We generated animals carrying a genomically integrated mir-124 promoter::gfp transgene and identified mir-124 promoter::GFP labelled cells as a subset of the C. elegans sensory neurons. We used fluorescence activated cell sorting (FACS) to isolate four distinct cell populations: mir-124 expressing (GFP+) and non-expressing (GFP-) cells from both wild-type and mutant animals. RNA samples obtained from the four cell populations were used for Affymetrix gene expression analysis to study the effect of mir-124 deletion on the transcriptome of mir-124 expressing (GFP+) and non-expressing (GFP-) cells.
The microRNA miR-124 controls gene expression in the sensory nervous system of Caenorhabditis elegans.
Specimen part
View SamplesProspectively isolated and characerized skeletal progenitor lineages
Identification and specification of the mouse skeletal stem cell.
Specimen part
View SamplesProspectively isolated and characerized skeletal progenitor lineages
Identification and specification of the mouse skeletal stem cell.
Specimen part
View SamplesIn order to identify the targets of GATA4-FOG2 action in mammalian heart development we performed Affymetrix microarray comparisons of gene expression in normal and mutant at embryonic (E) day E12.5 hearts. We compared RNA samples from both Fog2-null and Gata4ki/ki mutant E12.5 hearts to the wild-type control E12.5 hearts. We reasoned that as the phenotypes of the Fog2 knockout and Gata4ki/ki mutation (a V217G mutation that specifically cripples the interaction between GATA4 and FOG proteins) are similar, we should expect to identify a similar set of differentially expressed genes in both experiments. As an additional control, we expected to find the Fog2 gene expression absent in the mutant (null) Fog2 cardiac sample, but not Gata4ki/ki sample.
Cardiac expression of Tnnt1 requires the GATA4-FOG2 transcription complex.
Specimen part
View SamplesWe have demonstrated previously that mammalian sexual differentiation requires both GATA4 and FOG2 transcription regulators to assemble the functioning testis. We have now determined that the sexual development of female mice is profoundly affected by the loss of GATA4-FOG2 interaction. We have also identified the Dkk1 gene, encoding a secreted inhibitor of canonical -catenin signaling as a target of GATA4/FOG2 repression in the developing ovary. The tissue-specific ablation of the -catenin gene in the gonads disrupts female development while in the Gata4ki/ki/Dkk1-/- or Fog2-/-/Dkk1-/- embryos the normal ovarian gene expression pattern is partially restored. Control of ovarian development by the GATA4/FOG2 complex presents a novel insight into the crosstalk of transcriptional regulation and extracellular signaling in ovarian development.
Ovarian development in mice requires the GATA4-FOG2 transcription complex.
Specimen part
View SamplesMHCaCre induced knockout of Fog2flox.
Fog2 is critical for cardiac function and maintenance of coronary vasculature in the adult mouse heart.
Sex, Specimen part, Treatment
View SamplesMeig1-deficient mice show male germ cell development defect after they are 28 days old. To understand if the phenotype was caused by altered gene expression due to MEIG1 deficiency, total testicular RNA was isolated from 22 day old and 28 day old wild type and Meig1-deficient mice, microarray was conducted and gene expression was compared between wld-type and Meig1-deficient mice at the two time points.
A MEIG1/PACRG complex in the manchette is essential for building the sperm flagella.
Age, Specimen part
View Samples