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Mus musculus

ABSTRACT: Transcriptome profile of wildtype and Ret homozygote null mouse guts at E10.5 ,E12.5 and E14.5

PROVIDER: PRJNA400076 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5973200_1.fastq.gz	Fastqsanger.gz
	SRR5973200_2.fastq.gz	Fastqsanger.gz
	SRR5973210_1.fastq.gz	Fastqsanger.gz
	SRR5973210_2.fastq.gz	Fastqsanger.gz
	SRR5973220_1.fastq.gz	Fastqsanger.gz

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Transcriptome profile of wildtype and Ret homozygote null mouse guts at E10.5 ,E12.5 and E14.5

Project description:Total mRNA seq was perfomed on widtype and Ret null mouse embryonic gut at 3 stages of devlopment- E10.5, E12.5 and E14.5

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Testing the Ret and Sema3d genetic interaction in mouse enteric nervous system development

Project description:For most multigenic disorders, clinical manifestation (penetrance) and presentation (expressivity) are likely to be an outcome of genetic interaction between multiple susceptibility genes. Here, using gene knockouts in mice we evaluated genetic interaction between loss of Ret and loss of Sema3d, two Hirschsprung disease (HSCR) susceptibility genes. We intercrossed Ret and Sema3d double null heterozygotes to generate mice with the nine possible genotypes and assessed survival by counting various genotypes, myenteric plexus development by acetylcholinesterase (AchE) staining and embryonic day 12.5 (E12.5) gut transcriptome by RNA-sequencing. Survival rates of Ret wildtype, null heterozygote and null homozygote mice at E12.5, birth and weaning were not influenced by the genotypes at Sema3d locus and vice-versa. Loss of myenteric plexus was observed only in all Ret null homozygotes, irrespective of the genotypes at Sema3d locus, and Sema3d null heterozygote and homozygote mice had normal gut innervation. As compared to wildtype mice gut gene expression, loss of Ret in null homozygotes led to differential expression of ~300 genes, whereas loss of Sema3d in null homozygotes had no major consequence and there was no evidence supporting major interaction between the two genes influencing gut transcriptome. Overall, given the null alleles and phenotypic assays used, we did not find evidence for genetic interaction between Ret and Sema3d affecting survival, myenteric plexus formation or gut transcriptome.

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Single nuclei RNA-seq of mouse placental labyrinth development

Project description:Single nuclei RNA-sequencing of the mouse placenta at four developmental stages (E9.5, E10.5, E12.5, E14.5). Supplementary files include the expression matrices for the integrated datasets containing nuclei from E9.5, E10.5, E12.5, and E14.5 and the clustering annotations for either all nuclei (AllStages_AllNuclei) or subclustered trophoblast nuclei (AllStages_TrophoblastNuclei). Processed data as R objects for both AllStages_AllNuclei and AllStages_TrophoblastNuclei are available at https://figshare.com/projects/Single_nuclei_RNA-seq_of_mouse_placental_labyrinth_development/92354

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Project description:Purpose: The goals of this study are to characterize and analyze the emrbyonic heart transcriptome profiling (RNA-seq) at E9.5, E10.5, E12.5, E14.5 and E16.5. Methods: mRNA profiles of E9.5, E10.5, E12.5, E14.5 and E16.5 C57/Bl6 mouse embryonic hearts were generated by deep sequencing, n=3 or 4 for each age, using Illumina HiSeq2500. Results: Using an optimized data analysis workflow, we mapped at least 36 million sequence reads per sample to the mouse genome (build mm10) and identified 17,537 transcripts in the mouse hearts.

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Transcriptome profile of wildtype and Ret homozygote null male mouse guts at E10.5

Project description:Total mRNA seq was perfomed on widtype and Ret null male mouse embryonic gut at E10.5

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Transcriptome profile of wildtype and Ret homozygote null mouse guts at E11.5 and E12.5

Project description:Total mRNA seq was perfomed on widtype and Ret null mouse embryonic gut at 2 stages of devlopment- E11.5 and E12.5

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Project description:Mice lacking the zinc finger transcription factor Specificity protein 3 (Sp3) die prenatally in the C57Bl/6 background. To elucidate the cause of mortality we analyzed the potential role of Sp3 in embryonic heart development. Sp3 null hearts display defective looping at E10.5, and at E14.5 the Sp3 null mutants have developed a range of severe cardiac malformations. In an attempt to position Sp3 in the cardiac developmental hierarchy, we analysed the expression patterns of >15 marker genes in Sp3 null hearts. Expression of Cardiac ankyrin repeat protein (Carp) was downregulated prematurely after E12.5, while expression of the other marker genes was not affected. ChIP analysis revealed that Sp3 is bound to the Carp promoter region in vivo. Microarray analysis indicates that small molecule metabolism and cell-cell interactions are the most significantly affected biological processes in E12.5 Sp3 null myocardium. Since the epicardium showed distension from the myocardium, we studied expression of Wt1, a marker for epicardial cells. Wt1 expression was diminished in epicardium-derived cells in the myocardium of Sp3 null hearts. We conclude that Sp3 is required for normal cardiac development, and suggest that it has a crucial role in myocardial differentiation. ( Experiment Overall Design: Hearts were dissected from E12.5 wildtype (n=3) and Sp3 knockout (n=3) fetuses. Total RNA was isolated from individual hearts; 5Î¼g was used for labelling and hybridization to 430 2.0 Gene Chips (a total of 6).

2008-06-17 | E-GEOD-9124 | biostudies-arrayexpress

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