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Gene expression profiling of the tongue bud from Alk5 mutant mouse models

ABSTRACT: The overall goal of this project is to investigate the role of TGF-beta signaling in tissue-tissue interactions between myogenic precursors of craniofacial muscles and cranial neural crest cells (CNCCs). Here, we conducted gene expression profiling of the tongue bud from mice at embryonic day E13.5 with a CNCC-specific conditional inactivation of the TGF-beta receptor type 1 gene Alk5. These mice provide a model of microglossia as well as disrupted extraocular and masticatory muscle development, which are congenital birth defects commonly observed in several syndromic conditions.

ORGANISM(S): Mus musculus

PROVIDER: GSE52358 | GEO | 2014/06/18

SECONDARY ACCESSION(S): PRJNA227734

REPOSITORIES: GEO

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Gene expression profiling of the tongue bud from Alk5 mutant mouse models

Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in tissue-tissue interactions between myogenic precursors of craniofacial muscles and cranial neural crest cells (CNCCs). Here, we conducted gene expression profiling of the tongue bud from mice at embryonic day E13.5 with a CNCC-specific conditional inactivation of the TGF-beta receptor type 1 gene Alk5. These mice provide a model of microglossia as well as disrupted extraocular and masticatory muscle development, which are congenital birth defects commonly observed in several syndromic conditions. To investigate the adverse effects of dysfunctional TGF-beta signaling on tissue-tissue interactions between CNCCs and myogenic precursors of craniofacial muscles, we analyzed tongue bud tissue of mice with a CNCC-specific conditional inactivation of Alk5 (Wnt1-Cre; Alk5 fl/fl). We performed microarray analyses of the tongue bud of Alk5 fl/fl control mice and Wnt1-Cre; Alk5 fl/fl mutant mice, collected at embryonic day E13.5 (n=4 per group).

2014-06-18 | E-GEOD-52358 | biostudies-arrayexpress

Gene expression profiling of the mandibular arch from Alk5 mutant mouse models

Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in tissue-tissue interactions between myogenic precursors of craniofacial muscles and cranial neural crest cells (CNCCs). Here, we conducted gene expression profiling of the mandibular arch from mice at embryonic day E11.5 with a CNCC-specific conditional inactivation of the TGF-beta receptor type 1 gene Alk5. These mice provide a model of microglossia as well as disrupted extraocular and masticatory muscle development, which are congenital birth defects commonly observed in several syndromic conditions. To investigate the adverse effects of dysfunctional TGF-beta signaling on tissue-tissue interactions between CNCCs and myogenic precursors of craniofacial muscles, we analyzed mandibular arch tissue of mice with a CNCC-specific conditional inactivation of Alk5 (Wnt1-Cre; Alk5 fl/fl). We performed microarray analyses of the mandibular arch of Alk5 fl/fl control mice and Wnt1-Cre; Alk5 fl/fl mutant mice, collected at embryonic day E11.5 (n=4 per group).

2014-06-18 | E-GEOD-52357 | biostudies-arrayexpress

Gene expression profiling of the mandibular arch from Alk5 mutant mouse models

2014-06-18 | GSE52357 | GEO

Activation of TGF-beta pathway by areca nut constituents: A possible cause of Oral submucous fibrosis.

Project description:To understand the role of areca nut constituents in manifestation of Oral submucous fibrosis, we studied gene expression profile in epithelial cells following areca nut water extract treatment. A comaprison with TGF-beta induced gene expression changes were performed as epithelial cells were predicted to be source of TGF-beta. Control Vs Areca nut 5 ug/ml water extract (5H) (2), Contro Vs TGF-beta (2), Control Vs ALK5 (TbetaRI inhibitor) (2), Control Vs 5H + ALK5 inhibitor (2). (2)- Biological duplicates.

