Gene expression-based analysis of neural tube closure for the posterior neuropore of Splotch embryos at E9.5
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ABSTRACT: Three wildtype and three nullizygous embryonic posterior neural tube tissues were collected at embryonic day 9.5 and the gene expression patterns were profiled on CodeLink Mouse Whole Genome Bioarrays. Wild type versus nullizygous Splotch embryonic tissues were compared individually and as separate groups to determine classifiers and differences in expression due to the nullizygous mutation.
Project description:Three wildtype and three nullizygous embryonic posterior neural tube tissues were collected at embryonic day 9.5 and the gene expression patterns were profiled on CodeLink Mouse Whole Genome Bioarrays. Wild type versus nullizygous Fkbp8 embryonic tissues were compared individually and as separate groups to determine classifiers and differences in expression due to the nullizygous mutation.
Project description:Background: Spina bifida is one of the most common and life threatening human congenital defects. Despite considerable effort and investigations, the causes and mechanisms underlying this malformation remain poorly characterized. In order to better understand pathogenesis of this abnormality, we conducted a microarray study to compare gene expression profiles between two mouse models, CLX-Splotch and Fkbp8Gt(neo), that both have spina bifida. Results: To compare the gene expression profiles in these two mouse models we performed microarray analysis using Mouse Whole Genome CodeLink Bioarray. We compared the level of gene expression between wildtype and homozygous mutant embryos in Fkbp8Gt(neo) and CXL-Splotch separately. A total of 54 genes were determined to be differentially expressed (25 down, 29 up) in the posterior neural tube of Fkbp8Gt(neo) mice embryos; while 73 genes were differentially expressed (56 down, 17 up) in the CXL-Splotch mouse. The only two genes that showed decreased expression in both mutants were v-ski sarcoma viral oncogene homolog (Ski) and Zic1, a transcription factor member of the zinc finger family. Interestingly, when Gene Ontology (GO) analysis was performed on all of the differentially expressed genes, there was a striking enrichment of genes associated with mesoderm development and central nervous system development in CLX-Splotch, whereas in Fkbp8Gt(neo) genes involved in dorsal/ventral pattern formation, cell fate specification, and positive regulation of cell differentiation were distinguished. This SuperSeries is composed of the following subset Series: GSE25974: Gene expression-based analysis of neural tube closure for the posterior neuropore of Fkbp8 embryos at E9.5 GSE25975: Gene expression-based analysis of neural tube closure for the posterior neuropore of Splotch embryos at E9.5
Project description:Three wildtype and three nullizygous embryonic posterior neural tube tissues were collected at embryonic day 9.5 and the gene expression patterns were profiled on CodeLink Mouse Whole Genome Bioarrays.
Project description:Three wildtype and three nullizygous embryonic posterior neural tube tissues were collected at embryonic day 9.5 and the gene expression patterns were profiled on CodeLink Mouse Whole Genome Bioarrays.
Project description:Background: Spina bifida is one of the most common and life threatening human congenital defects. Despite considerable effort and investigations, the causes and mechanisms underlying this malformation remain poorly characterized. In order to better understand pathogenesis of this abnormality, we conducted a microarray study to compare gene expression profiles between two mouse models, CLX-Splotch and Fkbp8Gt(neo), that both have spina bifida. Results: To compare the gene expression profiles in these two mouse models we performed microarray analysis using Mouse Whole Genome CodeLink Bioarray. We compared the level of gene expression between wildtype and homozygous mutant embryos in Fkbp8Gt(neo) and CXL-Splotch separately. A total of 54 genes were determined to be differentially expressed (25 down, 29 up) in the posterior neural tube of Fkbp8Gt(neo) mice embryos; while 73 genes were differentially expressed (56 down, 17 up) in the CXL-Splotch mouse. The only two genes that showed decreased expression in both mutants were v-ski sarcoma viral oncogene homolog (Ski) and Zic1, a transcription factor member of the zinc finger family. Interestingly, when Gene Ontology (GO) analysis was performed on all of the differentially expressed genes, there was a striking enrichment of genes associated with mesoderm development and central nervous system development in CLX-Splotch, whereas in Fkbp8Gt(neo) genes involved in dorsal/ventral pattern formation, cell fate specification, and positive regulation of cell differentiation were distinguished. This SuperSeries is composed of the SubSeries listed below.
