Witke W, Schleicher M, Noegel A A
Max Planck Institute for Biochemistry, Martinsried, Federal Republic of Germany.
Cell. 1992 Jan 10;68(1):53-62. doi: 10.1016/0092-8674(92)90205-q.
We generated by gene disruption Dictyostelium cells that lacked both the F-actin cross-linking proteins, alpha-actinin and gelation factor. Several major cell functions, such as growth, chemotaxis, phagocytosis, and pinocytosis, were apparently unaltered. However, in all double mutants, development was greatly impaired. After formation of aggregates, cells were very rarely able to form fruiting bodies. This ability was rescued when mutant and wild-type strains were mixed in a ratio of 70 to 30. The developmental program in the mutant was not arrested, since the expression pattern of early and late genes remained unchanged. Development of the mutant was rendered normal when a functional alpha-actinin gene was introduced and expressed, showing the morphogenetic defect to be due to the absence of the two F-actin cross-linking proteins. These findings suggest the existence of a functional network allowing mutual complementation of certain actin-binding proteins.
我们通过基因破坏产生了缺乏F-肌动蛋白交联蛋白α-辅肌动蛋白和凝胶化因子的盘基网柄菌细胞。几种主要的细胞功能,如生长、趋化性、吞噬作用和胞饮作用,显然未发生改变。然而,在所有双突变体中,发育受到极大损害。聚集体形成后,细胞很少能够形成子实体。当突变体和野生型菌株以70比30的比例混合时,这种能力得以恢复。突变体中的发育程序并未停滞,因为早期和晚期基因的表达模式保持不变。当引入并表达功能性α-辅肌动蛋白基因时,突变体的发育恢复正常,表明形态发生缺陷是由于两种F-肌动蛋白交联蛋白的缺失所致。这些发现表明存在一个功能性网络,允许某些肌动蛋白结合蛋白相互互补。