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Gene expression profiling of Myf5-Cre;Smad4flox/flox mouse models of tongue development

ABSTRACT: We investigated Smad4-mediated TGF-beta signaling in the development of occipital somite-derived myogenic progenitors during tongue morphogenesis by comparing the transcriptomes of tongue derived from Myf5-Cre;Smad4flox/flox mutant and Myf5-Cre;Smad4flox/+ control mice at day E13.5. Based on gene expression profiles and functional studies, we elucidated the influences Smad4 activity and TGF-beta signaling have on the gene expression profiles underlying tongue development. The data are consistent with the hypothesis that TGF-beta-Smad4-FGF6 signaling cascade plays a crucial role in myogenic cell fate determination and lineage progression during tongue myogenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE35357 | GEO | 2012/02/03

SECONDARY ACCESSION(S): PRJNA152741

REPOSITORIES: GEO

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Gene expression profiling of Myf5-Cre;Smad4flox/flox mouse models of tongue development

Project description:We investigated Smad4-mediated TGF-beta signaling in the development of occipital somite-derived myogenic progenitors during tongue morphogenesis by comparing the transcriptomes of tongue derived from Myf5-Cre;Smad4flox/flox mutant and Myf5-Cre;Smad4flox/+ control mice at day E13.5. Based on gene expression profiles and functional studies, we elucidated the influences Smad4 activity and TGF-beta signaling have on the gene expression profiles underlying tongue development. The data are consistent with the hypothesis that TGF-beta-Smad4-FGF6 signaling cascade plays a crucial role in myogenic cell fate determination and lineage progression during tongue myogenesis. We obtained RNA samples from tongue tissues of mutant and control mouse embryos (C57BL/6J) at day E13.5 RNA and subjected them to analysis on Affymetrix GeneChip Mouse Genome 430 2.0 Arrays.

2012-02-03 | E-GEOD-35357 | biostudies-arrayexpress

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 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.

2013-04-11 | E-GEOD-45968 | biostudies-arrayexpress

MyoD, Myf5, myogenin, or hrGFP expressed in 2C5/7 myoD-/-;myf5-/- fibroblast cells

Project description:Gene expression changes induced by MyoD or Myf5 were examined in a double-knockout fibroblast cell line lacking endogenous functional myoD or myf5 genes. Use of this cell line precluded the possibility of auto- or cross-activation of endogenous myoD or myf5. Myogenin or hrGFP were expressed in parallel samples as controls. Following infection with retrovirus - expressing the relevant myogenic regulatory factor (MRF) from the viral LTR promoter and hrGFP through an IRES element in the same mRNA transcript - GFP+ cells were sorted by FACS and harvested for total RNA. Keywords: other

2005-09-07 | GSE3245 | GEO

Transcription profiling of mouse 2C5/7 myoD-/-;myf5-/- fibroblast cells expressing MyoD, Myf5, myogenin, or hrGFP

2008-06-12 | E-GEOD-3245 | biostudies-arrayexpress

TGF-beta-independent function of SMAD4 preconditions naïve CD8 T-cells to prevent severe microbiota-driven chronic intestinal inflammation [RNAseq]

Project description:SMAD4, a key mediator of TGF-beta signaling, plays a crucial role in T cells to prevent chronic intestinal inflammation through unknown mechanisms. We reveal that SMAD4 in CD8 T cells prevents chronic intestinal inflammation primarily in a TGF-beta-independent manner. Mechanistically, SMAD4, in CD8 T cells, acts as a basal and tonic repressor of TGF-beta-target genes at the transcriptional and epigenetic level, prior to any TGF-beta signal. SMAD4 deletion affects aberrantly a wide range of TGF-beta-target genes, thereby promoting accumulation and epithelial retention of CD8.alpha.beta T cells inversely to total TGF-beta signaling disruption. Moreover, SMAD4 deletion unleashes the expression of TGF-beta-signaling-repressors and hampers TGF-β-mediated CD8 T cell immunosuppression, eliciting their chronic activation. Hence, in a feedforward mechanism, SMAD4 both blocks the TGF-beta signature in CD8 T cells and pre-sensitizes them to TGF-beta.

2022-03-15 | GSE188933 | GEO

TGF-beta-independent function of SMAD4 preconditions naïve CD8 T-cells to prevent severe microbiota-driven chronic intestinal inflammation [ChIPseq]

2022-03-15 | GSE188932 | GEO

Transcription profiling timecourse of induced DACH1 expression in a human breast cancer cell line

Project description:The vertebrate homologues of Drosophila dachsund, DACH1 and DACH2, have been implicated as important regulatory genes in development. DACH1 plays a role in retinal and pituitary precursor cell proliferation and DACH2 plays a specific role in myogenesis. DACH proteins contain a domain (DS-domain) that is conserved with the proto-oncogenes Ski and Sno. Since the Ski/Sno proto-oncogenes repress AP-1 and SMAD signaling, we hypothesized that DACH1 might play a similar cellular function. Herein, DACH1 was found to be expressed in breast cancer cell lines and to inhibit TGF-beta induced apoptosis. DACH1 repressed TGF-beta induction of AP-1 and Smad signaling in gene reporter assays and repressed endogenous TGF-beta responsive genes by microarray analyses. DACH1 bound to endogenous NCoR and Smad4 in cultured cells and DACH1 co-localized with NCoR in nuclear dot-like structures. NCoR enhanced DACH1 repression and the repression of TGF-beta-induced AP-1 or Smad-signaling by DACH1 required the DACH1 DS domain. The DS-domain of DACH was sufficient for NCoR-binding at a Smad4-binding site. Smad4 was required for DACH1 repression of Smad signaling. In Smad4 null HTB-134 cells, DACH1 inhibited the activation of SBE-4 reporter activity induced by Smad2 or Smad3 only in the presence of Smad4. DACH1 participates in the negative regulation of TGF-beta signaling by interacting with NCoR and Smad4.

2007-07-19 | E-GEOD-685 | 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 analyses of SMAD4 knockdown in pancreatic cell line

Project description:The transforming growth factor β (TGF-β) signaling protein SMAD4 is lost in 60% of PDAC, and this has been associated with poorer prognosis. We expressed SMAD4 in human PDAC cell lines BxPC3, by selection of stable clones containing an inducible SMAD4 Tet-ON construct. After 24h of SMAD4 expression, TGF-β signaling-dependent G1-arrest was observed in BxPC3 cells with an increase in the G1-phase fraction from 48.9% to 71.5%. Microarray analysis of gene expression at 8h, 24h, and 48h after SMAD4 expression characterized the regulatory impact of SMAD4 expression in a SMAD4-null PDAC cell line and identified novel targets of TGF-β signaling.

2015-08-20 | GSE70940 | GEO

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