Comparison Between Sost-CreERT2 and wild type Cre- Gastrocnemius Skeletal Muscle Transcriptomes
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ABSTRACT:
PROVIDER: PRJNA490193 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7815360_1.fastq.gz | Fastqsanger.gz | |||
| SRR7815360_2.fastq.gz | Fastqsanger.gz | |||
| SRR7815370_1.fastq.gz | Fastqsanger.gz | |||
| SRR7815370_2.fastq.gz | Fastqsanger.gz | |||
| SRR7815361_1.fastq.gz | Fastqsanger.gz |
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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
Project description:Single cell cortical bone transcriptomics from Sost-Cre enriched cell population.
2023-01-24 | GSE208152 | GEO
Project description:Single Cell Cortical Bone Transcriptomics from Sost-Cre
| PRJNA858479 | ENA
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:RNA Sequencing Analysis of Nestin-creERT2, NG2-creERTM, and Synapsin-cre Tumors
| PRJNA481565 | ENA
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.
2013-08-17 | E-GEOD-44325 | biostudies-arrayexpress
Project description:All current smooth muscle cell (SMC) restricted Cre mice recombine floxed alleles in vascular and visceral SMCs. We generated a tamoxifen-inducible CreERT2 mouse, Itga8-CreERT2, and compared its activity to the widely used Myh11-CreERT2 mouse. Both CreERT2 mice showed similar activity in vascular SMCs; however, Itga8-CreERT2 displayed low activity in visceral SMC-containing tissues (e.g., intestine). Myh11-CreERT2 (but not Itga8-CreERT2) mice exhibited high levels of CreERT2 protein, tamoxifen-independent activity, and an altered transcriptome. Whereas Myh11-CreERT2-mediated knockout of Srf resulted in a lethal intestinal phenotype, loss of Srf with Itga8-CreERT2 (SrfItga8) revealed viable mice with attenuated vascular SMC contractile gene expression, but no evidence of intestinal pathology. Male and female SrfItga8 mice presented with vascular contractile incompetence; however, only male SrfItga8 mice showed systemic changes in blood pressure. These results establish the Itga8-CreERT2 mouse as an alternative to existing SMC Cre strains where gene loss may result in visceral myopathies that obfuscate accurate phenotyping in vascular SMCs.
2022-09-13 | GSE199244 | 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.
2013-08-17 | GSE44325 | GEO
Project description:RNA sequencing of FACS sorted microglia isolated from brain tissue of WT, Hexb-tdTomato, Hexb-CreERT2 and Hexb-KO mice was performed to test for potential differences in gene expression caused by the knock-in of tdTomato and CreERT2 into the Hexb locus.
2020-05-25 | GSE148410 | GEO
Project description:Using genetic fate-mapping with Cux2-Cre and Cux2-CreERT2 mice we demonstrated that the neocortical ventricular zone (VZ) contains radial glial cells (RGCs) with restricted fate potentials (Franco et al., 2012). Using the same mouse lines, Guo et al. (2013) concluded that the neocortical VZ does not contain lineage-restricted RGCs. We now show that the recombination pattern in Cux2-Cre/CreERT2 mice depends on genetic background and breeding strategies. We provide evidence that Guo et al. likely reached different conclusions because they worked with transgenic sublines with drifted transgene expression patterns. In Cux2-Cre and Cux2-CreERT2 mice that recapitulate the endogenous Cux2 expression pattern, the vast majority of fate-mapped neurons express Satb2 but not Ctip2, confirming that a restricted subset of all neocortical projection neurons belongs to the Cux2 lineage. This Matters Arising paper is in response to Guo et al. (2013), published in Neuron. See also the Matters Arising Response paper by Eckler et al. (2015), published concurrently with this Matters Arising in Neuron.
| S-EPMC4455040 | biostudies-literature