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Effect of Nkx2.5 mutation on gene expression profiles of mouse embryonic stem cells undergoing cardiac differentiation.

ABSTRACT: The purpose of this study was to determine the effect of Nkx2.5 mutation (R141C) on gene expression in mouse embryonic stem cells during their differentiation into cardiac progenitors.

ORGANISM(S): Mus musculus

PROVIDER: GSE83428 | GEO | 2017/12/31

SECONDARY ACCESSION(S): PRJNA325887

REPOSITORIES: GEO

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Genomic occupancy of TFs ISL1 and NKX2.5 in cardiac and neural populations

Project description:ChIP-sequencing demonstrated that ISL1 binds cardiac DNA in a cell-type-specific manner, and that NKX2.5 is both necessary and sufficient for this localization.

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Single cell RNA-sequencing (scRNA-seq) of ISL1 knockout (KO) or knockdown and NKX2.5 KO compared to WT in cardiac progenitors (CPs); scRNA-seq of ISL1 KO compared to WT in motor neuron progenitors (MNPs)

Project description:Previous evidence suggested ISL1 plays unique transcriptional roles between vastly different cell types in developing humans. Single cell RNA-sequencing (scRNA-seq) of in vitro progenitor cells detailed ISL1's cell-type-specific roles in human cardiac progenitors (CPs) and motor neuron progenitors (MNPs). In addition, scRNA-seq confirmed ISL1 and NKX2.5 likely regulate common transcriptional pathways.

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Activation of Nkx2.5 Transcriptional Program is Required for Adult Myocardial Repair

Project description:We show that cardiac-specific RNA-sequencing studies reveal a disrupted embryonic Nkx2.5 transcriptional profile despite histologically normal, Nkx2.5 loss-of-function adult myocardium. Yet, adult nkx2.5-/- fish exhibit an impaired ability to recover following ventricular apex amputation as illustrated by retention of fibrin and collagen in the injured area. Complex network analyses illuminate that Nkx2.5 is required to mount a proliferative response for cardiomyocyte renewal and to provoke proteolytic pathways necessary for sarcomere disassembly. Moreover, direct Nkx2.5 targets embedded in these distinct gene regulatory modules coordinate appropriate, multi-faceted injury responses. Altogether, our findings support a previously unrecognized, Nkx2.5-dependent regenerative circuit that invokes myocardial proliferation and dedifferentiation to ensure effective regeneration in the teleost heart.

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Transcription profiling of hearts from Nkx2.5 knockout mice (mouse model of congenital heart disease) at embryonic day 12.5 shows Nkx2.5 is not only crucial during early steps of cardiogenesis but also plays an important role at later developmental stages

Project description:The NK2 family of homeobox genes constitutes a family of transcription factors that play an important role in different developmental processes. Members of this group are characterized by two highly conserved protein domains: the homeodomain, conferring DNA binding activity, and the NK2-specific domain (NK2-SD) of yet unknown function. One of the best characterized members of this group is the early cardiogenic marker Nkx2.5. Loss of function of Nkx2.5 leads to embryonic lethality around E10.5 due to an arrest of heart development at the looping stage. We have further dissected the function of Nkx2.5 in vivo by creating a knockout mouse line harboring an in frame deletion of the NK2-SD by Cre/loxP mediated excision. Homozygous mutant mice die at E14.5 due to severe cardiac malformations, e.g. common AV canal, DORV, and VSD. Lack of the NK2-SD leads to downregulation of the ventricular markers MLC-2v and Irx4 specifically in the right ventricle, and is accompanied with reduced right ventricular function. This function of Nkx2.5 seems to be independent of its ability to bind target DNA, since lack of the NK2-SD does not alter the DNA binding activity of Csx/Nkx2.5 in vitro. Heterozygous mutant mice show a spectrum of cardiac defects related to cardiac septation and valve morphogenesis, but lack conduction system defects as reported for heterozygous Nkx2.5 mice. The phenotype observed in NK2-SD mutant mice shows that Nkx2.5 is not only crucial during early steps of cardiogenesis but also plays an important role at later developmental stages. Embryos were isolated at embryonic day 12.5. The entire embryo heart was taken and isolated in ice-cold PBS and immediately frozen on dry-ice. Total RNA was extracted from pooled samples of wildtype, heterozygous and mutant embryos.

