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Transcriptome changes in Slc7a5-null mouse embryos

ABSTRACT: Transcriptome changes in Slc7a5-null mouse embryos

PROVIDER: PRJEB24323 | ENA |

REPOSITORIES: ENA

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Transcriptome changes in Slc7a5-null mouse embryos

Project description:The effects of loss of the large neutral amino acid transporter Slc7a5 (aka Lat1) on mouse embryonic development were investigated. Slc7a5 fl/fl mice harbouring two copies of the Slc7a5 targeted allele (exon 1 of Slc7a5 flanked with two loxP sites), were crossed with a mouse line ubiquitously expressing cre recombinase under the Bal1 promoter (Bal1-cre) to obtain a global Slc7a5 knockout mouse (Poncet et al. 2014 PLoS One 9: e89547). Heterozygous Slc7a5+/- C57Bl/6 mice were viable and fertile and were bred free of Bal1-cre in subsequent generations. Slc7a5 -/- embryos were obtained by inter-crossing heterozygotes and a phenotype was apparent by E9.5. To identify the first cellular processes affected by Slc7a5 loss RNAseq was carried out to compare transcriptomes of null and wildtype E8.5 embryos.

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Comparative transcriptomic analysis between wild-type (WT) and Cables2-null embryos.

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Metabolomics of the interaction between PPAR-alpha and age in the PPAR-alpha-null mouse (NMR assay)

Project description:Regulation between the fed and fasted state in mammals is partially controlled by peroxisome proliferator activated receptor-alpha (PPAR-alpha). Expression of the receptor is high in liver, heart and skeletal muscle, but decreases with age. A combined 1H NMR spectroscopy and GC-MS metabolomic approach has been used to examine metabolism in liver, heart, skeletal muscle and adipose tissue in PPAR-alpha null mice and wild type controls during ageing between 3-13 months. For the PPAR-alpha-null mouse multivariate statistics highlighted hepatic steatosis, reductions in the concentrations of glucose and glycogen in both liver and muscle tissue, and profound changes in lipid metabolism in each tissue, reflecting known expression targets of the PPAR-alpha receptor. Hepatic glycogen and glucose also decreased with age for both genotypes. These findings indicate the development of age related hepatic steatosis in the PPAR-alpha-null mouse, with the normal metabolic changes associated with ageing exacerbating changes associated with genotype. Furthermore, the combined metabolomic and multivariate statistics approach provides a robust method for examining the interaction between age and genotype. </p> The GC-MS assay for this study can be found in the MetaboLights study MTBLS314.

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