lncRNA-induced nucleosome repositioning reinforces transcriptional repression of rRNA genes upon hypotonic stress
The activity of rRNA genes (rDNA) is regulated by pathways that target the transcription machinery or alter the epigenetic state of rDNA. Previous work has established that downregulation of rRNA synthesis in quiescent cells is accompanied by upregulation of PAPAS, a long noncoding RNA (lncRNA) that...
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| Main Authors: | , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
February 18, 2016
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| In: |
Cell reports
Year: 2016, Volume: 14, Issue: 8, Pages: 1876-1882 |
| ISSN: | 2211-1247 |
| DOI: | 10.1016/j.celrep.2016.01.073 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1016/j.celrep.2016.01.073 Verlag, lizenzpflichtig, Volltext: https://www.sciencedirect.com/science/article/pii/S2211124716300663 
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| Author Notes: | Zhongliang Zhao, Marcel Andre Dammert, Ingrid Grummt, and Holger Bierhoff |
| Summary: | The activity of rRNA genes (rDNA) is regulated by pathways that target the transcription machinery or alter the epigenetic state of rDNA. Previous work has established that downregulation of rRNA synthesis in quiescent cells is accompanied by upregulation of PAPAS, a long noncoding RNA (lncRNA) that recruits the histone methyltransferase Suv4-20h2 to rDNA, thus triggering trimethylation of H4K20 (H4K20me3) and chromatin compaction. Here, we show that upregulation of PAPAS in response to hypoosmotic stress does not increase H4K20me3 because of Nedd4-dependent ubiquitinylation and proteasomal degradation of Suv4-20h2. Loss of Suv4-20h2 enables PAPAS to interact with CHD4, a subunit of the chromatin remodeling complex NuRD, which shifts the promoter-bound nucleosome into the transcriptional “off” position. Thus, PAPAS exerts a “stress-tailored” dual function in rDNA silencing, facilitating either Suv4-20h2-dependent chromatin compaction or NuRD-dependent changes in nucleosome positioning. |
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| Item Description: | Gesehen am 08.10.2021 |
| Physical Description: | Online Resource |
| ISSN: | 2211-1247 |
| DOI: | 10.1016/j.celrep.2016.01.073 |