2007-12-13 | E-GEOD-528 | biostudies-arrayexpress

Nkx2.5 regulates Jarid2 during outflow tract morphogenesis

Project description:The transcription factor Nkx2.5 is required for specification of pharyngeal arch second heart field (SHF) progenitors that contribute to outflow tract (OFT) and right ventricle (RV) formation. Multiple sets of microarray data were analyzed to identify genes that are candidate targets of Nkx2.5 in the second heart field. These sets are: 1) publicly available data for cardiothoracic tissue from E9.5 Nkx2.5 wild-type, heterozygous and homozygous embryos; 2) an analysis of mouse E10.5 pharyngeal arch tissue; 3) an analysis of mouse E12.5 heart tissue; and 4) a temporal analysis of the cardiogenic cell line P19CL6. This combined analysis identified 11 genes (Lrrn1, Elovl2, Safb, Slc39a6, Khdrbs1, Hoxb4, Fez1, Ccdc117, Jarid2, Nrcam, and Enpp3) expressed in SHF-containing pharyngeal arch tissue whose regulation is dependent on Nkx2.5 expression. Refer to individual Series

2010-05-17 | E-GEOD-17936 | biostudies-arrayexpress

Nkx2.5 regulates Jarid2 during outflow tract morphogenesis

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The multi-lineage transcription factor ISL1 controls cardiomyocyte cell fate through interaction with NKX2.5

Project description:Congenital heart disease (CHD) is a leading cause of infant mortality in the US and is commonly thought to arise from perturbations of transcription factors (TFs) during cardiac development. ISLET1 (ISL1) is one such TF, although it also directs differentiation of other cell types, including motor neuron progenitors (MNPs) and pancreatic islet cells. Although cellular specificity of ISL1 function is likely achieved through combinatorial interactions, its essential cardiac interacting partners are unknown. By assaying ISL1 genomic occupancy in human iPSC-derived cardiac progenitors (CPs) or MNPs and leveraging the deep learning approach BPNet, we identified cell-type-specific motifs of other TFs that predicted ISL1 occupancy in each lineage, with the NKX2.5 motif being most closely associated to ISL1 in CPs. We demonstrated ISL1 forms a protein complex with NKX2.5 in CPs, and the two regulated similar gene networks. NKX2.5 co-occupied more than half of ISL1-bound loci, and ISL1 was dependent on NKX2.5 for CP-specific localization. Furthermore, overexpression of NKX2.5 in MNPs led to ISL1 redistribution to CP-specific loci. These results reveal how ISL1 can guide differential lineage choices through a combinatorial code that dictates genomic occupancy and transcription.

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RNA sequencing of hPSC-derived cardiac progenitors and endocardium

Project description:We utilized a dual reporting hPSC line that identified cells expressing NKX2.5 and endothelal cells to characterize discrete milestones during cardiac and vascular differentiaiton. Comparing populations that express either or both reporters to human umbilical vein endothelial cells, we document a unique molecular phenotype in hPSC-derived endocardium that points toward an important role for Wnt signaling during vascular specification of cardiac progenitors.

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Cardiac differentiation of embryonic stem cells recapitulates embryonic cardiac development.

Project description:Mouse embryonic stem cells can differentiate in vitro into spontaneously contracting cardiomyocytes. The main objective of this study was to investigate cardiogenesis in cultures of differentiating embryonic stem cells (ESCs) and to determine how closely it mimics in vivo cardiac development. We identified and isolated a population of cardiac progenitor cells (CPCs) through the use of a reporter DNA construct that allowed the expression of a selectable marker under the control of the Nkx2.5 enhancer. We proceeded to characterize these CPCs by examining their capacity to differentiate into cardiomyocytes and to proliferate. We then performed a large-scale temporal microarray expression analysis in order to identify genes that are uniquely upregulated or downregulated in the CPC population. We determined that the transcriptional profile of the mESC derived CPCs was consistent with pathways known to be active during embryonic cardiac development. We conclude that in vitro differentiation of mESCs recapitulates the early steps of mouse cardiac development. Keywords: embryonic stem cell, differentiation, cardiac progenitor, cardiogenesis

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Genomic occupancy of TFs ISL1 and NKX2.5 in cardiac and neural populations

Project description:Genomic occupancy of TFs ISL1 and NKX2.5 in cardiac and neural populations

| PRJNA800769 | ENA