| Co-Investigator(Kenkyū-buntansha) |
PARK Pyon Yuri Kobe Univ., Grad.school of Natural Science, Prof., 自然科学研究科, 教授 (20147094)
ICHINOSE Yuuki Okayama Univ., Fac. of Agriculture, Prof., 農学部, 教授 (50213004)
AKIMITSU Kazuya Kagawa Univ., Fac. of Agriculture, Prof., 農学部, 助教授 (80263888)
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| Research Abstract |
1. Molecular dissection of plant apoptosis using an oat cell free system
The host specific toxin, victorin induces apoptotic cell death in sensitive oat cultivars. We have developed an oat cell-free apoptosis system to investigate the execution mechanisms of plant apoptosis. Cell extracts derived from oat tissues undergoing victorin-induced apoptosis caused nuclear collapse and internucleosomal DNA fragmentation in isolated nuclei Pharmacological studies revealed that cysteine pretense, which is E-64-sensitive but insensitive to caspase-specific inhibitors, is a crucial component in the morphological change of isolated nuclei, and that nuclease and the cysteine protease act cooperatively to induce the apoptotic DNA laddering. Interestingly, this finding is contrasted with those in well-studied animal cell-free systems in which an apoptotic endonuclease is solely responsible for the DNA fragmentation.
2. Molecular mechanisms of induction and suppression of plant hypersensitive response tr
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iggered by proteinaccous elicitors INF] elicitin from Phytophthora infestans, harpin and flagellin from Pseudomonas syringae induce hypersensitive cell death. Pharmacological investigation of the signal transduction pathway leading to hypersensitive response (HR) revealed that HR requires de novo protein synthesis and protein phosphorylation. Flagellin is a newly identified HR elicitor, and its HR activity is regulated by post-translational glicosyl-modification. We also identified novel defense response-related plant genes, and characterized their structure, expression and function. One of the interesting plant genes, OPR is found to be induced specifically in compatible interactions. OPR may be involved in the suppression of plant defense response.
3. The mode of action of the host specific toxin, ACR toxin
Specificity in the interaction between rough lemon and the fungal pathogen Alternaria alternate rough lemon pathotype is determined by a host-selective toxin, ACR-toxin. The target site of ACR-toxin is mitochondrion, and mitochondrial DNA sequence, designated ACRS (ACR-toxin Sensitivity gene), is responsible for the toxin sensitivity. We identified that sensitivity/or insensitivity to ACR-toxin and hence specificity of the interaction between the A.alternata rough lemon pathotype and host plants is due to differential post-transcriptional processing of ACRS. Less
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