Rvs161p interacts with Fus2p to promote cell fusion in Saccharomyces cerevisiae.
Rvs161p interacts with Fus2p to promote cell fusion in Saccharomyces cerevisiae.
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DOI：
10.1083/jcb.141.3.567
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发表时间：
1998-05-04
期刊：
影响因子：
--
通讯作者：
Rose MD
中科院分区：
文献类型：
--
作者：
Brizzio V;Gammie AE;Rose MD
FUS 7先前通过在筛选双侧交配缺陷中导致细胞融合缺陷的突变来鉴定。在这里，我们表明，FUS 7是等位基因RVS 161/END 6，一个基因牵连在各种过程中，包括生存能力饥饿后，内吞作用，肌动蛋白细胞骨架组织。两条证据表明，RVS 161/END 6的内吞功能不是细胞融合所必需的。首先，其他几种内吞突变体没有表现出细胞融合缺陷。第二，我们分离了RVS 161/FUS 7的5个功能特异性等位基因，它们内吞作用有缺陷，但不交配，还有3个等位基因细胞融合有缺陷，但不内吞作用。肌动蛋白细胞骨架的组织在细胞融合突变体中是正常的，这表明Rvs 161 p在细胞融合中的功能不依赖于肌动蛋白组织。Rvs 161 p-GFP在细胞融合区的定位表明Rvs 161 p在细胞融合中起直接作用。双突变体的表型、Rvs 161 p和Fus 2 p的共沉淀以及Fus 2 p的稳定性强烈依赖于Rvs 161 p的交配功能的事实导致了Rvs 161 p需要与Fus 2 p相互作用以进行有效的细胞融合的结论。
FUS7 was previously identified by a mutation that causes a defect in cell fusion in a screen for bilateral mating defects. Here we show that FUS7 is allelic to RVS161/END6, a gene implicated in a variety of processes including viability after starvation, endocytosis, and actin cytoskeletal organization. Two lines of evidence indicate that RVS161/END6's endocytic function is not required for cell fusion. First, several other endocytic mutants showed no cell fusion defects. Second, we isolated five function-specific alleles of RVS161/FUS7 that were defective for endocytosis, but not mating, and three alleles that were defective for cell fusion but not endocytosis. The organization of the actin cytoskeleton was normal in the cell fusion mutants, indicating that Rvs161p's function in cell fusion is independent of actin organization. The three to fourfold induction of RVS161 by mating pheromone and the localization of Rvs161p-GFP to the cell fusion zone suggested that Rvs161p plays a direct role in cell fusion. The phenotypes of double mutants, the coprecipitation of Rvs161p and Fus2p, and the fact that the stability of Fus2p was strongly dependent on Rvs161p's mating function lead to the conclusion that Rvs161p is required to interact with Fus2p for efficient cell fusion.
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影响因子：
64.5
作者：
ELION, EA;GRISAFI, PL;FINK, GR
通讯作者：
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7.8
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