Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Anterior Heart Field (AHF)-conditional Mef2c Knockout

ABSTRACT: We have performed conditional inactivation of mef2c in the anterior heart field (AHF) of mice and observed a phenotypic spectrum of outflow tract anomalies in the conditional mutant hearts. In an effort to identify misregulated genes in the outflow tracts of the mutants, we have performed RNA-Seq on outflow tract samples dissected from E10.5 mutant and wild-type embryos. There are four wild-type samples and four mutant samples.

ORGANISM(S): Mus musculus

SUBMITTER: Brian Black

PROVIDER: E-GEOD-68147 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

MEF2C regulates outflow tract alignment and transcriptional control of Tdgf1.

Barnes Ralston M RM Harris Ian S IS Jaehnig Eric J EJ Sauls Kimberly K Sinha Tanvi T Rojas Anabel A Schachterle William W McCulley David J DJ Norris Russell A RA Black Brian L BL

Development (Cambridge, England) 20160125 5

Congenital heart defects are the most common birth defects in humans, and those that affect the proper alignment of the outflow tracts and septation of the ventricles are a highly significant cause of morbidity and mortality in infants. A late differentiating population of cardiac progenitors, referred to as the anterior second heart field (AHF), gives rise to the outflow tract and the majority of the right ventricle and provides an embryological context for understanding cardiac outflow tract a ...[more]

PMID: 26811383

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Project description:Acute myelogenous leukemia (AML) is driven by leukemic stem cells (LSC) generated by mutations that confer (or maintain) self-renewal potential coupled to an aberrant differentiation program. Using retroviral mutagenesis, we identified genes that generate LSC in collaboration with genetic disruption of the gene encoding interferon response factor 8 (Irf8), which induces a myeloproliferation in vivo. Amongst the targeted genes, we identified Mef2c, encoding a MADS transcription factor, and confirmed that over-expression induced a myelomonocytic leukemia in cooperation with Irf8 deficiency. Strikingly, several of the genes identified in our screen have been reported to be upregulated in the mixed-lineage leukemia (MLL) subtype. High MEF2C expression levels were confirmed in AML patient samples with MLL gene disruptions, prompting an investigation of the causal interplay. Using a conditional mouse strain, we demonstrated that Mef2c deficiency does not impair the establishment nor maintenance of LSC generated in vitro by MLL/ENL fusion proteins â?? however, its loss led to compromised homing and invasiveness of the tumor cells. Mef2c-dependent targets included several genes encoding matrix metalloproteinases and chemokine ligands and receptors, providing a mechanistic link to increased homing and motility. Thus an early event in LSC generation may be responsible for the aggressive nature of this leukemia subtype. Experiment Overall Design: For gene expression profiling of M/E cells, RNA was isolated from M/E-Mef2c del/- cells infected with MYs-iPAC (empty vector) or MYs-pMef2cASR after puromycin selection at three different time points, pooled, and hybridized against the Agilent Whole Mouse Genome Microarray 4x44K using the one-color service of Miltenyi. Transcript levels were verified by real-time RT-PCR using the SYBRGreen Reaction Mix (Roche Mannheim) in a Roche Light-Cycler. cDNA levels were normalized against Hprt transcript levels. Primers and amplification conditions are available upon request.

Dataset Information

Anterior Heart Field (AHF)-conditional Mef2c Knockout

Publications

MEF2C regulates outflow tract alignment and transcriptional control of Tdgf1.

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