Project description:The Mouse Genomes Project ( http://www.sanger.ac.uk/science/data/mouse-genomes-project ) uses using next-generation sequencing technologies to catalogue molecular variation in the common laboratory mouse strains, and a selected set of wild-derived inbred strains. Access to complete sequence of multiple inbred strains will add to these resources and will become a permanent foundation for a systems biology approach to phenotypic variation in the mouse. In this particular study, we have sequenced the transcriptome of whole-brain tissue from 16 laboratory mouse strains to examine differences in gene expression levels, differential RNA-editing, and for use in de novo gene prediction.
Project description:16 dietary protein preparations were digested according to a standardized invitro digestion (InfoGest) protocol, simulating gastrointestinal digestion. Resulting oligopeptide mixtures were subsequently analyzed by UPLC-MS using DDA shot-gun detection. Peak intensity data from MS1 spectra were obtained using Progenesis QI. MS1 peak data were matched and filtered based on overlap with the reference digest of Whey protein using a custom made script in R. MSMS fragmentation spectra were converted to .mgf format and de novo interpreted using SearchGUI 3.3.17 and RapidNOVOR algorithm. Raw data, peak intensity tables and de novo interpretaion data are provided.
Project description:We used an experimental mouse model to further evaluate whether constitutive p53 deficiency in the germ line may increase the rate of de novo CNV in the offspring. C57Bl6 mice with defined trp53 status (either +/+, +/- or -/-) were crossed with 129SvSL trp53+/+ mice and 129SvSL trp53-/- mice were crossed with C57Bl6 trp53+/+ mice. CNV were analyzed in DNA isolated from whole F1 embryos at 17.5 days and compared with liver DNA from their parents. One out of 36 embryo from trp53+/+ parents was detected to have a potential de novo CNV. No de novo CNV was detected in 84 embryos with a p53 deficient parent. These observations suggest that, in this mouse model, partial or complete deficiency of p53 function in the germ line does not increase the rate of CNV formation in the offspring. Affymetrix Mouse Diversity Genotyping Array was performed at The Jackson Lab
