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J. Cell Biol.,
Volume 141, Number 3, May 4, 1998 567-584
Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544-1014
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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