Project description:A nucleosome turnover map reveals that the stability of histone H4 Lys20 methylation depend on histone recycling in transcribed chromatin [ChIP]
Project description:Snf2 Family Protein Fft3 Suppresses Nucleosome Turnover to Promote Epigenetic Inheritance of Heterochromatin and Proper Replication of the Genome [BrdU IP]
Project description:Snf2 Family Protein Fft3 Suppresses Nucleosome Turnover to Promote Epigenetic Inheritance of Heterochromatin and Proper Replication of the Genome [H3K9me2 ChIP]
Project description:Snf2 Family Protein Fft3 Suppresses Nucleosome Turnover to Promote Epigenetic Inheritance of Heterochromatin and Proper Replication of the Genome [H3-FLAG ChIP]
Project description:Snf2 Family Protein Fft3 Suppresses Nucleosome Turnover to Promote Epigenetic Inheritance of Heterochromatin and Proper Replication of the Genome [HU + BrdU IP]
Project description:Heterochromatin enforces transcriptional gene silencing and can be epigenetically inherited, but the underlying mechanism has remained unclear.Here we show that histone deacetylation, a conserved feature of heterochromatin domains, blocks SWI/SNF subfamily remodelers involved in chromatin unraveling, thereby stabilizing modified nucleosomes that preserve gene silencing. Histone hyperacetylation, resulting from either the loss of a histone deacetylase (HDAC) or the direct targeting of histone acetyltransferase to heterochromatin, permits remodeler access, leading to silencing defects.The requirement for HDAC in heterochromatin silencing can be bypassedby impeding SWI/SNF activity. Highlighting the crucial role of remodelers, merely targeting SWI/SNF to heterochromatin, even in cells with functional HDAC, increases nucleosome turnover, causing defective gene silencing and compromised epigenetic inheritance. This study elucidates a fundamental mechanism whereby histone hypoacetylation, maintained by high HDAC levels in heterochromatic regions, ensures stable gene silencing and epigenetic inheritance,providing significant insights into genome regulation relevant to human diseases.
