Letter abstract
Nature Cell Biology 11, 1010 - 1016 (2009)
Published online: 5 July 2009 | doi:10.1038/ncb1914
Reversible acetylation of the chromatin remodelling complex NoRC is required for non-coding RNA-dependent silencing
Yonggang Zhou1,3, Kerstin-Maike Schmitz1,3, Christine Mayer1, Xuejun Yuan1, Asifa Akhtar2 & Ingrid Grummt1
The SNF2h (sucrose non-fermenting protein 2 homologue)-containing chromatin-remodelling complex NoRC silences a fraction of ribosomal RNA genes (rDNA) by establishing a heterochromatic structure at the rDNA promoter1, 2, 3. Here we show that the acetyltransferase MOF (males absent on the first) acetylates TIP5, the largest subunit of NoRC, at a single lysine residue, K633, adjacent to the TIP5 RNA-binding domain, and that the NAD+-dependent deacetylase SIRT1 (sirtuin-1) removes the acetyl group from K633. Acetylation regulates the interaction of NoRC with promoter-associated RNA (pRNA), which in turn affects heterochromatin formation, nucleosome positioning and rDNA silencing. Significantly, NoRC acetylation is responsive to the intracellular energy status and fluctuates during S phase. Activation of SIRT1 on glucose deprivation leads to deacetylation of K633, enhanced pRNA binding and an increase in heterochromatic histone marks. These results suggest a mechanism that links the epigenetic state of rDNA to cell metabolism and reveal another layer of epigenetic control that involves post-translational modification of a chromatin remodelling complex.
- German Cancer Research Center, Division of Molecular Biology of the Cell II, DKFZ-ZMBH Alliance, Im Neuenheimer Feld 581, D-69120 Heidelberg, Germany.
- European Molecular Biology Laboratory, Meyerhofstrasse 1, D-69117 Heidelberg, Germany.
- These authors contributed equally to this work.
Correspondence to: Ingrid Grummt1 e-mail: i.grummt@dkfz.de
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