• Proceedings of the Korean Society of Plant Pathology Conference
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• 2004.10a
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• pp.68-69
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• 2004

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• Proceedings of the Korean Society of Plant Pathology Conference
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• 2005.04a
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• pp.5-6
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• 2005

• The Plant Pathology Journal
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• v.39 no.5
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• pp.449-465
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• 2023

Plants are challenged by various pathogens throughout their lives, such as bacteria, viruses, fungi, and insects; consequently, they have evolved several defense mechanisms. In addition, plants have developed localized and systematic immune responses due to biotic and abiotic stress exposure. Animals are known to activate DNA damage responses (DDRs) and DNA damage sensor immune signals in response to stress, and the process is well studied in animal systems. However, the links between stress perception and immune response through DDRs remain largely unknown in plants. To determine whether DDRs induce plant resistance to pathogens, Arabidopsis plants were treated with bleomycin, a DNA damage-inducing agent, and the replication levels of viral pathogens and growth of bacterial pathogens were determined. We observed that DDR-mediated resistance was specifically activated against viral pathogens, including turnip crinkle virus (TCV). DDR increased the expression level of pathogenesis-related (PR) genes and the total salicylic acid (SA) content and promoted mitogen-activated protein kinase signaling cascades, including the WRKY signaling pathway in Arabidopsis. Transcriptome analysis further revealed that defense-and SA-related genes were upregulated by DDR. The atm-2atr-2 double mutants were susceptible to TCV, indicating that the main DDR signaling pathway sensors play an important role in plant immune responses. In conclusion, DDRs activated basal immune responses to viral pathogens.

• The Plant Pathology Journal
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• v.19 no.1
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• pp.19-23
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• 2003

Turnip crinkle vims (TCV) inoculation onto resistant Arabidopsis ecotype Dijon（Di-17) leads to a hypersensitive response (HR) on the inoculated leaves. A dominant gene, HRT, which confers an HR to TCV, has been cloned from Di-17 plants by map-based cloning. HRT is a LZ-NBS-LRR class resistance gene and it belongs to a small gene family that includes RPP8, which confers resistance to Peronospora parasitica Emco5. Outside of the LRR region, HRT and RPP8 proteins share 98% amino acid identity while their LRR regions are less conserved (87% identity). HRT-transformed Arabidopsis plants developed an HR but generally remained susceptible to TCV due to a dominant RRT allele, which is not compatible with resistance. However, several transgenic plants that over-expressed HRT much higher than Di-l7 showed micro-HR or no HR when inoculated with TCV and were resistant to infection. Both the HR and resistance are dependent on salicylic acid but independent of NPRI, ethylene, or jasmonic acid. Arabidopsis plants containing both TCV coat protein gene and HRT developed massive necrosis and death in seedlings, indicating that the TCV coat protein is an avirulence factor detected by the HRT.

• Proceedings of the Korean Society of Plant Pathology Conference
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• 2003.10a
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• pp.76.1-76
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• 2003

The coat protein (CP) of Turnip crinkle virus (TCV) is organized into 3 distinct domains, R domain (RNA-binding) connected by an arm, 5 domain and P domain. We have previously shown that the CP of TCV strongly suppresses RNA silencing, and have mapped N-terminal R domain of which is also the elicitor of resistance response in the Arabidopsis ecotype Di-17 carrying the HRT resistance gene. In order to map the region in the TCV CP that is responsible for silencing suppression, a series of CP mutants were constructed, transformed into Agrobacterium, coinfiltrated either with HC-Pro (the helper component proteinase of tobacco etch potyvirus) known as a suppressor of PTGS or GFP constructs into leaves of Nicotiana benthmiana expressing GFP transgenically. In the presence of HC-Pro, all CP mutants were well protected, accumulating mutant CP mRNAs and their proteins even 5 days post-infiltration (DPI). In the presence of GFP, some mutant constructs which showed the accumulation of CP mutants and GFP mRNAs at early stage but eventually degraded at 5 DPI. Only a mutant which carrying 4 amino acid deletion of R domain was tolerable to maintain suppressing activity, suggesting that the suppressing activity is not directly related with the eliciting activity. A transient assay also revealed that the mutants synthesized their proteins, suggesting that a full length of CP sequences and its intact structure are required to stabilize CP, which suppresses the RNA silencing.