該研究不僅為設計抗逆不減產作物提供了分子靶標（如編輯CPK3或SNC1磷酸化位點），還可能通過模擬TIR磷酸化機制，開發靶向SARM1的神經保護藥物，為阿爾茨海默病等疾病提供干預策略。

干旱、鹽脅迫以及低溫等非生物逆境導致植物受到滲透脅迫，嚴重威脅糧食安全。植物在脅迫響應中可能存在“有害應答”，即免疫信號過度激活（如NLR蛋白通過未知途徑被誘導），不僅拮抗ABA介導的脅迫耐受通路，還會導致生長停滯，嚴重威脅非生物逆境下的植物生存。如何限制免疫信號超激活的“有害應答”，是滲透脅迫下植物生長維持的關鍵。

中國科學院分子植物科學卓越創新中心趙楊研究組揭示了一種動植物保守的免疫剎車機制：通過磷酸化TIR結構域抑制其NAD+水解酶（NADase）活性，從而精準調控免疫信號強度，使植物在脅迫下兼顧防御與生長。

研究組過往研究鑒定到滲透早期信號元件BON1，發現其通過調控Ca2+信號協調滲透應答，并負調控NLR蛋白介導的免疫信號。滲透脅迫下，bon1突變體的免疫信號過度激活，從而嚴重抑制其生長。通過抑制子篩選，研究團隊發現SNC1（編碼一種含TIR結構域的NLR蛋白）的多個顯性失活突變可完全恢復bon1突變體的生長，證實SNC1是植物維持滲透脅迫下生長的核心因子。TIR結構域通過切割NAD+啟動防御反應，但過度激活會導致細胞死亡和生長停滯。因此，動態調節TIR信號的“開”與“關”，是植物實現“防御生長兩不誤”的關鍵。

近期研究發現，CPK3/4/6/11/27蛋白激酶響應滲透脅迫激發的Ca2+信號正調控脅迫應答。鑒于BON1調控滲透脅迫下Ca2+信號，團隊提出假說：BON1下游的CPK3/4/6/11/27激酶可能直接調控SNC1活性。通過遺傳與生化分析，最終鎖定CPK3為核心效應激酶。組成性激活形式的CPK3CPK3CA不僅能恢復滲透脅迫下bon1突變體的生長，還能抑制SNC1過表達導致的生長遲緩，而激酶失活突變的CPK3K107MΔK107則完全失效。機制解析表明，CPK3通過磷酸化TIR結構域的Ser26位點，抑制其NADase活性，從而阻斷免疫信號過度激活，猶如為防御反應安裝“剎車”，巧妙控制防御強度，保障植物生長。

值得注意的是，這一機制在動物中同樣保守，人類CAMK2D和TBK1激酶可磷酸化SARM1（包含TIR結構域蛋白）的對應位點（Ser567），抑制其NADase活性并阻斷細胞死亡。這一平行機制證實TIR磷酸化是跨物種保守的免疫-生長調控開關。

該研究不僅為設計抗逆不減產作物提供了分子靶標（如編輯CPK3或SNC1磷酸化位點），還可能通過模擬TIR磷酸化機制，開發靶向SARM1的神經保護藥物，為阿爾茨海默病等疾病提供干預策略。

相關研究成果以TIR immune signalling is blocked by phosphorylation to maintain plant growth為題，發表在《自然-植物》（Nature?Plants）上。研究工作得到中國科學院基礎與交叉前沿科研先導專項、中國科學院穩定支持基礎研究領域青年團隊計劃、上海市科學技術委員會等的支持。

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磷酸化修飾抑制TIR活性的保守分子機制