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Mol Cell Biol, May 1998, p. 2502-2513, Vol. 18, No. 5
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Posttranslational Regulation of Ty1 Retrotransposition by Mitogen-Activated Protein Kinase Fus3

Darryl Conte Jr.,1 Ellen Barber,1 Mukti Banerjee,1 David J. Garfinkel,2 and M. Joan Curcio1,*

Molecular Genetics Program, Wadsworth Center & School of Public Health, State University of New York at Albany, Albany, New York 12201-2002,1 and Gene Regulation and Chromosome Biology Laboratory, National Cancer Institute-Frederick Cancer Research and Development Center, ABL-Basic Research Program, Frederick, Maryland 21702-12012

Received 21 October 1997/Returned for modification 24 December 1997/Accepted 27 January 1998

Ty1 retrotransposons in Saccharomyces cerevisiae are maintained in a state of transpositional dormancy. We isolated a mutation, rtt100-1, that increases the transposition of genomic Ty1 elements 18- to 56-fold but has little effect on the transposition of related Ty2 elements. rtt100-1 was shown to be a null allele of the FUS3 gene, which encodes a haploid-specific mitogen-activated protein kinase. In fus3 mutants, the levels of Ty1 RNA, protein synthesis, and proteolytic processing were not altered relative to those in FUS3 strains but steady-state levels of TyA, integrase, and reverse transcriptase proteins and Ty1 cDNA were all increased. These findings suggest that Fus3 suppresses Ty1 transposition by destabilizing viruslike particle-associated proteins. The Fus3 kinase is activated through the mating-pheromone response pathway by phosphorylation at basal levels in naive cells and at enhanced levels in pheromone-treated cells. We demonstrate that suppression of Ty1 transposition in naive cells requires basal levels of Fus3 activation. Substitution of conserved amino acids required for activation of Fus3 derepressed Ty1 transposition. Moreover, epistasis analyses revealed that components of the pheromone response pathway that act upstream of Fus3, including Ste4, Ste5, Ste7, and Ste11, are required for the posttranslational suppression of Ty1 transposition by Fus3. The regulation of Ty1 transposition by Fus3 provides a haploid-specific mechanism through which environmental signals can modulate the levels of retrotransposition.

* Corresponding author. Mailing address: Molecular Genetics Program, Wadsworth Center & School of Public Health, SUNY at Albany, P.O. Box 22002, Albany, NY 12201-2002. Phone: (518) 473-6078. Fax: (518) 474-3181. E-mail: joan.curcio{at}wadsworth.org.

Mol Cell Biol, May 1998, p. 2502-2513, Vol. 18, No. 5
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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