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The MEF2C oncogene opposes Notch signalling in T versus B lineage decision and drives leukemia in the thymus context [array]

ABSTRACT: Overexpression of the oncogene MEF2C oposses NOTCH signalling in T versus B lineage decision, driving leukemia in the thymus context

ORGANISM(S): Homo sapiens

PROVIDER: GSE159506 | GEO | 2022/05/14

REPOSITORIES: GEO

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The MEF2C oncogene opposes Notch signalling in T versus B lineage decision and drives leukemia in the thymus context [ChIP-Seq]

Project description:Overexpression of the oncogene MEF2C opposes NOTCH signalling in T versus B lineage decision, driving leukemia in the thymus context

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The MEF2C oncogene opposes Notch signalling in T versus B lineage decision and drives leukemia in the thymus context

Project description:The MEF2C oncogene opposes Notch signalling in T versus B lineage decision and drives leukemia in the thymus context

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The MEF2C oncogene opposes Notch signalling in T versus B lineage decision and drives leukemia in the thymus context

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The MEF2C oncogene opposes Notch signalling in T versus B lineage decision and drives leukemia in the thymus context [array]

Project description:The MEF2C oncogene opposes Notch signalling in T versus B lineage decision and drives leukemia in the thymus context [array]

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The MEF2C oncogene opposes Notch signalling in T versus B lineage decision and drives leukemia in the thymus context [ChIP-Seq]

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MEF2C opposes Notch in lymphoid lineage decision and drives leukemia in the thymus.

Project description:Rearrangements that drive ectopic MEF2C expression have recurrently been found in patients with human early thymocyte progenitor acute lymphoblastic leukemia (ETP-ALL). Here, we show high levels of MEF2C expression in patients with ETP-ALL. Using both in vivo and in vitro models of ETP-ALL, we demonstrate that elevated MEF2C expression blocks NOTCH-induced T cell differentiation while promoting a B-lineage program. MEF2C activates a B cell transcriptional program in addition to RUNX1, GATA3, and LMO2; upregulates the IL-7R; and boosts cell survival by upregulation of BCL2. MEF2C and the Notch pathway, therefore, demarcate opposite regulators of B- or T-lineage choices, respectively. Enforced MEF2C expression in mouse or human progenitor cells effectively blocks early T cell differentiation and promotes the development of biphenotypic lymphoid tumors that coexpress CD3 and CD19, resembling human mixed phenotype acute leukemia. Salt-inducible kinase (SIK) inhibitors impair MEF2C activity and alleviate the T cell developmental block. Importantly, this sensitizes cells to prednisolone treatment. Therefore, SIK-inhibiting compounds such as dasatinib are potentially valuable additions to standard chemotherapy for human ETP-ALL.

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MEF2C hypofunction in neuronal and neuroimmune populations produces MEF2C haploinsufficiency syndrome behaviors in mice

Project description:Microdeletions of the MEF2C gene are linked to a syndromic form of autism termed MEF2C haploinsufficiency syndrome (MCHS). Here, we show that MCHS-associated missense mutations cluster in the conserved DNA binding domain and disrupt MEF2C DNA binding. DNA binding-deficient global Mef2c heterozygous mice (Mef2c-Het) display numerous MCHS-like behaviors, including autism-related behaviors, as well as deficits in cortical excitatory synaptic transmission. We find that hundreds of genes are dysregulated in Mef2c-Het cortex, including significant enrichments of autism risk and excitatory neuron genes. In addition, we observe an enrichment of upregulated microglial genes, but not due to neuroinflammation in the Mef2c-Het cortex. Importantly, conditional Mef2c heterozygosity in forebrain excitatory neurons reproduces a subset of the Mef2c-Het phenotypes, while conditional Mef2c heterozygosity in microglia reproduces social deficits and repetitive behavior. Together our findings suggest that MEF2C regulates typical brain development and function through multiple cell types, including excitatory neuronal and neuroimmune populations.

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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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Expression data from HUVEC adenovirally overexpressing MEF2C

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2013-06-01 | E-GEOD-46279 | biostudies-arrayexpress

Genome-wide maps of MEF2C and H3K27ac localization in HUVECs

Project description:MEF2C is one of the substantially expressed transcriptional factors in endothelial cells, but its genomic localization is unknown. This time, we established a new antibody for MEF2C, and performed ChIP-seq to identify MEF2C binding site in whole genome manner. H3K27Ac binding sites were also detected in the same way. We used chromatin immunoprecipitation with deep sequencing (ChIP-seq) of HUVECs treated with or without pitavastatin for 4hours, we identified MEF2C and H3K27Ac binding regions.HUVECs were used within the first 6 passages. For MEF2C studies, HUVECs were cultivated in medium EGM2MV containing pitavastatin at a concentration of 1 ?M, and same concentration of DMSO was used as a control sample. For H3K27ac, HUVECs were starved for 16 hours and harvested without statin treatment.

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