2013-05-22 | E-GEOD-38227 | biostudies-arrayexpress

Gene expression profiling of the tongue in Tgfbr2 mutant mouse models

Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in tongue development in order to study the contribution of cranial neural crest (CNC) cells towards the patterning of cranial mesoderm for proper tongue formation. Here, we conducted gene expression profiling of embryonic tongue tissue from wild type mice as well as those with a neural crest specific conditional inactivation of the Tgfbr2 gene. The latter mice provide a model of microglossia, a common congenital birth defect which is frequently observed with several syndromic conditions. To investigate the mechanism of microglossia resulting from dysfunctional TGF-Beta signaling during muscle development, we analyzed neural crest specific conditional inactivation of Tgfbr2 in mice (Tgfbr2fl/fl;Wnt1-Cre). We performed microarray analyses of tongue tissue of Tgfbr2fl/fl;Wnt1-Cre mutant mice and Tgfbr2fl/fl control mice at embryonic day E14.5 (n=3 per genotype) to examine the genes regulated by Tgf-beta during tongue muscle development.

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Project description:Extraocular Muscle is Defined by a Fundamentally Distinct Gene Expression Profile. Adult mouse extraocular, masticatory, and hindlimb (gastrocnemius/soleus) muscles of adult mice were compared using Affymetrix microarrays. Data form part of publication: Proceedings of the National Academy of Sciences USA 98:12062-12067, 2001. Keywords: parallel sample

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Transcription profiling of mouse extraocular, masticatory, and hindlimb muscles to compare putative muscle allotypes

2007-10-06 | E-GEOD-1062 | biostudies-arrayexpress

Gene expression profiling of the tongue in Tgfbr2 mutant mouse models

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Parallel Genome-Wide CRISPR Screens Clarify Executors of Epithelial-Mesenchymal Transition Mediated Immune resistance to CD8+ T cells

Project description:To investigate the role of tumor epithelial-to-mesenchymal plasticity in CD8+ T cell cytotoxicity, we generated two types of tumor cells with epithelial-like (Epi) or mesenchymal-like (Mes) features through an inducible EMT system. The parental KPC3-OVA cells were transduced with constitutively kinase active ALK5 cDNA (ALK5 CA) in doxycycline-induced system by Nakao et al. and Itoh et al, which initiated TGF-β signaling induced EMT. In this system, we firstly treated cells with TGF-β (5 ng/mL) for 2 days, then removed TGF-β ligands and added doxycycline to sustain cancer cells with mesenchymal feature. We proved the mesenchymal-like phenotype could maintain more than 16 days, which was long enough for all our experiments. Then we performed RNA-seq to investigate the differences between these two types of KPC3-OVA :: Tet-On ALK5 CA cells co-cultured with OT-1 CD8+ T cells or not.

2023-05-16 | GSE215803 | GEO

A multiple super-enhancer region establishes inter-TAD interactions and controls Hoxa function in cranial neural crest [PCHi-C]

Project description:Enhancer-promoter interactions preferentially occur within boundary-insulated topologically associating domains (TADs), limiting inter-TAD interactions. Enhancer clusters in linear proximity, termed super-enhancers (SEs), ensure high target gene expression levels. Little is known about SE topological regulatory impact during craniofacial development. Here, we identified 2232 genome-wide putative SEs in mouse cranial neural crest cells (CNCCs), 147 of which target genes establishing CNCC positional identity during face formation. In second pharyngeal arch (PA2) CNCCs, a multiple SE-containing region, partitioned into Hoxa Inter-TAD Regulatory Element 1 and 2 (HIRE1 and HIRE2), establishes long-range inter-TAD interactions selectively with Hoxa2, that is required for external and middle ear structures. HIRE2 deletion in a Hoxa2 haploinsufficient background results in microtia. HIRE1 deletion phenocopies the full homeotic Hoxa2 knockout phenotype and induces PA3 and PA4 CNCC abnormalities correlating with Hoxa2 and Hoxa3 transcriptional downregulation. Thus, SEs can overcome TAD insulation and regulate anterior Hoxa gene collinear expression in a CNCC subpopulation-specific manner during craniofacial development.

2023-04-28 | GSE211902 | GEO

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