Modulation of mRNA and lncRNA expression dynamics by the Set2-Rpd3S pathway

Ji Hyun Kim, Bo Bae Lee, Young Mi Oh, Chenchen Zhu, Lars M. Steinmetz, Yookyeong Lee, Wan Kyu Kim, Sung Bae Lee, Stephen Buratowski, Tae Soo Kim

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58 Scopus citations


H3K36 methylation by Set2 targets Rpd3S histone deacetylase to transcribed regions of mRNA genes, repressing internal cryptic promoters and slowing elongation. Here we explore the function of this pathway by analysing transcription in yeast undergoing a series of carbon source shifts. Approximately 80 mRNA genes show increased induction upon SET2 deletion. A majority of these promoters have overlapping lncRNA transcription that targets H3K36me3 and deacetylation by Rpd3S to the mRNA promoter. We previously reported a similar mechanism for H3K4me2-mediated repression via recruitment of the Set3C histone deacetylase. Here we show that the distance between an mRNA and overlapping lncRNA promoter determines whether Set2-Rpd3S or Set3C represses. This analysis also reveals many previously unreported cryptic ncRNAs induced by specific carbon sources, showing that cryptic promoters can be environmentally regulated. Therefore, in addition to repression of cryptic transcription and modulation of elongation, H3K36 methylation maintains optimal expression dynamics of many mRNAs and ncRNAs.

Original languageEnglish
Article number13534
JournalNature Communications
StatePublished - 28 Nov 2016

Bibliographical note

Funding Information:
This research was supported by grants to T.K. (Ewha Womans University Research Grant of 2013, the T.J. Park Science Fellowship of POSCO T.J. Park Foundation, the Basic Science Research Program of the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (NRF-2013R1A1A1008634 and NRF-2012R1A5A1048236), the National Research Foundation of Korea funded by Korean Government (NRF- 2013S1A2A2035342)), to L.M.S. (Deutsche Forschungsgemeinschaft and US National Institutes of Health GM068717) and to S.B. (US National Institutes of Health GM46498).

Publisher Copyright:
© The Author(s) 2016.


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