Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA286767 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:TNF ligand ectodysplasin-A1 contributes to embryonic mammary gland development. We searched for target genes of the Eda pathway using profiling of genes differentially expressed in Eda-null mammary buds after a short exposure to recombinant Fc-Eda-A1 protein. Microdissected E13.5 Eda-/- epithelial mammary buds from 5-6 embryos were pooled together. Other half of an embryo was used as a control and the other half as a treated sample. Littermates from 3 litters of B6CBA background were used for the analysis. Array and data analysis were performed in the Biomedicum Functional Genomics Unit (University of Helsinki, Finland).
2015-11-01 | E-GEOD-69781 | biostudies-arrayexpress
Project description:TNF ligand ectodysplasin-A1 contributes to embryonic mammary gland development. We searched for target genes of the Eda pathway using profiling of genes differentially expressed in Eda-null mammary buds after a short exposure to recombinant Fc-Eda-A1 protein.
2015-11-01 | GSE69781 | GEO
Project description:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Keywords: wildtype vs Myc-null
2007-06-30 | GSE7162 | GEO
Project description:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Hearts were taken from wide type and Myc-null Mouse embryos at E13.5 under the dissecting scope. Cardiac myocyte RNA was isolated using TRIZOL®Reagent Total RNA (100 ng) was hybridized to the Sentrix® MouseRef-8 Expression BeadChip that contains probes for ~24,000 transcripts. GeneChips were scanned using the Hewlett-Packard GeneArray Scanner G2500A. The data were analyzed with Illumina Inc. BeadStudio version 1.5.0.34 and normalized by rank invariant method.
2010-06-10 | E-GEOD-7162 | biostudies-arrayexpress
Project description:PGCs undergo two distinct stages of demethylation before reaching a hypomethylated ground state at E13.5. Stage 1 occurs between E7.25- E9.5 in which PGCs experience a global loss of cytosine methylation. However, discreet loci escape this global loss of methylation and between E10.5-E13.5, stage 2 of demethylation takes place. In this stage these loci are targeted by Tet1 and Tet2 leading to the loss of the remaining methylation and resulting in the epigenetic ground state. Our data shows that Dnmt1 is responsible for maintaining the methylation of loci that escape stage 1 demethylation, and that it functions in a UHRF1 independent manner. Our data further demonstrates that when these loci lose methylation prior to stage 2 it results in early activation of the meiotic program, which leads to precocious differentiation of the germ line resulting in a decreased pool of PGCs in the embryo and subsequent infertility in adult mice.
2016-09-13 | GSE74938 | GEO
Project description:Analysis of Gene Expression in PTHrP-/- Mammary Buds
| PRJNA118605 | ENA
Project description:Introgressed variants from other species can be an important source of genetic variation because they may arise rapidly, can include multiple mutations on a single haplotype, and have often been pretested by selection in the species of origin. Although introgressed alleles are generally deleterious, several studies have reported introgression as the source of adaptive alleles-including the rodenticide-resistant variant of Vkorc1 that introgressed from Mus spretus into European populations of Mus musculus domesticus. Here, we conducted bidirectional genome scans to characterize introgressed regions into one wild population of M. spretus from Spain and three wild populations of M. m. domesticus from France, Germany, and Iran. Despite the fact that these species show considerable intrinsic postzygotic reproductive isolation, introgression was observed in all individuals, including in the M. musculus reference genome (GRCm38). Mus spretus individuals had a greater proportion of introgression compared with M. m. domesticus, and within M. m. domesticus, the proportion of introgression decreased with geographic distance from the area of sympatry. Introgression was observed on all autosomes for both species, but not on the X-chromosome in M. m. domesticus, consistent with known X-linked hybrid sterility and inviability genes that have been mapped to the M. spretus X-chromosome. Tract lengths were generally short with a few outliers of up to 2.7 Mb. Interestingly, the longest introgressed tracts were in olfactory receptor regions, and introgressed tracts were significantly enriched for olfactory receptor genes in both species, suggesting that introgression may be a source of functional novelty even between species with high barriers to gene flow.
| S-EPMC8784167 | biostudies-literature
Project description:Gene expression profiling of Foxi3 null embryonic back skin epithelium
| PRJNA284263 | ENA
Project description:In this work we have analyzed the transcriptomic profiles of E13.5 mouse embryonic mammary buds. We show that Hoxd8 and Hoxd9, two gene members of the HoxD cluster, are transcribed during mammary bud development. Yet, unlike in other developmental contexts, their co-expression does not rely upon the same regulatory mechanism. Hoxd8 is regulated by the combined activity of closely located sequences and the most distant telomeric gene desert. On the other hand, Hoxd9 is controlled by an enhancer sequence also located within the telomeric gene desert, but which has no impact on Hoxd8 transcription, thus constituting an exception to the global regulations systematically observed at this locus. The latter DNA region is also involved in Hoxd gene regulation in other contexts and strongly interacts with Hoxd9 in all tissues analyzed so far as well as in other vertebrate species, indicating that its regulatory activity was already operational before the appearance of mammary glands. Within this DNA region and neighboring the CS39 limb enhancer, we further identified a short sequence conserved in therian mammals and capable of enhancer activity in the mammary buds. We propose that Hoxd gene regulation in embryonic mammary buds evolved by hijacking a preexisting regulatory landscape, which was already at work before the emergence of mammals in structures such like the limbs or the intestinal tract.
2016-11-21 | GSE84943 | GEO
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2021-05-05 | PXD022309 | Pride