Figure 2 Histone acetylation regulates gene expression Figure 2 | Histone acetylation regulates gene expression. a | Histone acetyltransferases (HAT) acetylate lysine tails; these marks keep the chromatin in an decondensed state, enabling the access of transcription factors (TF) and polymerases (Pol II) to the gene promoters. Proteins such as histone-lysine N-methyltransferase SETD2 and histone demethylase UTX, which are encoded by SETD2 and KDM6C (genes that are mutated in renal cancers), also maintain other open chromatin marks by removal (UTX) or addition (SETD2) of methyl groups (Me) to specific lysines. b | Following CpG methylation, methyl-CpG-binding domain proteins (MBD) bind to the methylated DNA and recruit histone deacetylases (HDAC), which remove acetyl groups (Ac). Additionally, the lysine-specific demethylase 5C (JARID1C) encoded by KDM5C, which is mutated in renal cancers, removes specific methyl groups in transcriptionally silenced regions of the genome. c | Following deacetylation (and other histone modifications) chromatin remodelling complexes are recruited to the region; these complexes bring nucleosomes together, causing DNA condensation and thus preventing access of TFs or polymerases to promoters. Morris, M. R. & Latif, F. (2016) The epigenetic landscape of renal cancer Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.168