanding the Dynamics of Blast Resistance in Rice- Magnaporthe oryzae Interactions

Basavantraya N Devanna et al. J Fungi (Basel). .

Abstract

Rice is a global food grain crop for more than one-third of the human population and a source for food and nutritional security. Rice production is subjected to various stresses; blast disease caused by Magnaporthe oryzae is one of the major biotic stresses that has the potential to destroy total crop under severe conditions. In the present review, we discuss the importance of rice and blast disease in the present and future global context, genomics and molecular biology of blast pathogen and rice, and the molecular interplay between rice-M. oryzae interaction governed by different gene interaction models. We also elaborated in detail on M. oryzae effector and Avr genes, and the role of noncoding RNAs in disease development. Further, rice blast resistance QTLs; resistance (R) genes; and alleles identified, cloned, and characterized are discussed. We also discuss the utilization of QTLs and R genes for blast resistance through conventional breeding and transgenic approaches. Finally, we review the demonstrated examples and potential applications of the latest genome-editing tools in understanding and managing blast disease in rice.

Keywords: CRISPR/Cas; Magnaporthe; QTLs; R-genes; resistance; resistance-breeding; rice.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic representation of the life cycle of the M. oryzae in rice.
Figure 2
Figure 2
Schematic presentation of mechanisms of Pi54 locus-mediated blast disease resistance. The Avr-Pi54 effector binds to Pi54 and its orthologs (blue) mainly at the non-LRR region, upstream to the LRR domain. The Pi54 loci perceive the M. oryzae signals through STI1, an anchor for defensome complex involving multiple proteins such as OsRac1 (Rac/Rop GTPase), RACK1A (Receptor of Activated C Kinase), RAR (Required for Mla12 Resistance), SGT1 (Suppressor of the G2 allele of skp1), MAPK6 (a rice Mitogen-Activated Protein Kinase), and Rboh (NADPH oxidases). The MAPK6-mediated downstream signaling pathways might induce various DR genes. Besides, a set of miRNAs induced by the Pi54 loci are playing a role disease-resistance response. This figure is partially adapted and modified with the latest information [89].
Figure 3
Figure 3
Schematic representation of the ‘Circular Model’ of plant–pathogen interaction. (This figure was originally drawn by Prof. Jonathan Jones, Sainsbury Lab, Norwich, UK, and it is being produced here with his permission).
Figure 4
Figure 4
Representation of role of phytohormones in rice during M. oryzae infection. (A) Auxin: Upon infection with M. oryzae, rice reduces the production of auxin and thereby induces SAR. However, the pathogen secretes auxins to counteract this host-induced SAR. (B) Cytokinin: The host CKs at higher concentration induce SA-mediated SAR. (C) Jasmonic acid: JA through induction of OsJAR1 induces resistance, whereas M. oryzae counteracts this through activation of miR319, which suppresses the expression of rice OsTCP21 and blocks the SAR-induced resistance. (D) Abscisic acid: ABA generally has antagonistic effects on blast disease resistance. M. oryzae induces the expression of rice NCED3 gene and thereby ABA biosynthesis and increased susceptibility to pathogens by inhibiting SAR.
Figure 5
Figure 5
Simplified diagrammatic representation of models on host disease-resistance mechanism. Gene for gene model (GFGM): Physical interaction of pathogen-derived PAMP (pathogen associated molecular pattern) with DR protein (pattern recognition receptor, PRR), resulting in PAMP-triggered immunity (PTI); physical interaction of Avr (effector) with R protein (NBS-LRR), resulting in effector-triggered immunity (ETI); Guard Model (GM): Interaction of effector with guardee triggers effector-triggered immunity (ETI) by their interaction with R protein (NBS-LRR). However, in the absence of R protein, binding of guardee with effector enhances the susceptibility/fitness of the pathogen (ETS); Decoy Model (DM): Interaction of effector with decoy triggers effector-triggered immunity (ETI) with the interaction of R protein (NBS-LRR), however, in the absence of R protein, there is no increase in the virulence/fitness of the pathogen.
Figure 6
Figure 6
Rice blast resistance genes identified and mapped on to different rice chromosomes.
Figure 7
Figure 7
Cloned and characterized blast resistance genes on different chromosomes.
See this image and copyright information in PMC

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