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Next Generation Sequencing of skin from wild-type and ADAM17 cKO (Sox9-Cre x ADAM17fl/fl) mice

ABSTRACT: Next Generation Sequencing of skin from wild-type and ADAM17 cKO (Sox9-Cre x ADAM17fl/fl) mice

PROVIDER: PRJNA421028 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6345750_1.fastq.gz	Fastqsanger.gz
	SRR6345750_2.fastq.gz	Fastqsanger.gz
	SRR6345751_1.fastq.gz	Fastqsanger.gz
	SRR6345751_2.fastq.gz	Fastqsanger.gz
	SRR6345752_1.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing of skin from wild-type and ADAM17 cKO (Sox9-Cre x ADAM17fl/fl) mice

Project description:Purpose: Transcriptomic analysis of ADAM17 cKO mice, a mouse model of atopic dermatitis. Methods: Skin was harvested from 10-week-old wild-type and ADAM17 cKO mice and were subjected to next generation sequencing as described. Results: Of 13,573 genes analyzed by GSA, 2514 differentially expressed genes (DEGs) were detected in ADAM17 cKO skin using a standard definition including both statistically significant change (P-value < 0.01; FDR < 0.05) and effect size (|fold change| > 2) . These DEGs included genes important in lipid metabolism and keratinization, consistent with the understanding of barrier dysfunction in atopic inflammation, as well as significant immunologic pathways in adaptive and innate immunity previously identified in the human AD transcriptome Conclusions: Our study reveals that the transcriptome of ADAM17 cKO mice capture a part of upregulated genes previously observed in human AD skin.

2018-05-01 | GSE107687 | GEO

m6A-seq analysis of Mettl3fl/fl (WT) and Mettl3fl/fl,LyzM-cre (cKO) bone-marrow-derived macrophages(BMDMs) transcriptomes

Project description:To investigate the role of RNA methyltransferase METTL3-mediated m6A modification in macrophage, we performed m6A-sequencing to map the m6A modification in bone-marrow-derived macrophages (BMDMs) from Mettl3fl/fl (WT) and Mettl3fl/fl,LyzM-cre (cKO) mice

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Conditional keratinocyte-specific ADAM17 knockout in mice alters skin homeostasis

Project description:This study investigates the role of ADAM17 (a disintegrin and metalloproteinase 17) in skin homeostasis. Here, we show that mice lacking ADAM17 in keratinocytes have a normal epidermal barrier and skin architecture at birth, but develop pronounced defects in epidermal barrier integrity soon after birth and chronic dermatitis as adults. The dysregulated expression of epidermal differentiation proteins becomes evident 2 days after birth, followed by transepidermal water loss and inflammatory immune cell infiltration. Our results identify a previously unappreciated critical role of the ADAM17/EGFR signaling axis in maintaining the homeostasis of the postnatal epidermal barrier. The genome-wide effects of ADAM17 deficiency were analyzed using Agilent Whole Mouse Genome microarrays. Conditional keratinocyte-specific ADAM17 knockout mice were generated by crossing Adam17flox/flox mice with keratin-14-Cre (Krt14-Cre) transgenic mice. Adam17flox/+Krt14-Cre mice were mated with Adam17flox/flox mice to generate pups of Adam17flox/flox Krt14-Cre positive (cKO) and Krt14-Cre negative (wild-type) control littermates. The genetic background was a mix of 129Sv and C57BL/6. As material, back skin tissue biopsies (postnatal day 10) from n = 2 wild-type skin and n = 2 ADAM17 epidermal KO skin (matched WT-cKO pairs from two different litters) were used in this study.

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m6A-seq analysis of Mettl3fl/fl (WT) and Mettl3fl/fl,LyzM-cre (cKO) bone-marrow-derived macrophages (BMDMs) transcriptomes after co-culturing with MC38 cells

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Identification of Sox9-Regulated Pathways During Early Pancreas Organogenesis

Project description:Sox9 target genes were identified by comparing gene expression in Sox9-ablated versus wild-type pancreata using microarray analysis. Sox9 was conditionally ablated in the developing pancreas via recombination of a Sox9-flox allele (Kist et al., 2002) using the Pdx1-Cre transgene (Gu et al., 2002). Total RNA was isolated and pooled from dorsal pancreatic epithelia of e12.5 Sox9fl/fl; Pdx1-Cre (mutant) versus Sox9fl/fl (wild-type) littermates for three biological replicates.

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