Cytophaga-flavobacterium gliding motility
Cytophaga-flavobacterium gliding motility
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DOI：
10.1159/000077870
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发表时间：
2004-01-01
影响因子：
1.2
通讯作者：
McBride, MJ
中科院分区：
文献类型：
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作者：
McBride, MJ
约翰逊黄杆菌与噬细胞-黄杆菌-拟杆菌群的许多其他成员一样，显示出快速的滑动运动。F.约翰逊氏菌以高达10 μ m/s的速率在表面上滑动。将胶乳球加入F.约翰逊氏菌与细胞结合，并沿细胞快速沿着推进，这表明在滑动过程中粘附分子沿细胞表面横向沿着移动。遗传分析已经确定了一些滑翔所需的g/d基因。三种Gld蛋白被认为是ATP结合盒转运蛋白的组分。其他五种Gld蛋白是定位于细胞质膜或外膜的脂蛋白。gld基因的破坏不仅导致运动性的丧失，而且导致对感染野生型细胞的噬菌体的抗性，以及消化不溶性多糖几丁质的能力的丧失。两个模型试图结合现有数据来解释F. johnsoniae滑动。版权所有（C）2004 S. Karger AG，巴塞尔。
Flavobacterium johnsoniae, like many other members of the Cytophaga-Flavobacterium-Bacteroides group, displays rapid gliding motility. Cells of F. johnsoniae glide over surfaces at rates of up to 10 mum/s. Latex spheres added to F. johnsoniae bind to and are rapidly propelled along cells, suggesting that adhesive molecules move laterally along the cell surface during gliding. Genetic analyses have identified a number of g/d genes that are required for gliding. Three Gld proteins are thought to be components of an ATP-binding-cassette transporter. Five other Gld proteins are lipoproteins that localize to the cytoplasmic membrane or outer membrane. Disruption of gld genes results not only in loss of motility, but also in resistance to bacteriophages that infect wild-type cells, and loss of the ability to digest the insoluble polysaccharide chitin. Two models that attempt to incorporate the available data to explain the mechanism of F. johnsoniae gliding are presented. Copyright (C) 2004 S. Karger AG, Basel.