Haploid Saccharomyces cerevisiae cells find each other during conjugat
ion by orienting their growth toward each other along pheromone gradie
nts (chemotropism). However, when their receptors are saturated for ph
eromone binding, yeast cells must select a mate by executing a default
pathway in which they choose a mating partner at random. We previousl
y demonstrated that this default pathway requires the SPAE gene. In th
is report we show that the default mating pathway also requires the AX
L1, FUS1, FUS2, FUS3, PEA2, RVS161, and BNI1 genes. These genes, inclu
ding SPA2, are also important for efficient cell fusion during chemotr
opic mating. Cells containing null mutations in these genes display de
fects in cell fusion that subtly affect mating efficiency. In addition
, we found that the defect in default mating caused by mutations in SP
AE is partially suppressed by multiple copies of two genes, FUS2 and M
FA2. These findings uncover a molecular relationship between default m
ating and cell fusion. Moreover, because axil mutants secrete reduced
levels of a-factor and are defective at both cell fusion and default m
ating, these results reveal an important role for a-factor in cell fus
ion and default mating. We suggest that default mating places a more s
tringent requirement on some aspects of cell fusion than does chemotro
pic mating.