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DUX4-r neomorphic activity depending on GTF2I in acute lymphoblastic leukemia [CUT&Tag]

ABSTRACT: DUX4-r neomorphic activity depending on GTF2I in acute lymphoblastic leukemia [CUT&Tag]

PROVIDER: PRJNA950006 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR24005319_1.fastq.gz	Fastqsanger.gz
	SRR24005319_2.fastq.gz	Fastqsanger.gz
	SRR24005320.fastq.gz	Fastqsanger.gz
	SRR24005320_1.fastq.gz	Fastqsanger.gz
	SRR24005320_2.fastq.gz	Fastqsanger.gz

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DUX4-r neomorphic activity depending on GTF2I in acute lymphoblastic leukemia [CUT&Tag]

Project description:Translocations producing rearranged versions of the transcription factor DUX4 (DUX4-r) are one of the most frequent causes of B-cell acute lymphoblastic leukemia (B-ALL). DUX4-r retains the DNA binding domain of wt DUX4, but is truncated on the C-terminal transcription activation domain. The precise mechanism through which DUX4-r causes leukemia is unknown and no targeted therapy is currently available. We found that the rearrangement leads to both a loss and a gain of function in DUX4-r. Loss of CBP/EP300 transcriptional co-activators interaction and inability to bind and activate repressed chromatin. Gain of interaction with the transcription factor GTF2I, which redirects DUX4-r toward leukemogenic targets. Importantly, this neomorphic activity exposes an Achilles' heel whereby DUX4-r positive leukemia cells are exquisitely sensitive to GTF2I targeting, which inhibits DUX4-r leukemogenic activity. Our work elucidates the molecular mechanism through which DUX4-r causes leukemia and suggest a possible therapeutic avenue tailored to this B-ALL subtype.

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DUX4-r neomorphic activity depending on GTF2I in acute lymphoblastic leukemia [RNA-seq]

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DUX4-r neomorphic activity depending on GTF2I in acute lymphoblastic leukemia [RNA-seq]

Project description:DUX4-r neomorphic activity depending on GTF2I in acute lymphoblastic leukemia [RNA-seq]

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DUX4-r exerts a neomorphic activity that depends on GTF2I in acute lymphoblastic leukemia

Project description:DUX4-r exerts a neomorphic activity that depends on GTF2I in acute lymphoblastic leukemia

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DUX4-r exerts a neomorphic activity that depends on GTF2I in acute lymphoblastic leukemia.

Project description:Translocations producing rearranged versions of the transcription factor double homeobox 4 (DUX4-r) are one of the most frequent causes of B cell acute lymphoblastic leukemia (B-ALL). DUX4-r retains the DNA binding domain of wild-type DUX4 but is truncated on the C-terminal transcription activation domain. The precise mechanism through which DUX4-r causes leukemia is unknown, and no targeted therapy is currently available. We found that the rearrangement leads to both a loss and a gain of function in DUX4-r. Loss of CBP/EP300 transcriptional coactivator interaction leads to an inability to bind and activate repressed chromatin. Concurrently, a gain of interaction with the general transcription factor 2 I (GTF2I) redirects DUX4-r toward leukemogenic targets. This neomorphic activity exposes an Achilles' heel whereby DUX4-r-positive leukemia cells are exquisitely sensitive to GTF2I targeting, which inhibits DUX4-r leukemogenic activity. Our work elucidates the molecular mechanism through which DUX4-r causes leukemia and suggests a possible therapeutic avenue tailored to this B-ALL subtype.

| S-EPMC10881058 | biostudies-literature

DUX4-r exerts a neomorphic activity that depends on GTF2I in acute lymphoblastic leukemia

Project description:This SuperSeries is composed of the SubSeries listed below.

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Murine Adult Cortex: Gtf2i (+/Δex2 ) VS WT (+/+)

Project description:Transcriptional profiling of mouse cortex tissue comparing control animals with Gtf2i-mutated mouse (Gtf2i+/Δex2 ). Goal was to determine the specific deregulated genes in the cortex of mutated animals.

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Expression data from GTF2i mutated ES cells

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Project description:The aim of this study is to define the molecular mechanisms underlying DUX4-associated toxicity in the context of facioscapulohumeral muscular dystrophy (FSHD). DUX4 is a transcription factor, which induces cell death by activating the transcription of its targets. No molecule able to directly control DUX4 activity is currently known. By using a tandem affinity purification protocol combined to mass spectrometry analysis, we identified Matrin 3 (MATR3), as the first cellular factor able to directly block DUX4 toxic activity. We found that MATR3 binds to the DNA binding domain of DUX4 blocking the activation of its genomic targets.

2023-08-21 | PXD011073 | Pride

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