Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Myc mild overexpression in the heart in a mosaic fashion induces matabolic changes and triggers hipertrophic protection pathways without a pathological phenotype

ABSTRACT: Recently, it was described that mammalian cells are able to eliminate those with relative lower Myc levels in the epiblast through cell competition. We have described that cardiomyocytes during heart development are also able to complete eliminating cells with lower Myc levels. We have also shown that adult cardiomyocytes respond in the same way over long periods of time when cell competition is induced by overexpressing Myc in a mosaic fashion. We therefore have developed an RNASeq assay to further understand the mechanism of elimination of WT cells and the effect of mild Myc overexpression in cardiomyocytes. Myc overexpression in a mosaic fashion in adult cardiomyocytes, 2 hearts were analyzed and two wild type littermates were used as controls

ORGANISM(S): Mus musculus

SUBMITTER: Fatima Sanchez-Cabo

PROVIDER: E-GEOD-58858 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Cell competition promotes phenotypically silent cardiomyocyte replacement in the mammalian heart.

Villa Del Campo Cristina C Clavería Cristina C Sierra Rocío R Torres Miguel M

Cell reports 20140904 6

Heterogeneous anabolic capacity in cell populations can trigger a phenomenon known as cell competition, through which less active cells are eliminated. Cell competition has been induced experimentally in stem/precursor cell populations in insects and mammals and takes place endogenously in early mouse embryonic cells. Here, we show that cell competition can be efficiently induced in mouse cardiomyocytes by mosaic overexpression of Myc during both gestation and adult life. The expansion of the My ...[more]

PMID: 25199831

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Project description:Ventricular chambers are essential for the rhythmic contraction and relaxation that occurs in every hearbeat throughout life. Congenital abnormalities in ventricular chamber formation cause severe human heart defects. How the early trabecular meshwork of myocardial fibres forms and subsequently develops into mature chambers is still poorly understood. Here we show that Notch signalling first connects chamber endocardium and myocardium to sustain trabeculation and later coordinates ventricular patterning and compaction with coronary vessel development to give rise to the mature chamber via a temporal sequence of ligand signalling determined by the glycosyltransferase Manic Fringe (Mfng). The early endocardial expression of Mfng favours Dll4-Notch1 signalling, Which induces trabeculation in the developing ventricle.Ventricular maturation and compaction in turn require Mfng and Dll4 downregulation in the endocardium, Which allows myocardial Jag1- And Jag2- Signalling to Notch1 in this tissue.Timely and spatial perturbation of this signalling equilibrium severely disrupts heart chamber formation. Our results open a new research avenue into the pathogenesis of cardiomyopathies. Dll4 and Notch1 conditional KOs using Nfact1 and/or Tie2 driven Cre expression: RNA was isolated from pooled whole hearts of 8 (Nfact1) or 9 (Tie2) E9.5 embryos per replicate. Dll4flox;Nfatc1-Cre and WT siblings (4 KO and 4 WT replicates), Notch1flox;Nfatc1-Cre and WT siblings (3 KO and 2 WT replicates), Dll4flox;Tie2-Cre and WT siblings (3 KO and 3 WT replicates). Jag1, Jag2 and Jag1Jag2 conditional KOs using cTnT driven Cre expression: RNA was isolated from pooled heart ventricles of 4 E15.5 embryos per replicate. Jag1flox;cTnT-Cre and WT siblings (3 KO and 3 WT replicates), Jag2flox;cTnT-Cre and WT siblings (3 KO and 2 WT replicates). Jag1flox;jag2flox;cTnT-Cre and WT siblings (3 KO and 2 WT replicates). MFng Gain Of Function using Tie2 driven Cre expression: RNA was isolated from pooled heart ventricles of 4 E15.5 embryos per replicate. MFng;Tie2-Cre and WT siblings (4 GOF and 4 WT replicates). For Dll4, Noth1 and Jag1 KOs, libraries were prepared using the standard Illumina TrueSeq RNASeq library preparation kit and sequenced in a GAIIx Illumina sequencer using a 75bp single end elongation protocol. For Jag2 and Jag1Jag2 KOs and MFng GOF libraries were prepared prepared using the NEBNext Ultra RNA Library Prep Kit for Illumina and sequenced in a HiSeq2500 Illumina sequencer using a 61bp single end elongation protocol

Dataset Information

Myc mild overexpression in the heart in a mosaic fashion induces matabolic changes and triggers hipertrophic protection pathways without a pathological phenotype

Publications

Cell competition promotes phenotypically silent cardiomyocyte replacement in the mammalian heart.

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