Pathogenicity of viroid - circular RNA pathogen; Analysis of destructive effects of viroid infection on a host miRNA/gene expression network

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H04455
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Plant protection science
• Research Institution: Hirosaki University
• Principal Investigator: SANO Teruo 弘前大学, 農学生命科学部, 教授 (30142699)
• Co-Investigator(Kenkyū-buntansha): 種田 晃人 弘前大学, 理工学研究科, 准教授 (70332492) ; 葛西 厚史 弘前大学, 農学生命科学部, 研究員 (80633982)
• Research Collaborator: Jaroslav Matoušek Institute of Plant Molecular Biology, Biology Centre ASCR v.v.i ; Adkar Purushothama CR Université de Sherbrooke, RNA Group/Groupe ARN
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: ウイロイド / RNAサイレンシング / DCL2 / DCL4 / miR398a-3p / SOD1 / CCS1

Outline of Final Research Achievements

We analyzed adverse effects of viroid infection upon the network of host gene expression and found that accumulation of a viroid-specific small RNA derived from the position 39-59 of PSTVd genome caused down-regulation of callose synthase gene (CalS11-like) expression through RNA silencing pathway. We also developed novel viroid-resistant tobacco plants expressing viroid-specific small RNAs and identified a key nucleotide which attenuates PSTVd pathogenicity.
RNAi-mediated down-regulation of DCL2 and DCL4 made tomato plants susceptible to viroid infection. The plants infected with PSTVd produced severe systemic necrosis and died 3 to 4 months after infection, in which the expression level of CCS1, SOD1, and miR398 was abnormally elevated.
Although plants generate reactive oxygen species by fundamental innate immunity to counteract viroid infection, it became clear that abnormality in RNA silencing mechanism disturbs the defense mechanism and intensifies disease symptoms.

Free Research Field

植物病理学