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Expression data from distinct populations of iMC from the small intestine of Ackr4(+/gfp) mice

ABSTRACT: Mesenchymal cells play key roles in modulating tissue homeostasis in various organs, including the intestine. Here we show that the murine intestinal mesenchymal cells are heterogenous, comprising at least three distinct populations. In this dataset, we include the expression data obtained from sorted subsets of CD45-Ter119-EPCAM-GP38+CD31- murine intestinal mesenchymal cell (iMC) populations. The iMC populations were separated into: CD146+ cells, which expressed CD9 and CD29, but not Ackr4, SCA1, ICAM1 or PDGFRa; GFP+ fibroblasts, which expressed Ackr4, SCA1, ICAM1 and PDGFRa; and GFP- fibroblasts, which also expressed SCA1, ICAM1 and PDGFRa, but were negative for Ackr4 expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE113665 | GEO | 2018/04/26

REPOSITORIES: GEO

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Expression data from distinct populations of iMC from the small intestine of Ackr4(+/gfp) mice

Project description:Expression data from distinct populations of iMC from the small intestine of Ackr4(+/gfp) mice

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Exome Sequencing of Ackr4-deficient mice in generation 12 (backcrossing to C57BL/6)

Project description:Purpose: The goal of this study was to compare exome sequences of Ackr4-deficient mice with C57BL/6 wildtype sequences to understand phenotypic differences which can not be explained by Ackr4-deficiency. Methods: Tail DNA of one wild-type (WT, C57BL/6) and atypical chemokine receptor 4 knockout (Ackr4−/−) mice was sequenced by exome sequencing using an Illumina NovaSeq 6000 sequencing system (2x 100bp). After demultiplexing (Illumina bcl2fastq 2.19) and adapter trimming (Skewer, 0.2.2), the trimmed reads were aligned with to the murine genome (mm10) with Burrows-Wheeler Aligner (BWA-mem 0.7.2-cegat). Reads aligned to multiple sides with the same mapping score were discarded. Further, duplicated reads were removed with SAMtool 0.1.18. Genetic variants were identified with Verscan 2.4.2-cegat and variants with a frequency of ≥ 2% were annotated with SnpEff (version 4.2 with GRCm38.75). Results: 100,000 to 140,000 million sequence reads per mouse were mapped to the mouse genome (build mm10). Each mouse had approx. 20,000 variants (insertions, deletions, SNPs) compared to the reference genome. In Ackr4-/- mice, 3,367 variants were present in both mice analysed, yet not detected in the C57BL/6 mouse used as control. 1781 of these 'shared' variants were present on the chromosome with the targeted Ackr4 allele (Chr9) and predominantly in close proximity to the Ackr4 locus, indicating that these variants originate from the 129-genetic background which was used for targeted mutagenesis during the generation of these mice. Conclusions: Our study shows that Ackr4-/- mice in generation F12 after backcrossing to the C57BL/6 background are still congenic for 129-derived DNA around the targeted Ackr4 locus, indicating that passenger mutations can influence the phenotype of these mice.

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Gene expression signatures of splenic CD31+ACKR4+ and CD31+ACKR4- endothelial cells from Ackr4GFP/wt mice

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