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Cell biology of spatial regulation of formation of the cell wall

细胞壁形成空间调控的细胞生物学

基本信息

批准号：
03454015
负责人：
HOGETSU Taizo
金额：
$ 4.03万
依托单位：
The University of Tokyo
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1991
资助国家：
日本
起止时间：
1991 至 1993
项目状态：
已结题

项目摘要

1.Involvement of cortical microtubules in localized deposition of the cell wall was demonstrated in formation of bordered pit in Taxus. 2.A method to observe three dimensional structure of the wall was established. It was found in pea epicotyls by this method that cellulose microfibrils are interrupted immediately after entering into the pit areas. This indicates that the plasma membrane(PM) domains of secondary thickenings and pit areas activate and inactivate cellulose synthase, respectively. 3.Hemicellulose was distributed only in secondary thickenings. This indicates that depositions of cellulose and hemicellulose are controlled at least in part by the same mechanism. 4.Disruption of microtubules by amiprophos-methyl disordered deposition patterns of cellulose and hemicellulose in the same way as did the deposition pattern of the secondary thickening. This means that microtubules define the boundary between the thickening and the pit. 5.Based on the above results, I proposed the following hypothesis : Golgi vesicles carrying cellulose synthase and hemicelluloses fuse only with the PM of the secondary thickenings. Cellulose synthases carried to the PM synthesize cellulose microfibrils in the PM of the thickening but lose their activity when entering into the PM of the pit. Cortical microtubules define the boundary between the PM domains in the thickening and the pit. 6.Toward proving this hypothesis, separation and identification of PM proteins related to wall synthesis was tried using Closterium cells. Some differences in spot patterns of two dimensional PAGE were detected between PM proteins of cells synthesizing much and little cellulose.

1.皮层微管参与了细胞壁的局部沉积，在红豆杉具缘纹孔的形成中得到证实。2.建立了一种观察壁面三维结构的方法。用这种方法在豌豆上胚轴中发现，纤维素微纤丝在进入纹孔区后立即中断。这表明，质膜（PM）领域的次生加厚和纹孔区激活和抑制纤维素合成酶，分别。3.半纤维素仅分布在次生加厚中。这表明纤维素和半纤维素的沉积至少部分地由相同的机制控制。4.破坏微管amiprostin-甲基无序沉积模式的纤维素和半纤维素以同样的方式没有沉积模式的次生增厚。这意味着微管定义了增厚和凹陷之间的边界。5.基于以上结果，笔者提出以下假设：携带纤维素合成酶和半纤维素的高尔基体囊泡只与次生加厚的PM融合。纤维素酶被携带到颗粒膜中，在增厚的颗粒膜中合成纤维素微纤丝，但当进入纹孔的颗粒膜中时失去活性。皮层微管定义的PM域之间的边界增厚和坑。6.为了证明这一假设，分离和鉴定PM蛋白质相关的壁合成尝试使用新月藻细胞。纤维素合成多、少的细胞PM蛋白的双向电泳图谱存在一定差异。