Comparison Between Sost-CreERT2 and wild type Cre- Gastrocnemius Skeletal Muscle Transcriptomes
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PROVIDER: PRJNA490193 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: The purpose of this study is to identify the age when the skeletal muscle phenotype in Sost-CreERT2 mice occurs. Methods: Gastrocnemius skeletal muscle mRNA profiles of 1-month-old Sost-CreERT2 and wild type Cre- male mice and 3-month-old Sost-CreERT2 and wild type Cre- female mice were generated by deep sequencing, in triplicate, using HiSeq4000. The sequencing data were first assessed using FastQC (Babraham Bioinformatics, Cambridge, UK) for quality control. Then all sequenced libraries were mapped to the mm10 mouse genome using STAR RNA-seq aligner with the following parameter: “--outSAMmapqUnique 60”. The reads distribution across the genome was assessed using bamutils (from ngsutils). Uniquely mapped sequencing reads were assigned to mm10 refSeq genes using featureCounts (from subread) with the following parameters: “-s 2 -p –Q 10”. Quality control of sequencing and mapping results was summarized using MultiQC. Genes with read count per million (CPM) > 0.5 in more than 2 of the samples were kept. The data was normalized using TMM (trimmed mean of M values) method. Differential expression analysis was performed using edgeR. False discovery rate (FDR) was computed from p-values using the Benjamini-Hochberg procedure. Results: In the male mice there were 1,857 2fold upregulated genes and 1,959 2fold downregulated genes, whereas in females there were 37 upregulated and 34 downregulated genes. Only 14 upregulated and 21 downregulated genes overlapped between males and females. A pathway analysis of the male gastrocnemius was performed showing that inflammation mediated by chemokine and cytokine signaling pathways was the major upregulated pathway in Sost-CreERT2 as compared to wild type Cre– male mice. The Wnt signaling pathway was the major downregulated pathway in the Sost-CreERT2 male mice.
2018-11-29 | GSE119761 | GEO
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Project description:Single-cell sorted cells from the osteocytic cell line Ocy454 were screened for high- and low-Sost/sclerostin expression to see changes in other gene expressions related to Sost/sclerostin.
2018-08-22 | GSE102958 | GEO
Project description:WNT signaling is critical in most aspects of skeletal development and homeostasis, and antagonists of WNT signaling are emergning as key regulatory proteins with great promise as therapeutic agents for bone disorders. Until recently Sost and its paralog Sostdc1 have been described as growth factors with highly restricted expression in the adult where Sost was assumed 'osteocyte-' and Sostdc1 'kidney-' specific. Here we show that these two proteins emerged throgh ancestral genome duplication and their expression patterns have diverged to span complimentary domains in most organ systems including musculoskeletal, cardiovascular, nervous, digestive, reproductive and respiratory. In the developing limb, Sost and Sostdc1 display dynamic expression patterns with Sost being restricted to the distal ectoderm and Sostdc1 to the proximal ectoderm and the mesenchyme. While Sostdc1-/- mice lack any obvious limb and skeletal defects, Sost-/- mice recapitulate the hand defects described for sclerosteosis patients. However, elevated WNT signaling in Sost-/-; Sostdc1-/- mice causes misregulation of SHH signaling, ectopic activation of Sox9 in the digit 1 field and ultimately preaxial polydactyly. In addition, we show that the syndactyly documented in Sclerosteosis is present in both Sost-/- and Sost-/-; Sostdc1-/- mice, and is driven by misregulation of Fgf8 in the AER, a region lacking Sost and Sostdc1 expression. This study highlights the complexity of WNT signaling in skeletal biology and disease and emphasizes how redundant mechanisms and non-cell autonomous effects can synergize to unveil new intricate phenotypes caused by elevated WNT signaling. Five arrays were analyzed, consisting of two total embryonic fore-limb RNA (experimental) and three total embryonic forelimb RNA (reference) samples at E11.5 DPC mouse (C57Bl6 strain). Embryos were not pooled to generate samples. Each time point has 3 to 5 biological replicates for limb bud samples, duplicates for whole embryos. Comparisons were made between limb bud samples and whole embryo at the same stage, fore-limb samples of different stages, hind-limb samples of different stages, and fore-limb samples compared to hind-limb samples at the same or the next stage.
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Project description:WNT signaling is critical in most aspects of skeletal development and homeostasis, and antagonists of WNT signaling are emergning as key regulatory proteins with great promise as therapeutic agents for bone disorders. Until recently Sost and its paralog Sostdc1 have been described as growth factors with highly restricted expression in the adult where Sost was assumed 'osteocyte-' and Sostdc1 'kidney-' specific. Here we show that these two proteins emerged throgh ancestral genome duplication and their expression patterns have diverged to span complimentary domains in most organ systems including musculoskeletal, cardiovascular, nervous, digestive, reproductive and respiratory. In the developing limb, Sost and Sostdc1 display dynamic expression patterns with Sost being restricted to the distal ectoderm and Sostdc1 to the proximal ectoderm and the mesenchyme. While Sostdc1-/- mice lack any obvious limb and skeletal defects, Sost-/- mice recapitulate the hand defects described for sclerosteosis patients. However, elevated WNT signaling in Sost-/-; Sostdc1-/- mice causes misregulation of SHH signaling, ectopic activation of Sox9 in the digit 1 field and ultimately preaxial polydactyly. In addition, we show that the syndactyly documented in Sclerosteosis is present in both Sost-/- and Sost-/-; Sostdc1-/- mice, and is driven by misregulation of Fgf8 in the AER, a region lacking Sost and Sostdc1 expression. This study highlights the complexity of WNT signaling in skeletal biology and disease and emphasizes how redundant mechanisms and non-cell autonomous effects can synergize to unveil new intricate phenotypes caused by elevated WNT signaling.
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