Gene expression analysis in Pbx1; Emx1-cre mutant cortex at embryonic day 15.5
Ontology highlight
ABSTRACT: the goal of the study was to compare gene expression between control and Pbx1; Emx1-cre mutant corteces at e15.5 E15.5 whole cortex was dissected for the analysis. Control embryo genotype was Pbx1F/+. Mutant embryo genotype was Pbx1F/-; Emx1-cre. 4 corteces of each genotype were used for the analysis: 4 controls and 4 mutants, 8 samples total.
Project description:the goal of the study was to compare gene expression between control and Pbx1; Emx1-cre mutant corteces at e12.5 E12.5 whole cortex was dissected for the analysis. Control embryo genotype was Pbx1F/+. Mutant embryo genotype was Pbx1F/-; Emx1-cre. 4 corteces of each genotype were used for the analysis: 4 controls and 4 mutants, 8 samples total.
Project description:We demonstrate using conditional mutagenesis that Pbx1, with and without Pbx2+/ sensitization, regulates regional identity and laminar patterning of the developing mouse neocortex in cortical progenitors (Emx1-Cre) and in newly generated neurons (Nex1-Cre). Pbx1/2 mutants have three salient molecular phenotypes of cortical regional and laminar organization: hypoplasia of the frontal cortex, ventral expansion of the dorsomedial cortex, and ventral expansion of Reelin expression in the cortical plate of the frontal cortex, concomitant with an inversion of cortical layering in the rostral cortex. Molecular analyses, including PBX ChIP-seq, provide evidence that PBX promotes frontal cortex identity by repressing genes that promote dorsocaudal fate. Chromatin immunoprecipitation was performed using antibody against Pbx1/2/3 (sc-888, Santa Cruz). Wild type E15.5 mouse whole cortex was used for the analysis.
Project description:We demonstrate using conditional mutagenesis that Pbx1, with and without Pbx2+/ sensitization, regulates regional identity and laminar patterning of the developing mouse neocortex in cortical progenitors (Emx1-Cre) and in newly generated neurons (Nex1-Cre). Pbx1/2 mutants have three salient molecular phenotypes of cortical regional and laminar organization: hypoplasia of the frontal cortex, ventral expansion of the dorsomedial cortex, and ventral expansion of Reelin expression in the cortical plate of the frontal cortex, concomitant with an inversion of cortical layering in the rostral cortex. Molecular analyses, including PBX ChIP-seq, provide evidence that PBX promotes frontal cortex identity by repressing genes that promote dorsocaudal fate.
Project description:This is RNA sequencing performed with embryonic day 12 (E12) microdissected mouse cortices with the following genotypes: Emx1 Cre/ +; Zbtb7a +/+ (WT), Emx1 Cre/+; Zbtb7a fl/+ (cHet) and Emx1 Cre/+; Zbtb7a fl/fl (cKO). The goal of this study was to understand the impact ot Zbtb7a knockout during cortical development.
Project description:The mammalian genome contains two ERK/MAP kinase kinase genes, Mek1 and Mek2, which encode dual-specificity kinases responsible for ERK/MAP kinase activation. To define the function of ERK/MAPK signaling pathway in lung development, we performed tissue-specific deletions of Mek1 function in a Mek2 null background. Inactivation of both Mek genes in mesenchyme resulted in several phenotypes including giant omphalocele, skeletal defects, pulmonary hypoplasia, abnormal trachea patterning, and death at birth. Microarray analysis with RNA extracted from lungs of E15.5 Dermo1+/Cre, Mek1+/flox;Mek2-/-;Dermo1+/Cre and Mek1flox/flox;Mek2-/-;Dermo1+/Cre embryos was performed to evaluate the molecular impact of the loss of all Mek alleles in mesenchyme on lung development. . Total RNA was isolated from lungs of E15.5 Dermo1+/Cre embryos (control), from E15.5 Mek1+/flox;Mek2- /-;Dermo1+/Cre embryos (experimental) and from E15.5 Mek1flox/flox;Mek2-/-;Dermo1+/Cre embryos (experimental). Four specimens were analyzed per genotype.
Project description:This is RNA sequencing performed with embryonic day 12 (E12) microdissected mouse cortices with the following genotypes: Emx1 Cre/ +; Zbtb7a +/+ (WT) and Emx1 Cre/+; Zbtb7a fl/fl (cKO). The goal of this study was to understand the impact ot Zbtb7a knockout during cortical development.
Project description:Purpose: Our lab has previously shown that Scleraxis (Scx) is require for proper valve development in vivo. In order to fully explore gene networks regulated by Scx during the vital stages of valve remodeling , high throughput RNA-squencing was performed. Results:There were a total of 18,810 genes were detected. A total of 864 genes were differentially expressed Scx null AVC regions: 645 being upregulated and 217 downregulated. In this data set, we include expression data from atrioventricular canal (AVC) regions from Scx null and wild-type littermate controls at embryonic day 15.5. A total of 6 samples were analyzed; 3 valve regions from E15.5 Scx-/- mice, and 3 from E15.5 Scx+/+ wild-type littermate controls. Differential expression read counts are ranked based on p-value (<0.05).