Ty1 retrotransposition is
regulated at a posttranslational step by Fus3, a member of the mitogen-activated protein (MAP) kinase family [Conte et al. (1998) MCB, in
press ]. In fus3delta mutants, the rate of Ty1 transposition
is elevated 18- to 56-fold. We showed that this is likely due to
increased levels of Ty1 cDNA and of processed forms of Ty1 proteins that
are associated with virus-like particles. Recently, Madhani et al. [Cell
91:673 (1997)] demonstrated that a kinase-independent function of Fus3
negatively regulates the expression of invasive growth genes. Fus3 does
this by blocking activation of the invasive growth MAP kinase Kss1 by
the mating pathway. The following results suggest that Fus3 represses
Ty1 transposition via the same pathway. First, the hypertransposition
defect of fus3delta mutants requires a functional mating pathway
upstream of Fus3. Second, the hypertransposition defect also requires
STE12 and TEC1 , which regulate the expression of invasive
growth genes. This indicates that expression of an invasive growth
gene(s) is required for hypertransposition and is supported by the
finding that kss1delta mutants have a lower level of Ty1
transposition. Finally, fus3 catalytic mutants partially suppress
hypertransposition, suggesting that a kinase-independent function of
Fus3 inhibits Ty1 transposition. These results support the model that
Fus3 inhibits Ty1 transposition by negatively regulating the expression
of invasive growth genes.
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