Transcription of Two Long Noncoding RNAs Mediates Mating-Type Control of Gametogenesis in Budding Yeast
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van Werven-2012-Transcription of Two.pdf
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Author(s) • • • • • • • • •
van Werven, Folkert J.
Neuert, Gregor
Hendrick, Natalie
Buratowski, Stephen
van Oudenaarden, Alexander
Primig, Michael
Lardenois, Aurelie
van Werven, Folkert J.
van Oudenaarden, Alexander
Amon, Angelika B
Date Issued
September 2012
Journal
Cell
Publisher
Elsevier
Citation
Van Werven, Folkert J., Gregor Neuert, Natalie Hendrick, Aurelie Lardenois, Stephen Buratowski, Alexander van Oudenaarden, Michael Primig, and Angelika Amon. “Transcription of Two Long Noncoding RNAs Mediates Mating-Type Control of Gametogenesis in Budding Yeast.” Cell 150, no. 6 (September 2012): 1170–1181. © 2012 Elsevier Inc.
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Final published version
Abstract
The cell-fate decision leading to gametogenesis is essential for sexual reproduction. In S. cerevisiae, only diploid MATa/α but not haploid MATa or MATα cells undergo gametogenesis, known as sporulation. We find that transcription of two long noncoding RNAs (lncRNAs) mediates mating-type control of sporulation. In MATa or MATα haploids, expression of IME1, the central inducer of gametogenesis, is inhibited in cis by transcription of the lncRNA IRT1, located in the IME1 promoter. IRT1 transcription recruits the Set2 histone methyltransferase and the Set3 histone deacetylase complex to establish repressive chromatin at the IME1 promoter. Inhibiting expression of IRT1 and an antisense transcript that antagonizes the expression of the meiotic regulator IME4 allows cells expressing the haploid mating type to sporulate with kinetics that are indistinguishable from that of MATa/α diploids. Conversely, expression of the two lncRNAs abolishes sporulation in MATa/α diploids. Thus, transcription of two lncRNAs governs mating-type control of gametogenesis in yeast.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Massachusetts Institute of Technology. Department of Physics
Koch Institute for Integrative Cancer Research at MIT
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DOI of Published Version
https://doi.org/10.1016/j.cell.2012.06.049