Project description:Maternal diabetes is a teratogen that can lead to neural tube closure defects in the offspring. We therefore sought to compare gene expression profiles at the site of neural tube closure between stage-matched embryos from normal dams, and embryos from diabetic dams. Neurulation-stage mouse embryos at 8.5 days of gestation were used to prepare neural tissue at the anterior aspect of neural tube closure site 1. Tissue was procured from the open neural tube immediately anterior of the closure site, and from the closed neural tube immediately posterior to the closure site by laser microdissection. For each sample, 10 sections were pooled, total RNA was extracted, and 7 ng of total RNA were used for expression profiling by Tag sequencing using an Applied Biosystems SolidSAGE kit for library construction, and an AB SOLiD 5500 XL instrument for sequencing. Sequence reads were mapped to RefSeq RNA, and count data per gene were obtained using a modified version of the Applied Biosystems SOLiDâ?¢ SAGEâ?¢ Analysis Software. diabetic dam - closed neural tube // diabetic dam - open neural tube // normal dam - closed neural tube // normal dam - open neural tube
Project description:The overall goal of this project is to investigate the role of TGF-beta signaling in epithelial cells as it pertains to the orientation of muscle fibers in the soft palate during embryogenesis. Here, we first conducted gene expression profiling of the anterior and posterior portions of the palate from wild-type mice. In addition, we also conducted gene expression profiling of the posterior palate in mutant mice with an epithelium-specific conditional inactivation of the Tgfbr2 gene. The latter mice provide a model of submucosal cleft palate, which is a congenital birth defect commonly observed in many syndromic conditions. To investigate the adverse effects of dysfunctional TGF-Beta signaling on tissue-tissue interaction between the palatal epithelium and myofibers during palatogenesis, we analyzed mice with an epithelial cell-specific conditional inactivation of Tgfbr2 (Tgfbr2fl/fl;K14-Cre). We performed microarray analyses of anterior palatal tissue and posterior palatal tissue of E15.5 Tgfbr2fl/fl control mice (n=5, each region), and posterior palatal tissue of Tgfbr2fl/fl;K14-Cre mutant mice, collected at embryonic day 15.5 (n=5). Control samples and mutant samples are from separate litters.
Project description:Delta-like 3 (Dll3) is a divergent ligand and modulator of the Notch signaling pathway only identified so far in mammals. Null mutations of Dll3 disrupt cycling expression of Notch targets Hes1, Hes5, and Lfng, but not of Hes7. Compared with Dll1 or Notch1, the effects of Dll3 mutations are less severe for gene expression in the presomitic mesoderm, yet severe segmentation phenotypes and vertebral defects result in both human and mouse. Reasoning that Dll3 specifically disrupts key regulators of somite cycling, we carried out functional analysis to identify targets accounting for the segmental phenotype. Using microdissected embryonic tissue from somitic and presomitic mesodermal tissue, we identified new genes enriched in these tissues, including Limch1, Rphn2, and A130022J15Rik. Surprisingly, we only identified a small number of genes disrupted by the Dll3 mutation. These include Uncx, a somite gene required for rib and vertebral patterning, and Nrarp, a; regulator of Notch/Wnt signaling in zebrafish and a cycling gene in mouse. To determine the effects of Dll3 mutation on Nrarp, we characterized the cycling expression of this gene from early (8.5 dpc) to late (10.5 dpc) somitogenesis. Nrarp displays a distinct pattern of cycling phases when compared to Lfng and Axin2 (a Wnt pathway gene) at 9.5 dpc but appears to be in phase with Lfng by 10.5 dpc. Nrarp cycling appears to require Dll3 but not Lfng modulation. In Dll3 null embryos, Nrarp displayed static patterns. However, in Lfng null embryos, Nrarp appeared static at 8.5 dpc but resumed cycling expression by 9.5 and dynamic expression at 10.5 dpc stages. By contrast, in Wnt3a null embryos, Nrarp expression was completely absent in the presomitic mesoderm. Towards identifying the role of Dll3 in regulating somitogenesis, Nrarp emerges as a potentially important regulator that requires Dll3 but not Lfng for normal function. Experiment Overall Design: To enrich for genes in the somite level tissues that are specifically disrupted by Dll3 mutation, we compared microdissected tissues from wild-type and Dll3 mutant embryos. We generated biological replicate pools from Dll3+/+ (wild-type) or Dll3neo/neo embryos for a total of six pools. Microarray analysis using Affymetrix MOE430A arrays was carried out on the biological pool triplicates for both wild-type and mutant genotypes.
Project description:RNA-sequencing profiling analysis was performed on TS23 humerus tissue from control mice(splotch-delayed). The purpose of this profiling analysis was to identify the transcriptome and expression profile of the developing humerus rudiment and associated joints at embryonic theiler stage 23 (E14.5) during mouse skeletal development.
Project description:Microarray profiling analysis was performed on TS23 humerus tissue from muscle-less mutant (splotch-delayed) mice and compared to control littermates. The purpose of this profiling analysis was to identify differentially expressed genes between muscle-less and control embryonic (TS23) humerus tissue, in order to determine mechanosensitive genes that impact skeletal development.