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Vol. 9, Issue 6, 1395-1410, June 1998
Princeton University, Princeton, New Jersey 08544-1014
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
phenotypically and genetically characterized four cell fusion mutants,
fus6/spa2, fus7/rvs161, fus1, and fus2.
First, we examined the complete array of single and double mutants. In all cases but one, double mutants exhibited stronger cell fusion defects than single mutants. The exception was rvs161
fus2, suggesting that Rvs161p and Fus2p act in
concert. Dosage suppression analysis showed that Fus1p and Fus2p act
downstream or parallel to Rvs161p and Spa2p. Second, electron
microscopic analysis was used to define the mutant defects in cell
fusion. In wild-type prezygotes vesicles were aligned and clustered
across the cell fusion zone. The vesicles were associated with regions
of cell wall thinning. Analysis of Fus
zygotes indicated
that Fus1p was required for the normal localization of the vesicles to
the zone of cell fusion, and Spa2p facilitated their clustering. In
contrast, Fus2p and Rvs161p appeared to act after vesicle positioning.
These findings lead us to propose that cell fusion is mediated in part
by the localized release of vesicles containing components essential
for cell fusion.
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