bHLHの転写因子の変異により,アーモンドの化が可能になった
R Sánchez-Pérez1,2,3, S Pavan4,5, R Mazzeo2,3,6
1Department of Plant Breeding, CEBAS-CSIC, Campus Universitario de Espinardo, 30100 Espinardo, Spain. rsanchez@cebas.csic.es stefano.pavan@uniba.it.
まとめ
アーモンドの家畜化には 遺伝子の変異を特定することで 甘い核の選択が含まれていました このbHLH2転写因子の変異は,野生の杏仁に含まれる毒性化合物であるアミグダリンの生成を阻害します.
科学分野:
- 植物遺伝学
- 農業科学
- 生物化学
背景:
- 野生のアーモンドには 毒性のあるアミグダリンという シアノゲン系ジグルコシドが含まれています
- アーモンドの栽培は 毒性のない甘い核の選択によって 進められました
研究 の 目的:
- アーモンドの甘い核の特徴の 遺伝的根拠を特定するためです
- アミグダリン生物合成とその調節の基礎となる分子機構を理解する.
主な方法:
- ゲノムシーケンシングとアーモンド参照ゲノムの組み立て
- マップベースのクローニングで,F1集団をカーネル味のために分離する.
- 転写因子と関連する遺伝子の機能的特徴.
主要な成果:
- 5つの基本的なヘリックス・ループ・ヘリックス (bHLH) 転写因子 (bHLH1-bHLH5) を含む46キロ塩基基の遺伝子クラスターが特定されました.
- bHLH2転写因子はアミグダリン生物合成遺伝子 (PdCYP79D16とPdCYP71AN24) を調節する.
- bHLH2の特定の点変異は,これらの遺伝子の転写を妨げ,甘い核につながります.
結論:
- アーモンドの甘い核の特徴は,bHLH2転写因子の変異によって制御されます.
- このbHLH2の遺伝的変異は,アーモンドの養殖過程で,アミグダリン生成の喪失に起因する.
- この経路を理解することで作物の改善と 植物二次代謝物の進化の洞察が得られます
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