Saunders W, Lengyel V, Hoyt M A
Department of Biological Sciences, University of Pittsburgh, Pennsylvania 15260, USA.
Mol Biol Cell. 1997 Jun;8(6):1025-33. doi: 10.1091/mbc.8.6.1025.
Two Saccharomyces cerevisiae kinesin-related motors, Cin8p and Kip1p, perform an essential role in the separation of spindle poles during spindle assembly and a major role in spindle elongation. Cin8p and Kip1p are also required to prevent an inward spindle collapse prior to anaphase. A third kinesin-related motor, Kar3p, may act antagonistically to Cin8p and Kip1p since loss of Kar3p partially suppresses the spindle collapse in cin8 kip1 mutants. We have tested the relationship between Cin8p and Kar3p by overexpressing both motors using the inducible GAL1 promoter. Overexpression of KAR3 results in a shrinkage of spindle size and a temperature-dependent inhibition of the growth of wild-type cells. Excess Kar3p has a stronger inhibitory effect on the growth of cin8 kip1 mutants and can completely block anaphase spindle elongation in these cells. In contrast, overexpression of CIN8 leads to premature spindle elongation in all cells tested. This is the first direct demonstration of antagonistic motors acting on the intact spindle and suggests that spindle length is determined by the relative activity of Kar3p-like and Cin8p/Kip1p-like motors.
两种与酿酒酵母驱动蛋白相关的马达蛋白,Cin8p和Kip1p,在纺锤体组装过程中纺锤极的分离中发挥着重要作用,并且在纺锤体延长中起主要作用。在后期之前,Cin8p和Kip1p对于防止纺锤体向内塌陷也是必需的。第三种与驱动蛋白相关的马达蛋白Kar3p,可能与Cin8p和Kip1p起拮抗作用,因为Kar3p的缺失部分抑制了cin8 kip1突变体中的纺锤体塌陷。我们通过使用可诱导的GAL1启动子过表达这两种马达蛋白,来测试Cin8p和Kar3p之间的关系。KAR3的过表达导致纺锤体大小缩小以及对野生型细胞生长的温度依赖性抑制。过量的Kar3p对cin8 kip1突变体的生长具有更强的抑制作用,并且可以完全阻断这些细胞中后期纺锤体的延长。相反,CIN8的过表达导致所有测试细胞中纺锤体过早延长。这是首次直接证明拮抗马达蛋白作用于完整纺锤体,并表明纺锤体长度由Kar3p样和Cin8p/Kip1p样马达蛋白的相对活性决定。