Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA188166 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The aim of this experiment was to investigate the dysregulation of gene expression in whole E12.5 embryos containing a gene trap (CH) or point mutation (H275R) within the Klf3 gene Affymetrix microarrays were performed on RNA from wildtype, Klf3 H275R/H275R, Klf3 H275R/+, Klf3 CH homozygous and Klf3 CH heterozygous E12.5 embryos Four wildtype replicates, three Klf3 H275R/H275R replicates, four Klf3 H275R/+ replicates, four Klf3 CH homozygous replicates and two Klf3 CH heterozygous replicates of whole E12.5 embryos, litter-matched where possible.
2013-01-31 | E-GEOD-43908 | biostudies-arrayexpress
Project description:The aim of this experiment was to investigate the dysregulation of gene expression in whole E12.5 embryos containing a gene trap (CH) or point mutation (H275R) within the Klf3 gene Affymetrix microarrays were performed on RNA from wildtype, Klf3 H275R/H275R, Klf3 H275R/+, Klf3 CH homozygous and Klf3 CH heterozygous E12.5 embryos
2013-01-31 | GSE43908 | GEO
Project description:To study Hnrnpu function during cortical development we preformed single-cell RNA sequencing (scRNA-seq) on mouse neutrosphere cultures derived from E13 ICR cortices, 24 hours following treatment with CRISPR/CAS9 and two sgRNA sequences targeting mouse Hnrnpu. In parallel, we analyzed bulk RNA-seq from dissected cortices of E13 embryos in which Hnrnpu conditional truncation in the telencephalon was driven by Emx1::Cre. Additionally, we analyzed MARS-Seq trancriptomal profiles of cortices of E13 embryos carrying homozygous heterozygous or wildtype alleles of Hnrnpu truncation (Emx1::Cre driver) in combination with homozygous or heterozygous conditional deletion of Tp53
2022-06-07 | GSE181527 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. The Vsx2 homeobox gene is expressed in the newly formed retinal domain during early eye development and mutations in the Vsx2 gene cause congenital microphthalmia. The primary disruptions in the early retina are compromised retinal identity (lineage infidelity), reduced proliferation, and delayed neurogenesis. One goal of the study was to use gene expression profiling to predict genetic interactions between Vsx2 and candidate functional interactors that contribute to the early retinal phenotype of the Vsx2-null mouse strain ocular retardation J (orJ). The orJ allele is a spontaneous, recessive allele caused by the presence of a premature stop codon in the Vsx2 homeodomain. The datasets contained within are from three independent experimental designs. One was to compare the retinal gene expression profiles from E12.5 embryos that are one of three genotypes: the orJ-homozygous mutant, the combinatorial orJ; Mitfmi heterozygous mutant, and the orJ-heterozygous mouse (control). Another analysis was to compare the gene expression profiles of E12.5 orJ-homozygous mutant retinal tissues cultured for 24 hour in the presence or absence of the RXR antagonist HX531. The other analysis was to compare the gene expression profiles of E12.5 orJ-homozygous mutant retinal tissues cultured for 24 hour in the presence or absence of the gamma-Secretase antagonist Dibenzazipine (DBZ).
2023-05-19 | GSE227056 | GEO
Project description:These datasets contain the transcriptomes from E12.5 mouse retinal tissues from embryos carrying three different combinations of the Vsx2 ocular retardation J (orJ) allele and the Mitf mi (mi) allele: orJ-heterozygous, which serves as the control, orJ-homozygous, and orJ-homozygous; mi-heterozygous. The orJ allele is a recessive loss of function and the mi allele is semi-dominant. Mitf is direct target of repression by Vsx2 in the retina and is an established causal factor in the orJ ocular phenotype of microphthalmia. The goal of this analysis was to determine if blocking Mitf function in the orJ mutant would restore retinal gene expression to wild type levels. All libraries were prepared and sequenced together, facilitating direct comparisons of the gene expression profiles across the 3 genotypes.
2023-05-19 | GSE227055 | GEO
Project description:MyD88 is an adaptor protein in Toll-like receptor and interleukin 1 receptor mediated signaling pathways that plays an essential role in activation of immune responses following pathogen recognition. We investigate that role in the zebrafish embryo model by using a zebrafish mutant line that contains a premature stop condon in the gene encoding MyD88, leading to a truncated protein that lacks domains important for its normal function. We infected these MyD88 mutants and wildtype individuals with Salmonella typhimurium and Edwardsiella tarda to compare the resulting immune response by transcriptome profiling on total RNA isolated from single embryos. The data derived from these microarray experiments confirms the vital role of MyD88 in pathogen recognition and provides many leads for further research. This microarray study was designed to determine the effect of a truncation of the MyD88 protein on the innate immune response of zebrafish embryos during infection with Salmonella typhimurium and Edwardsiella tarda. Embryos used in this study are derived from an incross between parents heterozygous for the mutation. Both homozygous mutants and their wildtype siblings were selected by genotyping after being injected with the bacteria or PBS as control. RNA was isolated from single embryos and each treatment group consisted of three embryos: (1) Homozygous mutants injected with PBS 8 hours post infection (hpi), (2) wildtype siblings injected with PBS 8hpi, (3) S. typhimurium-infected homozygous mutants 8hpi, (4) S. typhimurium-infected wildtype siblings 8hpi, (5) Homozygous mutants injected with PBS 8 hours post infection (hpi) (E.tarda control), (6) wildtype siblings injected with PBS 8hpi (E. tarda control), (7) E. tarda-infected homozygous mutants 8hpi, (8) E. tarda-infected wildtype siblings 8hpi. Embryos were grown at 28.5M-bM-^@M-^S30M-BM-0C in egg water and manually dechorionated at 24 hours post fertilization (hpf). Subsequently, embryos were infected at 28 hpf by micro-injecting 200 colony forming units (CFU) of S. typhimurium SL1027 or E. Tarda FL-F60, or were mock-injected with buffer as a control. After injections embryos were transferred into fresh egg water and incubated for 8 h or 4 days at 28M-BM-0C. After the incubation period, single embryos were snap-frozen in liquid nitrogen and RNA was isolated for microarray analysis. All treatment groups were analyzed using a common reference approach.
