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Article

Remodeling Yeast Gene Transcription by Activating the Ty1 Long Terminal Repeat Retrotransposon under Severe Adenine Deficiency

, &
Pages 5543-5554 | Received 12 Mar 2008, Accepted 20 Jun 2008, Published online: 27 Mar 2023
 

Abstract

The Ty1 long terminal repeat (LTR) retrotransposon of Saccharomyces cerevisiae is a powerful model to understand the activation of transposable elements by stress and their impact on genome expression. We previously discovered that Ty1 transcription is activated under conditions of severe adenine starvation. The mechanism of activation is independent of the Bas1 transcriptional activator of the de novo AMP biosynthesis pathway and probably involves chromatin remodeling at the Ty1 promoter. Here, we show that the 5′ LTR has a weak transcriptional activity and is sufficient for the activation by severe adenine starvation. Furthermore, we demonstrate that Ty1 insertions that bring Ty1 promoter sequences into the vicinity of a reporter gene confer adenine starvation regulation on it. We provide evidence that similar coactivation of genes adjacent to Ty1 sequences occurs naturally in the yeast genome, indicating that Ty1 insertions can mediate transcriptional control of yeast gene expression under conditions of severe adenine starvation. Finally, the transcription pattern of genes adjacent to Ty1 insertions suggests that severe adenine starvation facilitates the initiation of transcription at alternative sites, partly located in the 5′ LTR. We propose that Ty1-driven transcription of coding and noncoding sequences could regulate yeast gene expression in response to stress.

ACKNOWLEDGMENTS

We are grateful L. Bénard and M. Springer for stimulating discussions and comments on the manuscript. Thanks also go to M. Bétermier and C. Condon for helpful comments on the manuscript. We are grateful to E. Dubois for providing plasmids and to J. Lederout for technical help with riboprobe synthesis.

This work was supported by grants from the CNRS (UPR 9073) and Université Paris-Diderot Paris 7. G.S. was a recipient of a fellowship from the CNRS and of a fellowship from the Association pour la Recherche contre le Cancer.

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