Project description:We have identified candidate genes from the Feml2 QTL influencing femur length through allele specific expression analysis of growth plates in C57BL/6J x CAST/EiJ F1 hybrids. This work provides the foundation to identify novel genes affecting bone geometry.
Project description:Sequencing files provided here are mouse liver RNA-seq in two mouse strains: C57BL/6J and CAST/EiJ. This is part of a larger study published in PLoS Genetics (2021) "Harnessing natural variation to identify cis regulators of sex-biased gene expression in a multi-strain mouse liver model" that includes DNase-seq and H3K27ac ChIP-seq in mouse liver from the same two strains. This allows us to identify strain-shared ("core") and strain-unique sex-biased genes and enhancers.
Project description:Technical control for allelic detection using Smart-seq3. Liver RNA from pure C57BL6/J and CAST/EiJ strains was combined at varying ratios (0:1, 1:7, 1:3, 3:5, 1:1, 5:3, 3:1, 7:1, 1:0) for a total of 200 pg RNA per sample.
Project description:Sequencing files provided here are mouse liver ChIP-seq for the activating histone mark H3K27ac in two mouse strains: C57BL/6J and CAST/EiJ. This is part of a larger study published in PLoS Genetics (2021) "Harnessing natural variation to identify cis regulators of sex-biased gene expression in a multi-strain mouse liver model" that includes RNA-seq and DNase-seq in mouse liver from the same two strains. This allows us to identify strain-shared ("core") and strain-unique sex-biased genes and enhancers.
Project description:Sequencing files provided here are mouse liver DNase-seq in two mouse strains: C57BL/6J and CAST/EiJ. This is part of a larger study published in PLoS Genetics (2021) "Harnessing natural variation to identify cis regulators of sex-biased gene expression in a multi-strain mouse liver model" that includes RNA-seq and H3K27ac ChIP-seq in mouse liver from the same two strains. This allows us to identify strain-shared ("core") and strain-unique sex-biased genes and enhancers.
Project description:Male C3H/HeOuJ and CAST/EiJ mice were treated with diethylnitrosamine to induce liver tumours. We collected liver samples from untreated P15 mice for control experiments. Liver tissue samples were snap frozen in liquid nitrogen and total RNA was extracted using the AllPrep 96 DNA/RNA Kit (Qiagen) according to the manufacturer’s instructions. Libraries were prepared using the TruSeq Stranded Total RNA Library Prep Kit with Ribo-Zero Gold (Illumina) and sequenced on an Illumna HiSeq4000 to produce 150bp paired-end reads.
Project description:To determine if genetic background can modulate severity of an infection, we studied the host responses to influenza infections in the eight genetically highly diverse Collaborative Cross (CC) founder mice. The CC founder (C57BL/6J, 129S1/SvlmJ, CAST/EiJ, PWK/PhJ) were intranasally infected with influenza A/HK/01/68 (H3N2) with 20μl virus solution (1x101 ffu) or mock infected (with PBS). After infection lung was collected at different time points (mock_d3), d3, d5).
Project description:To determine if genetic background can modulate severity of an infection, we studied the host responses to influenza infections in the eight genetically highly diverse Collaborative Cross (CC) founder mice. The CC founder (C57BL/6J, 129S1/SvlmJ, CAST/EiJ, PWK/PhJ) were intranasally infected with influenza A/HK/01/68 (H3N2) with 20μl virus solution (1x101 ffu) or mock infected (with PBS). After infection lung was collected at different time points (mock_d3), d3, d5).
Project description:We report testis H3K4me3 enrichment in an F1 male from a C57BL/6J (B6) x CAST/Eij (CAST) cross (B6 mother, CAST father). This mouse is heterozygous at PRDM9 for a humanized allele (Davies et al. Nature 2016) and the CAST allele. After filtering of promoter H3K4me3 regions, these data serve as a measure of PRDM9 binding enrichment on each homologue. We found that both crossovers and non-crossovers (observed by sequencing F2/F4/F5 genomic DNA) are depleted at "asymmetric" Double-Strand Break hotspots where PRDM9 primarily binds only one of the two homologues. This proves that PRDM9 plays an important role in promoting inter-homologue interactions and can explain why increasing PRDM9 binding asymmetry predicts hybrid infertility. See Li, Bitoun, Altemose et al. 2018 (pending) for a complete summary.
