Elucidation of information transmission networks formed by plant immunity and various environmental factors

2020 Fiscal Year Final Research Report

• Project/Area Number: 19K16165
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 44030:Plant molecular biology and physiology-related
• Research Institution: Nagoya University
• Principal Investigator: Mika Nomoto 名古屋大学, 遺伝子実験施設, 助教 (70825736)
• Project Period (FY): 2019-04-01 – 2021-03-31
• Keywords: 植物ホルモン / 転写因子 / 植物免疫

Outline of Final Research Achievements

We demonstrate that SA-induced NPR1 is recruited to JA-responsive promoter regions that are co-occupied by a JA-induced transcription complex consisting of MYC2 activator and MED25 mediator subunit. In presence of SA, NPR1 replaces JA-regulated JAZ repressors by directly interacting with MYC2 and inhibiting its transcriptional activity. We find that NPR1-mediated suppression of MYC2 is a major immune mechanism for curtailing virulence of pathogens that attempt to hijack JA signaling for their own benefit, underscoring NPR1-mediated antagonism as a driver of versatile immune responses.

Free Research Field

植物分子・生理科学

Academic Significance and Societal Importance of the Research Achievements

本研究のアプローチは、SAやJA以外のホルモンシグナル、さらには転写因子を標的とする光受容体のファイトクロムや、多様なリン酸化酵素などにも適用可能である。例えば、ジベレリンやオーキシンなどの植物ホルモンシグナルは、他の環境応答や内生の情報伝達機構に影響を与えると考えられるが、その転写制御ネットワークは不明な点が多い。本研究成果に基づき、ジベレリンやオーキシンシグナルの転写補助因子を用いた相互作用解析を行い、それらの標的転写因子群を網羅的に同定することが可能になると考えられる。