Cell fusion in yeast is the process by which two haploid cells fuse to
form a diploid zygote. To dissect the pathway of cell fusion, we phen
otypically and genetically characterized four cell fusion mutants, fus
6/spa2, fus7/rvs161, fus1, and fus2. First, we examined the complete a
rray of single and double mutants. In all cases but one, double mutant
s exhibited stronger cell fusion defects than single mutants. The exce
ption was rvs161 Delta fus2 Delta, suggesting that Rvs161p and Fus2p a
ct in concert. Dosage suppression analysis showed that Fus1p and Fus2p
act downstream or parallel to Rvs161p and Spa2p. Second, electron mic
roscopic analysis was used to define the mutant defects in cell fusion
. In wild-type prezygotes vesicles were aligned and clustered across t
he cell fusion zone. The vesicles were associated with regions of cell
wall thinning. Analysis of Fus(-) zygotes indicated that Fus1p was re
quired for the normal localization of the vesicles to the zone of cell
fusion, and Spa2p facilitated their clustering. In contrast, Fus2p an
d Rvs161p appeared to act after vesicle positioning. These findings le
ad us to propose that cell fusion is mediated in part by the localized
release of vesicles containing components essential for cell fusion.