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Analysis of gene expression in the mouse embryo pharyngeal arch

ABSTRACT: This study was conducted to examine normal gene expression in the pharyngeal arch during mouse embryonic development Wild type embryonic tissue containing the pharyngeal arches was collected from five independent samples (n=5) at stage E10.5 by dissection. Total RNA was isolated for analysis by Affymetrix mouse genome 430A GeneChip.

ORGANISM(S): Mus musculus

SUBMITTER: Jeremy Barth

PROVIDER: E-GEOD-17934 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Jarid2 is among a set of genes differentially regulated by Nkx2.5 during outflow tract morphogenesis.

Barth Jeremy L JL Clark Christopher D CD Fresco Victor M VM Knoll Ellen P EP Lee Benjamin B Argraves W Scott WS Lee Kyu-Ho KH

Developmental dynamics : an official publication of the American Association of Anatomists 20100701 7

Nkx2.5, a transcription factor implicated in human congenital heart disease, is required for regulation of second heart field (SHF) progenitors contributing to outflow tract (OFT). Here, we define a set of 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. Further investigation shows that Jarid2, which has been implicated in OFT morphogenesis, is a direct target ...[more]

PMID: 20549724

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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

Differential gene expression between wild type and Pax9-null pharyngeal arch tissue

Project description:The aim of this study was to identify differentially expressed genes within the pharyngeal arches of Pax9-null embryos at E9.5. Mice null for Pax9 die in the neonatal period with complex cardiovascular defects, caused by abnormal morphogenesis of the pharyngeal arch arteries.

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Analysis of gene expression in the mouse embryo pharyngeal arch

Project description:This study was conducted to examine normal gene expression in the pharyngeal arch during mouse embryonic development

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Gene expression in mouse embryonic heart

Project description:This study was conducted to examine normal gene expression in the heart during mouse embryonic development. Wild type embryo hearts (n=5) were collected at stage E12.5 and total RNA was isolated for analysis by Affymetrix mouse genome 430A GeneChip.

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Single-cell transcriptomics of mouse wildtype and Hoxa2-/- pharyngeal arches 1 and 2 at E10.5.

Project description:The Hox genes play a key role in specifying the axial identity of neural crest cells (NCCs) migrating into the pharyngeal arches of the developing mouse embryo. In the absence of Hoxa2, NCC derivatives of the second pharyngeal arch (PA2) duplicate those formed by NCCs of the first arch (PA1). In this study, we use bulk and single-cell RNAseq to establish the molecular mechanisms driving this phenotypic reversion to a ground state. Comparing the transcriptomes of PA1 and PA2 in wildtype and Hoxa2-/- embryos during NCC migration and differentiation, we find that Hoxa2-/- PA2 does not revert to a molecular ‘ground state’ corresponding to the NCC derivatives. This separation of phenotypic and molecular states has significant implications for our understanding of NCC biology. We also identify putative targets through which HOXA2 likely acts to impart PA2 identity. The heterogenous expression of these targets within the PAs and their responses to the absence of HOXA2 suggest that subsets of NCCs may respond to HOXA2 activity in distinct manners related to their ultimate fate. To understand the heterogeneity of neural crest cells (NCCs) and other tissues of pharyngeal arches (PAs) 1 and 2 in the mouse embryo at E10.5, during NCC differentiation, we collected PA1 and PA2 from wildtype embryos and Hoxa2-/- embryos. We used the 10x Chromium single-cell sequencing system to compare the transcriptional profiles between PA1 and PA2 as well as wildtype and Hoxa2-/- PAs.

2021-02-09 | GSE164108 | GEO

Transcriptomes of mouse wildtype and Hoxa2-/- pharyngeal arches 1 and 2 at E9.0, E9.5, E10.0, and E10.5.

Project description:The Hox genes play a key role in specifying the axial identity of neural crest cells (NCCs) migrating into the pharyngeal arches of the developing mouse embryo. In the absence of Hoxa2, NCC derivatives of the second pharyngeal arch (PA2) duplicate those formed by NCCs of the first arch (PA1). In this study, we use bulk and single-cell RNAseq to establish the molecular mechanisms driving this phenotypic reversion to a ground state. Comparing the transcriptomes of PA1 and PA2 in wildtype and Hoxa2-/- embryos during NCC migration and differentiation, we find that Hoxa2-/- PA2 does not revert to a molecular ‘ground state’ corresponding to the NCC derivatives. This separation of phenotypic and molecular states has significant implications for our understanding of NCC biology. We also identify putative targets through which HOXA2 likely acts to impart PA2 identity. The heterogenous expression of these targets within the PAs and their responses to the absence of HOXA2 suggest that subsets of NCCs may respond to HOXA2 activity in distinct manners related to their ultimate fate. To understand the specification of axial identity in neural crest cells (NCCs), we collected pharyngeal arches (PAs) 1 and 2 from mouse embryos at four time points during NCC migration and the beginning of differentiation (E9.0, E9.5, E10.0, and E10.5). We collected these tissues from both wildtype embryos and embryos homozygous for a mutation abrogating Hoxa2 expression. By performing comparative analysis of these tissues, we set out to understand the molecular underpinnings of NCC axial identity, as well as the mechanistic role of Hoxa2 in establishing PA2 identity.

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scRNA-seq timeline of first pharyngeal arch migratory stream in zebrafish

Project description:scRNA-seq timeline of first pharyngeal arch migratory stream in zebrafish

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Differential gene expression between wild type and Pax9-null pharyngeal arch tissue

Project description:Differential gene expression between wild type and Pax9-null pharyngeal arch tissue

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Transcription profiling following expression of the transcription factor Hoxa2 in first branchial arch cells

Project description:Branchial arches are transient tissue bands in the head region of all vertebrate embryos. Although initially formed from similar components, each arch will give rise to different head and neck structures.<br><br>To understand the molecular control of inter-branchial arch identity, we forced expression of the transcription factor Hoxa2 (the main determinant of second branchial arch fate) in first branchial arch mice cells, and analyzed changes in global expression.<br><br>

2013-12-13 | E-MEXP-3837 | biostudies-arrayexpress

scRNA-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO)

Project description:We performed scRNA-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO). We dissected primarily the cardiac region but also the regions dorsal to the heart and the pharyngeal arches to capture the progenitor cells that migrate into the heart and the neural crest cells. For time points E10.5 and E11.5, we primarily dissected the regions behind the heart and included less of the overall cardiac region. We included pharyngeal arches for all time points and, at E11.5, we excluded the first arch. For Tbx1 null embryos, we also generated scRNA-seq data for WT and mutant embryos from the same pool of dissociated cells used for scATAC-seq.

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