野生リンゴが腐爛病に抵抗する分子メカニズムを解明(Study Reveals Resistance Mechanism of Wild Apple Against Valsa Canker)

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2026-08-25 中国科学院(CAS)

中国科学院新疆生态与地理研究所の研究チームは、野生リンゴ(Malus sieversii)がリンゴ胴枯病(Valsa canker)に抵抗する分子機構を解明した。病原菌Valsa maliに感染した野生リンゴを解析し、長鎖非コードRNA(lncRNA)「MsLNC1」が病害抵抗性に重要な役割を果たすことを特定した。転写因子MsWRKY65はMsLNC1のプロモーターに結合して発現を促進し、MsLNC1はさらにMsTRX5のプロモーター領域に結合してRNAポリメラーゼIIを呼び込み、その発現を活性化する。MsTRX5は細胞内の酸化還元状態を調節し、一酸化窒素(NO)の早期バーストを誘導するとともに過剰な過酸化水素(H₂O₂)を抑制し、防御反応を強化する。このMsWRKY65–MsLNC1–MsTRX5カスケードは、果樹の免疫におけるlncRNAの機能を示すとともに、耐病性リンゴ育種や遺伝子編集の標的としての応用が期待される。

野生リンゴが腐爛病に抵抗する分子メカニズムを解明(Study Reveals Resistance Mechanism of Wild Apple Against Valsa Canker)
The proposed mode of action of MsWRKY65-MsLNC1-MsTRX5 module. (Image by XIEG)

<関連情報>

新規MsWRKY65– MsLNC1 –MsTRX5モジュールは、野生リンゴ(Malus sieversii) にバルサ病抵抗性を付与する Novel MsWRKY65–MsLNC1–MsTRX5 module confers Valsa canker resistance in wild apple (Malus sieversii)

Xiaojie Liu,Mingqi Zhao,Huawei Liu Jianglin Zhu,Tohir A Bozorov,Xuejing Wen,Yakupjan Haxim,Lili Huang,Zongrang Liu,Daoyuan Zhang
Horticulture Research  Published:22 July 2026
DOI:https://doi.org/10.1093/hr/uhag299

Abstract

Valsa mali is a devastating fungal pathogen that causes systemic necrosis and trunk dieback in apple trees, a disease widely known as ‘apple canker’. While this pathogen poses a serious threat to woody plants, the molecular basis of host resistance remains poorly understood. Here, we investigated whether long non-coding RNAs (lncRNAs) contribute to defence against V. mali in Malus sieversii. Through systematic screening, we identified a key pathogen-responsive MsLNC1, 388-nt sense lncRNA. Ectopic overexpression of MsLNC1 enhanced resistance, whereas its knockdown compromised resistance in apple plantlets. MsLNC1 is downstream of MsWRKY65, which exerts its regulatory effect by binding to the W-box motif within its promotor. MsWRKY65 acts as a positive regulator in mediating the resistance of M. sieversii to V. mali. Additionally, thioredoxin H5 (MsTRX5), the neighboring gene of MsLNC1, exhibits a significant resistance function against V. mali. Genetic and molecular evidence demonstrates that MsLNC1, which binds to two 20-bp homologous regions with the MsTRX5 promoter, and physically interacts with RNA Polymerase II (Pol II) components, enhances MsTRX5 transcription. Collectively, our results demonstrate that MsLNC1 functions upstream of MsTRX5 and, together with MsWRKY65, forms a previously uncharacterized regulatory module that controls V. mali resistance in wild apple.

細胞遺伝子工学
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