Mol. Cells 2019; 42(9): 637-645
Published online September 19, 2019
https://doi.org/10.14348/molcells.2019.0070
© The Korean Society for Molecular and Cellular Biology
Correspondence to : jjeon@khu.ac.kr (JSJ); khsohn@postech.ac.kr (KHS)
This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/.
Effector-triggered immunity (ETI) is an effective layer of plant defense initiated upon recognition of avirulence (Avr) effectors from pathogens by cognate plant disease resistance (R) proteins. In rice, a large number of
Keywords allelism, Magnaporthe oryzae, Pi5, Pii, resistance, rice
Pathogen infection causes tragic damage to host plants and serious reduction of crop yield. Resulting from their co-evolution, pathogens and plants have developed efficient mechanisms to evade detection and activate disease resistance, respectively (Huang et al., 2014). Pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI) have emerged as two key immunity layers in plants. Whereas PTI is associated with the perception of PAMPs by pattern recognition receptors (PRRs), ETI is the second tier of immunity where the plant recognizes secreted effector proteins which, in the absence of resistance proteins, might dampen PTI and benefit the pathogen (Jones and Dangl, 2006). ETI is often associated with rapid development of programmed cell death at the site of infection termed the hypersensitive response (HR) (Maekawa et al., 2011), a strong resistance mechanism that prevents microbial proliferation. The specific recognition of pathogen-derived avirulence (Avr) effectors by corresponding disease resistance (R) proteins activates ETI in plants. R proteins typically carry nucleotide-binding (NB) and leucine-rich repeat (LRR) (NLR) domains with varying N-terminal toll/interleukin 1 or coiled-coil domains. Recently, it was discovered that some NLRs carry effector-sensing decoy domains at their C-terminal regions (Cui et al., 2015).
In order to understand the mechanism of disease resistance to the rice blast fungus
Despite the effective disease resistance against blast fungus conferred by NLRs in rice, the rapid onset of genetic variability and pathogenicity of blast fungus has led to the disarmament of resistance conferred by specific
Twelve PCR primer sets (Supplementary Table S1) were designed across the
To analyze gene expression, total RNA from leaf blades of four-week-old transgenic plants was extracted using RNAiso Plus according to the manufacturer’s protocol (Takara Bio, Japan). Reverse transcription was performed according to the manufacturer’s protocol using ReverTra Ace® qPCR RT Master Mix with gDNA Remover (Toyobo, Japan). The cDNA obtained was used as template to measure expression by quantitative PCR (qPCR) with gene-specific primers (Supplementary Table S1). Three biological replications were carried out for each sample.
Full-length cDNAs of
To produce transgenic rice plants, the
To identify
For blast fungus inoculation,
In order to verify the pair of NLRs as orthologues of
To test if Pii-1 and Pii-2 are required for AVR-Pii recognition in
To further investigate whether the Pii-1/Pii-2 pair is required, we generated a series of binary constructs carrying
In order to verify if the transgenic plants expressing
The high similarity of the
Exo70F3 was previously reported as an interactor of AVR-Pii and critical for
The requirement of Pi5-1 and Pi5-2 in
The similarity of resistance specificity conferred by
Cell death is often an indicator of defense induced by ETI. Therefore, LM phenotypes have been studied in-depth to understand the molecular aspect of defense (Wu et al., 2008). Cell death phenotypes in tobacco are observed when expressing
The sequence variation in NB-LRR genes is the result of a long co-evolution between rice and rice blast. Therefore, the significant difference in the last intron of
The sequence similarity, resistance spectrum, and location on the chromosome raised the question about the identity of AVR-Pii and AVR-Pi5 effectors. AVR-Pii was previously isolated via an association genetics approach among 23
The Exo70 protein in the exocyst complex is important in tethering and fusion of the vesicles and plasma membrane at the site of polarized exocytosis (Munson and Novick, 2006). In plants, OsExo70F3 is known to interact with AVR-Pii and is critical for
Mol. Cells 2019; 42(9): 637-645
Published online September 30, 2019 https://doi.org/10.14348/molcells.2019.0070
Copyright © The Korean Society for Molecular and Cellular Biology.
