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Magnaporthe oryzae Effector AVR-Pii Helps to Establish Compatibility by Inhibition of the Rice NADP-Malic Enzyme Resulting in Disruption of Oxidative Burst and Host Innate Immunity.
Mol Cells. 2016 May 31; 39(5):426-38.MC

Abstract

Plant disease resistance occurs as a hypersensitive response (HR) at the site of attempted pathogen invasion. This specific event is initiated in response to recognition of pathogen-associated molecular pattern (PAMP) and subsequent PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI). Both PTI and ETI mechanisms are tightly connected with reactive oxygen species (ROS) production and disease resistance that involves distinct biphasic ROS production as one of its pivotal plant immune responses. This unique oxidative burst is strongly dependent on the resistant cultivars because a monophasic ROS burst is a hallmark of the susceptible cultivars. However, the cause of the differential ROS burst remains unknown. In the study here, we revealed the plausible underlying mechanism of the differential ROS burst through functional understanding of the Magnaporthe oryzae (M. oryzae) AVR effector, AVR-Pii. We performed yeast two-hybrid (Y2H) screening using AVR-Pii as bait and isolated rice NADP-malic enzyme2 (Os-NADP-ME2) as the rice target protein. To our surprise, deletion of the rice Os-NADP-ME2 gene in a resistant rice cultivar disrupted innate immunity against the rice blast fungus. Malic enzyme activity and inhibition studies demonstrated that AVR-Pii proteins specifically inhibit in vitro NADP-ME activity. Overall, we demonstrate that rice blast fungus, M. oryzae attenuates the host ROS burst via AVR-Pii-mediated inhibition of Os-NADP-ME2, which is indispensable in ROS metabolism for the innate immunity of rice. This characterization of the regulation of the host oxidative burst will help to elucidate how the products of AVR genes function associated with virulence of the pathogen.

Authors+Show Affiliations

Division of Integrative Bioscience and Biotechnology, College of Life Sciences, Sejong University, Seoul 143-747, Korea.Division of Integrative Bioscience and Biotechnology, College of Life Sciences, Sejong University, Seoul 143-747, Korea.Division of Integrative Bioscience and Biotechnology, College of Life Sciences, Sejong University, Seoul 143-747, Korea.Division of Integrative Bioscience and Biotechnology, College of Life Sciences, Sejong University, Seoul 143-747, Korea.Division of Integrative Bioscience and Biotechnology, College of Life Sciences, Sejong University, Seoul 143-747, Korea.Division of Integrative Bioscience and Biotechnology, College of Life Sciences, Sejong University, Seoul 143-747, Korea.Division of Integrative Bioscience and Biotechnology, College of Life Sciences, Sejong University, Seoul 143-747, Korea.Division of Integrative Bioscience and Biotechnology, College of Life Sciences, Sejong University, Seoul 143-747, Korea.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27126515

Citation

Singh, Raksha, et al. "Magnaporthe Oryzae Effector AVR-Pii Helps to Establish Compatibility By Inhibition of the Rice NADP-Malic Enzyme Resulting in Disruption of Oxidative Burst and Host Innate Immunity." Molecules and Cells, vol. 39, no. 5, 2016, pp. 426-38.
Singh R, Dangol S, Chen Y, et al. Magnaporthe oryzae Effector AVR-Pii Helps to Establish Compatibility by Inhibition of the Rice NADP-Malic Enzyme Resulting in Disruption of Oxidative Burst and Host Innate Immunity. Mol Cells. 2016;39(5):426-38.
Singh, R., Dangol, S., Chen, Y., Choi, J., Cho, Y. S., Lee, J. E., Choi, M. O., & Jwa, N. S. (2016). Magnaporthe oryzae Effector AVR-Pii Helps to Establish Compatibility by Inhibition of the Rice NADP-Malic Enzyme Resulting in Disruption of Oxidative Burst and Host Innate Immunity. Molecules and Cells, 39(5), 426-38. https://doi.org/10.14348/molcells.2016.0094
Singh R, et al. Magnaporthe Oryzae Effector AVR-Pii Helps to Establish Compatibility By Inhibition of the Rice NADP-Malic Enzyme Resulting in Disruption of Oxidative Burst and Host Innate Immunity. Mol Cells. 2016 May 31;39(5):426-38. PubMed PMID: 27126515.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Magnaporthe oryzae Effector AVR-Pii Helps to Establish Compatibility by Inhibition of the Rice NADP-Malic Enzyme Resulting in Disruption of Oxidative Burst and Host Innate Immunity. AU - Singh,Raksha, AU - Dangol,Sarmina, AU - Chen,Yafei, AU - Choi,Jihyun, AU - Cho,Yoon-Seong, AU - Lee,Jea-Eun, AU - Choi,Mi-Ok, AU - Jwa,Nam-Soo, Y1 - 2016/05/03/ PY - 2016/04/08/received PY - 2016/04/14/accepted PY - 2016/4/30/entrez PY - 2016/4/30/pubmed PY - 2017/3/9/medline KW - AVR-effectors KW - NADP-Malic enzyme KW - gene-for-gene interaction KW - reactive oxygen species KW - rice SP - 426 EP - 38 JF - Molecules and cells JO - Mol Cells VL - 39 IS - 5 N2 - Plant disease resistance occurs as a hypersensitive response (HR) at the site of attempted pathogen invasion. This specific event is initiated in response to recognition of pathogen-associated molecular pattern (PAMP) and subsequent PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI). Both PTI and ETI mechanisms are tightly connected with reactive oxygen species (ROS) production and disease resistance that involves distinct biphasic ROS production as one of its pivotal plant immune responses. This unique oxidative burst is strongly dependent on the resistant cultivars because a monophasic ROS burst is a hallmark of the susceptible cultivars. However, the cause of the differential ROS burst remains unknown. In the study here, we revealed the plausible underlying mechanism of the differential ROS burst through functional understanding of the Magnaporthe oryzae (M. oryzae) AVR effector, AVR-Pii. We performed yeast two-hybrid (Y2H) screening using AVR-Pii as bait and isolated rice NADP-malic enzyme2 (Os-NADP-ME2) as the rice target protein. To our surprise, deletion of the rice Os-NADP-ME2 gene in a resistant rice cultivar disrupted innate immunity against the rice blast fungus. Malic enzyme activity and inhibition studies demonstrated that AVR-Pii proteins specifically inhibit in vitro NADP-ME activity. Overall, we demonstrate that rice blast fungus, M. oryzae attenuates the host ROS burst via AVR-Pii-mediated inhibition of Os-NADP-ME2, which is indispensable in ROS metabolism for the innate immunity of rice. This characterization of the regulation of the host oxidative burst will help to elucidate how the products of AVR genes function associated with virulence of the pathogen. SN - 0219-1032 UR - https://www.unboundmedicine.com/medline/citation/27126515/Magnaporthe_oryzae_Effector_AVR_Pii_Helps_to_Establish_Compatibility_by_Inhibition_of_the_Rice_NADP_Malic_Enzyme_Resulting_in_Disruption_of_Oxidative_Burst_and_Host_Innate_Immunity_ L2 - https://dx.doi.org/10.14348/molcells.2016.0094 DB - PRIME DP - Unbound Medicine ER -