Lechler T, Li R
Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA.
J Cell Biol. 1997 Jul 14;138(1):95-103. doi: 10.1083/jcb.138.1.95.
We have developed a biochemical approach for identifying the components of cortical actin assembly sites in polarized yeast cells, based on a permeabilized cell assay that we established for actin assembly in vitro. Previous analysis indicated that an activity associated with the cell cortex promotes actin polymerization in the bud. After inactivation by a chemical treatment, this activity can be reconstituted back to the permeabilized cells from a cytoplasmic extract. Fractionation of the extract revealed that the reconstitution depends on two sequentially acting protein factors. Bee1, a cortical actin cytoskeletal protein with sequence homology to Wiskott-Aldrich syndrome protein, is required for the first step of the reconstitution. This finding, together with the severe defects in actin organization associated with the bee1 null mutation, indicates that Bee1 protein plays a direct role in controlling actin polymerization at the cell cortex. The factor that acts in the second step of the reconstitution has been identified by conventional chromatography. It is composed of a novel protein, Pca1. Sequence analysis suggests that Pca1 has the potential to interact with SH3 domain-containing proteins and phospholipids.
我们基于为体外肌动蛋白组装建立的透化细胞检测方法,开发了一种用于鉴定极化酵母细胞中皮质肌动蛋白组装位点成分的生化方法。先前的分析表明,与细胞皮质相关的一种活性促进了芽中肌动蛋白的聚合。经化学处理失活后,这种活性可以从细胞质提取物中重新恢复到透化细胞中。对提取物进行分级分离显示,这种恢复依赖于两个依次起作用的蛋白质因子。Bee1是一种皮质肌动蛋白细胞骨架蛋白,与威斯科特-奥尔德里奇综合征蛋白具有序列同源性,是恢复过程第一步所必需的。这一发现,连同与bee1基因缺失突变相关的肌动蛋白组织严重缺陷,表明Bee1蛋白在控制细胞皮质处的肌动蛋白聚合中起直接作用。在恢复过程第二步起作用的因子已通过传统色谱法鉴定出来。它由一种新蛋白质Pca1组成。序列分析表明,Pca1有可能与含SH3结构域的蛋白质和磷脂相互作用。