Fus3 controls Ty1 transpositional dormancy through the invasive growth MAPK pathway

Citation
D. Conte et Mj. Curcio, Fus3 controls Ty1 transpositional dormancy through the invasive growth MAPK pathway, MOL MICROB, 35(2), 2000, pp. 415-427
Citations number
56
Categorie Soggetti
Microbiology
Journal title
MOLECULAR MICROBIOLOGY
ISSN journal
0950382X → ACNP
Volume
35
Issue
2
Year of publication
2000
Pages
415 - 427
Database
ISI
SICI code
0950-382X(200001)35:2<415:FCTTDT>2.0.ZU;2-A
Abstract
Fus3, the mitogen-activated protein kinase (MAPK) of the mating pheromone r esponse pathway, inhibits a post-translational step of Ty1 retrotranspositi on. Fus3 also inhibits haploid invasive growth by blocking cross-activation of invasive growth gene expression by the pheromone response signal cascad e. Here, we show that Fus3 kinase activity and dosage co-ordinately regulat e Ty1 transposition and invasive growth. A chromosomal copy of the kinase-d efective fus3-K42R allele fails to inhibit either Ty1 transposition or inva sive growth. When overexpressed, kinase-defective Fus3 weakly inhibits both Ty1 transposition and invasive growth, but is much less inhibitory than wi ld-type Fus3 expressed at the same level. Moreover, increasing the dosage o f wild-type Fus3 intensifies the inhibition of both Ty1 transposition and i nvasive growth. To demonstrate that Fus3 regulates Ty1 transposition via it s negative regulation of the invasive growth pathway, we show by epistatic analysis that the invasive growth pathway transcription factors Ste12. and Tec1 are both required for Fus3-mediated inhibition of Ty1 transposition. W hen haploid invasive growth is stimulated by high-copy expression of TEC1, by expression of the dominant hypermorphic allele STE11-4 or by deletion of HOG1, Ty1 transposition is concomitantly activated. In summary, these resu lts demonstrate that the haploid invasive growth pathway activates Ty1 tran sposition at both transcriptional and post-transcriptional levels and that Fus3 inhibits Ty1 transposition by inhibiting the invasive growth pathway.