Project/Area Number |
11660048
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
植物保護
|
Research Institution | Kagawa University |
Principal Investigator |
AKIMITSU Kazuya Kagawa University, Agriculture, Associate Professor, 農学部, 助教授 (80263888)
|
Project Period (FY) |
1999 – 2000
|
Project Status |
Completed (Fiscal Year 2000)
|
Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2000: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1999: ¥2,000,000 (Direct Cost: ¥2,000,000)
|
Keywords | ACR-toxin / Alternaria / Brown spot disease / Citrus / Host-specific toxin / tRNA-Ala / mitochondria / receptor |
Research Abstract |
Rough lemon is sensitive to host-selective toxin ACR-toxin and susceptible to its producer Alternaria alternata rough lemon pathotype. The target site of ACR-toxin is rough lemon mitochondrion, and the toxin has no effect on mitochondria from resistant plants. We have cloned a receptor gene, ACRS gene, which confers the toxin sensitivity by expressing in Escherichia coli cells. Coding region of the gene is located in the group II intron of tRNA-Ala in mitochondrial genome, and translates the pore-forming oligometric receptor to ACR-toxin. ACRS gene locates at mitochondrial genomes from both toxin-sensitive and insensitive citrus. However, the transcripts suffer a processing to be dysfunctional in toxin-insensitive citrus, while those in toxin-sensitive rough lemon remain intact without the processing. To determine whether ACRS is translated in mitochondria, proteins from isolated mitochondria of toxin-sensitive rough lemon and insensitive citrus were analyzed by western blot with anti-ACRS antibodies. The antibodies detected peptides on blot from only rough lemon mitochondria, while no peptides detected by the antibodies from any resistant citrus mitochondria tested. These results demonstrated that the post-transcriptional modification of this mitochondrial ACRS gene regulates specificity in the toxin-plant interactions, in which RNA processing in mitochondria plays a key role in controlling sensitivity to ACR-toxin in citrus.
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