近日，北京大學生命科學學院蛋白質與植物基因研究國家重點實驗室的瞿禮嘉教授實驗室最新在線發表在《植物細胞》（Plant Cell）上的研究成果介紹植物肌醇原初功能的研究新進展。這項研究得到了化學學院趙美萍教授研究組的大力支持，是生命科學學院與化學學院科研合作的又一重要成果。
長期以來人們都知道，肌醇在動物細胞中是一種重要的調節性小分子，參與許多生理生化過程，包括信號傳導和生物膜的合成等。植物細胞中也有肌醇分子，之前的研究發現，植物細胞中的肌醇分子參與了更加多樣的過程，包括形成植酸等儲存物質、調節植物細胞抗逆、促進種子脫水、修飾生長素、參與細胞壁組成等；但是，在這些眾多的生物學過程中，肌醇分子最原初的功能到底是什麼，一直是植物學界的一個未解之謎。
模式植物擬南芥基因組中有三個肌醇磷酸合酶（MIPS）編碼基因，肌醇磷酸合酶控制的是肌醇合成的限速步驟；他們的實驗首先證明這三個MIPS基因都是有功能的基因，它們都可以互補酵母相應基因的缺失突變體ino1。隨後他們發現這三個基因在擬南芥胚胎發育過程中表現出各不相同的動態表達模式。進一步的遺傳多突變體構建實驗表明，mips1 mips2雙突變體以及mips1 mips2 mips3三突變體是胚胎致死的，mips1 mips3 以及mips1 mips2+/- 雙突變體表現出異常的胚胎發育。瞿教授實驗室的研究還發現，這些多突變體胚胎中生長素的分布模式以及生長素運輸蛋白PIN1的亞細胞定位都不正常；而mips1 mips3雙突變體的膜運輸也出現了異常。值得注意的是，如果在雙突變體中過量表達磷脂醯肌醇合酶2基因，將有限的肌醇轉化為膜系統所必需的磷脂醯肌醇，就可以在很大程度上減輕突變體的子葉和內膜系統缺陷。這些研究證明，植物細胞中肌醇的原初功能是作為底物合成磷脂醯肌醇以及磷脂醯肌醇磷酸，維持內膜系統的結構完整和運輸功能；而內膜系統的結構完整和運輸功能又直接影響生長素調控的植物胚胎發育過程。（生物谷Bioon.com）
生物谷推薦原文出處：
The Plant Cell doi: 10.1105/tpc.111.083337
d-myo-Inositol-3-Phosphate Affects Phosphatidylinositol-Mediated Endomembrane Function in Arabidopsis and Is Essential for Auxin-Regulated Embryogenesis[W][OA]
Yu Luoa, Genji Qina, Jun Zhanga, Yuan Liangb, Yingqi Songa, Meiping Zhaob, Tomohiko Tsugec, Takashi Aoyamac, Jingjing Liua, Hongya Gua,d and Li-Jia Qua,d,1
In animal cells, myo-inositol is an important regulatory molecule in several physiological and biochemical processes, including signal transduction and membrane biogenesis. However, the fundamental biological functions of myo-inositol are still far from clear in plants. Here, we report the genetic characterization of three Arabidopsis thaliana genes encoding d-myo-inositol-3-phosphate synthase (MIPS), which catalyzes the rate-limiting step in de novo synthesis of myo-inositol. Each of the three MIPS genes rescued the yeast ino1 mutant, which is defective in yeast MIPS gene INO1, and they had different dynamic expression patterns during Arabidopsis embryo development. Although single mips mutants showed no obvious phenotypes, the mips1 mips2 double mutant and the mips1 mips2 mips3 triple mutant were embryo lethal, whereas the mips1 mips3 and mips1 mips2+/? double mutants had abnormal embryos. The mips phenotypes resembled those of auxin mutants. Indeed, the double and triple mips mutants displayed abnormal expression patterns of DR5:green fluorescent protein, an auxin-responsive fusion protein, and they had altered PIN1 subcellular localization. Also, membrane trafficking was affected in mips1 mips3. Interestingly, overexpression of PHOSPHATIDYLINOSITOL SYNTHASE2, which converts myo-inositol to membrane phosphatidylinositol (PtdIns), largely rescued the cotyledon and endomembrane defects in mips1 mips3. We conclude that myo-inositol serves as the main substrate for synthesizing PtdIns and phosphatidylinositides, which are essential for endomembrane structure and trafficking and thus for auxin-regulated embryogenesis.