Kieu Thi Xuan Vo1,8, Sang-Kyu Lee1,8, Morgan K. Halane2, Min-Young Song1, Trung Viet Hoang1, Chi-Yeol Kim1,3, Sook-Young Park4, Junhyun Jeon5, Sun Tae Kim6, Kee Hoon Sohn2,7,*, and Jong-Seong Jeon1,*
1Graduate School of Biotechnology and Crop Biotech Institute, Kyung Hee University, Yongin 17104, Korea, 2Department of Life Sciences, Pohang University of Science and Technology, Pohang 37673, Korea, 3Present address: Department of Agricultural Biotechnology, Seoul National University, Seoul 08826, Korea, 4Department of Plant Medicine, Sunchon National University, Suncheon 57922, Korea, 5Department of Biotechnology, Yeungnam University, Gyeongsan 38541, Korea, 6Department of Plant Bioscience, Pusan National University, Miryang 46241, Korea, 7School of Interdisciplinary Bioscience and Bioengineering, Pohang University of Science and Technology, Pohang 37673, Korea, 8These authors contributed equally to this work.
Correspondence to:jjeon@khu.ac.kr (JSJ); khsohn@postech.ac.kr (KHS)
This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/.
Effector-triggered immunity (ETI) is an effective layer of plant defense initiated upon recognition of avirulence (Avr) effectors from pathogens by cognate plant disease resistance (R) proteins. In rice, a large number of
Keywords: allelism, Magnaporthe oryzae, Pi5, Pii, resistance, rice
Pathogen infection causes tragic damage to host plants and serious reduction of crop yield. Resulting from their co-evolution, pathogens and plants have developed efficient mechanisms to evade detection and activate disease resistance, respectively (Huang et al., 2014). Pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI) have emerged as two key immunity layers in plants. Whereas PTI is associated with the perception of PAMPs by pattern recognition receptors (PRRs), ETI is the second tier of immunity where the plant recognizes secreted effector proteins which, in the absence of resistance proteins, might dampen PTI and benefit the pathogen (Jones and Dangl, 2006). ETI is often associated with rapid development of programmed cell death at the site of infection termed the hypersensitive response (HR) (Maekawa et al., 2011), a strong resistance mechanism that prevents microbial proliferation. The specific recognition of pathogen-derived avirulence (Avr) effectors by corresponding disease resistance (R) proteins activates ETI in plants. R proteins typically carry nucleotide-binding (NB) and leucine-rich repeat (LRR) (NLR) domains with varying N-terminal toll/interleukin 1 or coiled-coil domains. Recently, it was discovered that some NLRs carry effector-sensing decoy domains at their C-terminal regions (Cui et al., 2015).
In order to understand the mechanism of disease resistance to the rice blast fungus
Despite the effective disease resistance against blast fungus conferred by NLRs in rice, the rapid onset of genetic variability and pathogenicity of blast fungus has led to the disarmament of resistance conferred by specific
Twelve PCR primer sets (Supplementary Table S1) were designed across the
To analyze gene expression, total RNA from leaf blades of four-week-old transgenic plants was extracted using RNAiso Plus according to the manufacturer’s protocol (Takara Bio, Japan). Reverse transcription was performed according to the manufacturer’s protocol using ReverTra Ace® qPCR RT Master Mix with gDNA Remover (Toyobo, Japan). The cDNA obtained was used as template to measure expression by quantitative PCR (qPCR) with gene-specific primers (Supplementary Table S1). Three biological replications were carried out for each sample.
Full-length cDNAs of
To produce transgenic rice plants, the
To identify
For blast fungus inoculation,
In order to verify the pair of NLRs as orthologues of
To test if Pii-1 and Pii-2 are required for AVR-Pii recognition in
To further investigate whether the Pii-1/Pii-2 pair is required, we generated a series of binary constructs carrying
In order to verify if the transgenic plants expressing
The high similarity of the
Exo70F3 was previously reported as an interactor of AVR-Pii and critical for
The requirement of Pi5-1 and Pi5-2 in
The similarity of resistance specificity conferred by
Cell death is often an indicator of defense induced by ETI. Therefore, LM phenotypes have been studied in-depth to understand the molecular aspect of defense (Wu et al., 2008). Cell death phenotypes in tobacco are observed when expressing
The sequence variation in NB-LRR genes is the result of a long co-evolution between rice and rice blast. Therefore, the significant difference in the last intron of
The sequence similarity, resistance spectrum, and location on the chromosome raised the question about the identity of AVR-Pii and AVR-Pi5 effectors. AVR-Pii was previously isolated via an association genetics approach among 23
The Exo70 protein in the exocyst complex is important in tethering and fusion of the vesicles and plasma membrane at the site of polarized exocytosis (Munson and Novick, 2006). In plants, OsExo70F3 is known to interact with AVR-Pii and is critical for
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