2012-12-10 | E-GEOD-39274 | biostudies-arrayexpress
Project description:Palb2 interacts with BRCA1 and BRCA2 in supercomplexes involved in DNA repair via homologous recombination. Heterozygous germline mutations in PALB2 confer a moderate risk of breast cancer while biallelic PALB2 mutations are linked to a severe form of Fanconi anaemia characterized by early childhood solid tumours and severe chromosomal instability. In contrast to BRCA1- or BRCA2-associated cancers, breast tumours in heterozygous PALB2 mutation carriers do not show loss of the wild type allele, suggesting PALB2 might be haploinsufficient for tumour suppression. To study the role of PALB2 in development and tumourigenesis, we have generated Palb2GT mouse mutants using a gene trap approach. Whereas Palb2GT/GT homozygous mutant embryos died at mid-gestation due to massive apoptosis, Palb2GT/+ heterozygous mice were viable and did not show any obvious abnormalities. Deletion of p53 alleviated the phenotype of Palb2GT/GT embryos, but did not rescue embryonic lethality. In addition, loss of p53 did not significantly collaborate with Palb2 heterozygosity in tumourigenesis in heterozygous or homozygous p53 knockout mice. Tumours arising in Palb2GT/+;p53+/– or Palb2GT/+;p53–/– compound mutant mice retained the wild type Palb2 allele and did not display increased genomic instability.
2011-01-21 | GSE26723 | GEO
Project description:Palb2 interacts with BRCA1 and BRCA2 in supercomplexes involved in DNA repair via homologous recombination. Heterozygous germline mutations in PALB2 confer a moderate risk of breast cancer while biallelic PALB2 mutations are linked to a severe form of Fanconi anaemia characterized by early childhood solid tumours and severe chromosomal instability. In contrast to BRCA1- or BRCA2-associated cancers, breast tumours in heterozygous PALB2 mutation carriers do not show loss of the wild type allele, suggesting PALB2 might be haploinsufficient for tumour suppression. To study the role of PALB2 in development and tumourigenesis, we have generated Palb2GT mouse mutants using a gene trap approach. Whereas Palb2GT/GT homozygous mutant embryos died at mid-gestation due to massive apoptosis, Palb2GT/+ heterozygous mice were viable and did not show any obvious abnormalities. Deletion of p53 alleviated the phenotype of Palb2GT/GT embryos, but did not rescue embryonic lethality. In addition, loss of p53 did not significantly collaborate with Palb2 heterozygosity in tumourigenesis in heterozygous or homozygous p53 knockout mice. Tumours arising in Palb2GT/+;p53+/– or Palb2GT/+;p53–/– compound mutant mice retained the wild type Palb2 allele and did not display increased genomic instability. Comparison of 15 Palb2GT/+;p53-/- and 11 Palb2+/+;p53-/- lymphomas. Spleen/liver DNA of the same animal was used as reference material.
2011-01-21 | E-GEOD-26723 | biostudies-arrayexpress
Project description:The aim of this experiment was to investigate the role of KLF3 in regulating gene expression at different stages throughout the erythroid maturation process. Affymetrix microarrays were performed on fetal liver cells (both TER119- progenitor cells and TER119+ erythroblast cells) from E14.5 wildtype and Klf3 KO mice. Four wildtype TER119- replicates, four Klf3 KO TER119- replicates, four wildtype TER119+ replicates, three Klf3 KO TER119+ replicates. All are from E14.5 fetal liver.
2012-02-07 | E-GEOD-35592 | biostudies-arrayexpress
Project description:Heterogeneous Tg(hsp70-hRASG12V) embryos were obtained by mating the male homozygous transgenic fish to wildtype females. They were raised to 24 hour-post fertilization (hpf) stage and received heatshock at 37°C in waterbath for one hour, and kept in 28.5°C till 30hpf for RNA extraction. Wildtype embryos receiving the same heatshock treatment were used as controls. Each microarray sample was prepared by pooling 50 embryos and biological duplication was used.
2013-02-16 | GSE44364 | GEO