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ETS1 recruits cBAF to hijack the hematopoietic stem cell MYB enhancer in T-cell leukemia.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE263952 | GEO | 2025/09/25

REPOSITORIES: GEO

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ETS1 recruits cBAF to hijack the hematopoietic stem cell MYB enhancer in T-cell leukemia [dataset 1]

Project description:Notch signaling is the most prevalent oncogenic pathway in T-ALL, but clinical trials showed that pan-Notch inhibitors caused dose-limiting toxicities. Thus, we shifted our focus from Notch to ETS1, which is one of the top transcription factors that most frequently co-bind Notch-occupied regulatory elements in the T-ALL context. A top essential ETS1-dependent element was a Notch-bound enhancer at +140kb from MYB that we named the ETS-MYB enhancer (E-Me). Using genetically engineered mouse models and chromatin profiling, we showed that the E-Me selectively promotes self-renewal of hematopoietic stem cells, becomes inactive in committed T cell progenitors; and is reactivated to promote Notch-induced transformation.

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ETS1 recruits cBAF to hijack the hematopoietic stem cell MYB enhancer in T-cell leukemia [dataset 2]

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ETS1 recruits cBAF to hijack the hematopoietic stem cell MYB enhancer in T-cell leukemia.

Project description:ETS1 recruits cBAF to hijack the hematopoietic stem cell MYB enhancer in T-cell leukemia.

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ETS1 recruits cBAF to hijack the hematopoietic stem cell MYB enhancer in T-cell leukemia [dataset 2]

Project description:ETS1 recruits cBAF to hijack the hematopoietic stem cell MYB enhancer in T-cell leukemia [dataset 2]

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ETS1 recruits cBAF to hijack the hematopoietic stem cell MYB enhancer in T-cell leukemia [dataset 1]

Project description:ETS1 recruits cBAF to hijack the hematopoietic stem cell MYB enhancer in T-cell leukemia [dataset 1]

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An enhancer RNA recruits KMT2A to regulate transcription of Myb.

Project description:The Myb proto-oncogene encodes the transcription factor c-MYB, which is critical for hematopoiesis. Distant enhancers of Myb form a hub of interactions with the Myb promoter. We identified a long non-coding RNA (Myrlin) originating from the -81-kb murine Myb enhancer. Myrlin and Myb are coordinately regulated during erythroid differentiation. Myrlin TSS deletion using CRISPR-Cas9 reduced Myrlin and Myb expression and LDB1 complex occupancy at the Myb enhancers, compromising enhancer contacts and reducing RNA Pol II occupancy in the locus. In contrast, CRISPRi silencing of Myrlin left LDB1 and the Myb enhancer hub unperturbed, although Myrlin and Myb expressions were downregulated, decoupling transcription and chromatin looping. Myrlin interacts with the KMT2A/MLL1 complex. Myrlin CRISPRi compromised KMT2A occupancy in the Myb locus, decreasing CDK9 and RNA Pol II binding and resulting in Pol II pausing in the Myb first exon/intron. Thus, Myrlin directly participates in activating Myb transcription by recruiting KMT2A.

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Project description:The Myb proto-oncogene encodes the transcription factor c-MYB, which is critical for hematopoiesis. Distant enhancers of Myb form a hub of interactions with the Myb promoter. We identified a long non-coding RNA (Myrlin) originating from the -81 kb murine Myb enhancer. Myrlin and Myb are coordinately regulated during erythroid differentiation. Myrlin TSS deletion using CRISPR/Cas9 reduced Myrlin and Myb expression and LDB1 complex occupancy at the Myb enhancers, compromising enhancer contacts and reducing RNA Pol II occupancy in the locus. In contrast, CRISPRi silencing of Myrlin left LDB1 and the Myb enhancer hub unperturbed, although Myrlin and Myb expression were downregulated, decoupling transcription and chromatin looping. Myrlin interacts with the MLL1 complex. Myrlin CRISPRi compromised MLL1 occupancy in the Myb locus, decreasing CDK9 and RNA Pol II binding and resulting in Pol II pausing in the Myb first exon/intron. Thus, Myrlin directly participates in activating Myb transcription by recruiting MLL1.

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Project description: Not available

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Regulation of MYB by distal enhancer elements in human myeloid leukemia.

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Project description:The success of hematopoietic stem cell transplantation (HSCT) lies with the ability of the engrafting immune system to remove residual leukemia cells via a graft-versus-leukemia effect (GvL), caused either spontaneously post-HSCT or via donor lymphocyte infusion. GvL effects can also be initiated by allogenic mismatched natural killer cells, antigen-specific T cells, and activated dendritic cells of leukemic origin. The history and further application of this GvL effect and the main mechanisms will be discussed and reviewed in this chapter.

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