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MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia [ATAC-seq]

ABSTRACT: MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia [ATAC-seq]

PROVIDER: PRJNA418959 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6304620_1.fastq.gz	Fastqsanger.gz
	SRR6304620_2.fastq.gz	Fastqsanger.gz
	SRR6304611_1.fastq.gz	Fastqsanger.gz
	SRR6304611_2.fastq.gz	Fastqsanger.gz
	SRR6304621_1.fastq.gz	Fastqsanger.gz

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MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia [mutant MEF2C]

Project description:In acute myeloid leukemia, chemotherapy resistance remains prevalent and poorly understood. Using functional proteomics of patient AML specimens, we identified MEF2C S222 phosphorylation as a specific marker of primary chemoresistance. We found that transgenic Mef2cS222A/S222A mice engineered to block MEF2C phosphorylation exhibited normal hematopoiesis, but were resistant to leukemogenesis induced by MLL-AF9. MEF2C phosphorylation was required for leukemia stem cell maintenance, induced by MARK kinases in cells, and blocked by selective MARK inhibitor MRT199665, which caused apoptosis of MEF2C-activated human AML cell lines and primary patient specimens, but not those lacking MEF2C. These findings identify signaling-dependent dysregulation of transcription factor control as a determinant of therapy response in AML, with immediate potential for improved diagnosis and therapy for this disease.

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MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia

Project description:MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia

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MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia [ATAC-seq]

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MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia [inhibitor MRT199665]

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MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia [inhibitor MRT199665]

Project description:MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia [inhibitor MRT199665]

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MEF2C Phosphorylation Is Required for Chemotherapy Resistance in Acute Myeloid Leukemia.

Project description:In acute myeloid leukemia (AML), chemotherapy resistance remains prevalent and poorly understood. Using functional proteomics of patient AML specimens, we identified MEF2C S222 phosphorylation as a specific marker of primary chemoresistance. We found that Mef2cS222A/S222A knock-in mutant mice engineered to block MEF2C phosphorylation exhibited normal hematopoiesis, but were resistant to leukemogenesis induced by MLL-AF9 MEF2C phosphorylation was required for leukemia stem cell maintenance and induced by MARK kinases in cells. Treatment with the selective MARK/SIK inhibitor MRT199665 caused apoptosis and conferred chemosensitivity in MEF2C-activated human AML cell lines and primary patient specimens, but not those lacking MEF2C phosphorylation. These findings identify kinase-dependent dysregulation of transcription factor control as a determinant of therapy response in AML, with immediate potential for improved diagnosis and therapy for this disease.Significance: Functional proteomics identifies phosphorylation of MEF2C in the majority of primary chemotherapy-resistant AML. Kinase-dependent dysregulation of this transcription factor confers susceptibility to MARK/SIK kinase inhibition in preclinical models, substantiating its clinical investigation for improved diagnosis and therapy of AML. Cancer Discov; 8(4); 478-97. ©2018 AACR.This article is highlighted in the In This Issue feature, p. 371.

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Regulation of lymphoid versus myeloid fate choice by Mef2c

Project description:Despite recent advances in the identification of lymphoid-restricted progenitors, the transcription factors essential for their generation remain to be identified. Here we describe an unexpected role for the myeloid oncogene Mef2c in multipotent progenitors (MPPs), where it is required for pan-lymphoid differentiation. Mef2c deficiency was associated with profound defects in B, T, NK cell and common lymphoid progenitor production and an enhanced myeloid output. Mef2c deficiency in MPPs leads to downregulation of several key lymphoid regulators and the upregulation of the myeloid factor C/EBPa. Our studies also show that Mef2c is a critical transcriptional target of PU.1 during lymphopoiesis. Thus, Mef2c is a crucial component of the transcriptional network that regulates lymphoid specification and cell fate choice in MPPs.

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Project description:MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia [mutant MEF2C]

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MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia

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

2018-07-23 | GSE107073 | GEO

Impact of MEF2C on chromatin accessibility of mouse BM pre-B and myeloid cells

Project description:We analyzed the chromatin accessibility of control and Mef2c deficient mouse BM pre-B and myeloid cells by ATAC-seq analysis.

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