DOT1L Inhibits SIRT1 and SUV39H1-Mediated H3K9 Modification to Maintain Gene Expression (ATACseq)

Methylation of histone 3 on lysine 79 (H3K79) is broadly associated with active gene expression in eukaryotes, and the H3K79 methyltransferase DOT1L is indispensable for specific leukemia subtypes like those with MLL-translocations. We found that suppression of the histone deacetylase SIRT1 rescued MLL-AF9 leukemia cells from their dependence on DOT1L. We show that upon DOT1L inhibition, SIRT1 is required for the acquisition of a repressive chromatin state consistent with facultative heterochromatin around MLL-AF9 target genes in leukemia and other genes possess an H3K79me2(hi), H3K9ac(hi), H3K9me2(low) histone modification profile in normal hematopoietic stem and progenitor cells.

Dataset features

Information

Specifications

Application:	ChIP-seq analysis
Number of samples:	6
Release date:	Mar 30 2015
Last update date:	Oct 10 2018
Access:	Public
Diseases:	Leukemia
Dataset link	DOT1L Inhibits SIRT1 and SUV39H1-Mediated H3K9 Modification to Maintain Gene Expression (ATACseq)

Experimental Protocol

Examination of histone modifications and a chromatin modifier with and without drug treatment and RNA interference.

Repositories

GEO

ArrayExpress

ENA

BioProject

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Contact

Richard Koche