Rxivist logo

Rxivist combines preprints from bioRxiv with data from Twitter to help you find the papers being discussed in your field. Currently indexing 73,530 bioRxiv papers from 320,012 authors.

Epigenomic translocation of H3K4me3 broad domains following super-enhancer hijacking

By Aneta Mikulasova, Marco Trevisan-Herraz, Kent Fung, Cody Ashby, Nefeli Karataraki, Gareth J. Morgan, Anne Corcoran, Sophie Hambleton, Brian A. Walker, Daniel Rico, Lisa J Russell

Posted 12 Feb 2020
bioRxiv DOI: 10.1101/2020.02.12.938563

Chromosomal translocations are important drivers of haematological malignancies whereby proto-oncogenes are activated by juxtaposition with super-enhancers, often called super-enhancer hijacking. We analysed the epigenomic consequences of rearrangements between the enhancers of the immunoglobulin heavy chain locus (IGH) and proto-oncogene CCND1 that are common in B-cell malignancies. By integrating BLUEPRINT epigenomic data with DNA breakpoint detection, we characterised the normal chromatin landscape of the human IGH locus and its dynamics after pathological genomic rearrangement. We detected an H3K4me3 broad domain (BD) within the IGH locus of healthy B-cells that was absent in samples with IGH-CCND1 translocations. The appearance of H3K4me3-BD over CCND1 in the latter was associated with overexpression and extensive chromatin accessibility of this locus. We observed similar cancer-specific H3K4me3-BDs associated with super-enhancer hijacking of other common oncogenes in B-cell (MAF, MYC and FGFR3) and in T-cell malignancies (LMO2, TLX3 and TAL1). Our analysis suggests that H3K4me3-BDs are created by super-enhancers and supports the new concept of epigenomic translocation, where the relocation of H3K4me3-BDs accompanies the translocation of super-enhancers.

Download data

No bioRxiv download data for this paper yet.

Altmetric data


PanLingua

Sign up for the Rxivist weekly newsletter! (Click here for more details.)


News