Vallen E A, Hiller M A, Scherson T Y, Rose M D
Department of Molecular Biology, Lewis Thomas Laboratory, Princeton University, New Jersey 08544-1014.
J Cell Biol. 1992 Jun;117(6):1277-87. doi: 10.1083/jcb.117.6.1277.
The yeast KAR1 gene is essential for mitotic growth and important for nuclear fusion. Mutations in KAR1 prevent duplication of the spindle pole body (SPB), and affect functions associated with both the nuclear and cytoplasmic microtubules. The localization of hybrid Kar1-lacZ proteins, described elsewhere (Vallen, E. A., T. Y. Scherson, T. Roberts, K. van Zee, and M. D. Rose. 1992. Cell. In press), suggest that the protein is associated with the SPB. In this paper, we report a deletion analysis demonstrating that the mitotic and karyogamy functions of KAR1 are separate and independent, residing in discrete functional domains. One region, here shown to be essential for mitosis, coincided with a part of the protein that is both necessary and sufficient to target Karl-lacZ hybrid proteins to the SPB (Vallen, E. A., T. Y. Scherson, T. Roberts, K. van Zee, and M. D. Rose. 1992. Cell. In press). Complementation testing demonstrated that deletions in this interval did not affect nuclear fusion. A second region, required only for karyogamy, was necessary for the localization of a Kar3-lacZ hybrid protein to the SPB. These data suggest a model for the roles of Kar1p and Kar3p, a kinesin-like protein, in nuclear fusion. Finally, a third region of KAR1 was found to be important for both mitosis and karyogamy. This domain included the hydrophobic carboxy terminus and is sufficient to target a lacZ-Kar1 hybrid protein to the nuclear envelope (Vallen E. A., T. Y. Scherson, T. Roberts, K. van Zee, and M. D. Rose. 1992. Cell. In press). Altogether, the essential mitotic regions of KAR1 comprised 20% of the coding sequence. We propose a model for Kar1p in which the protein is composed of several protein-binding domains tethered to the nuclear envelope via its hydrophobic tail.
酵母KAR1基因对于有丝分裂生长至关重要,且对核融合也很重要。KAR1基因的突变会阻止纺锤极体(SPB)的复制,并影响与核微管和细胞质微管相关的功能。其他地方已描述过的杂交Kar1-lacZ蛋白的定位(Vallen, E. A., T. Y. Scherson, T. Roberts, K. van Zee, and M. D. Rose. 1992. Cell. In press)表明该蛋白与SPB相关。在本文中,我们报告了一项缺失分析,结果表明KAR1的有丝分裂和核融合功能是分开且独立的,分别存在于不同的功能结构域中。一个区域,此处显示对有丝分裂至关重要,与将Karl-lacZ杂交蛋白靶向至SPB所必需且足够的蛋白质部分相重合(Vallen, E. A., T. Y. Scherson, T. Roberts, K. van Zee, and M. D. Rose. 1992. Cell. In press)。互补试验表明该区间的缺失不影响核融合。第二个区域,仅对核融合是必需的,是将Kar3-lacZ杂交蛋白定位到SPB所必需的。这些数据提示了一个关于Kar1p和Kar3p(一种类驱动蛋白)在核融合中作用的模型。最后,发现KAR1的第三个区域对有丝分裂和核融合均很重要。该结构域包括疏水的羧基末端,并且足以将lacZ-Kar1杂交蛋白靶向至核膜(Vallen E. A., T. Y. Scherson, T. Roberts, K. van Zee, and M. D. Rose. 1992. Cell. In press)。总之,KAR1的必需有丝分裂区域占编码序列的20%。我们提出了一个关于Kar1p的模型,其中该蛋白由几个通过其疏水尾部与核膜相连的蛋白质结合结构域组成。