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Analysis of skin of keratinocyte-specific OTULIN-deficient mice by single-cell RNA-sequencing

ABSTRACT: Analysis of skin of keratinocyte-specific OTULIN-deficient mice by single-cell RNA-sequencing

PROVIDER: PRJNA681782 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13172442.fastq.gz	Fastqsanger.gz
	SRR13172443.fastq.gz	Fastqsanger.gz
	SRR13172444.fastq.gz	Fastqsanger.gz
	SRR13172445.fastq.gz	Fastqsanger.gz
	SRR13172446.fastq.gz	Fastqsanger.gz

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Analysis of skin of keratinocyte-specific OTULIN-deficient mice by single-cell RNA-sequencing

Project description:In order to unravel the functional role of the linear deubiquitinase OTULIN, we performed single-cell RNA-sequencing on total skin of mice lacking OTULIN selectively in keratinocytes. Keratinocyte-specific OTULIN knock-out (KO) mice develop delineated inflammatory lesion. Through single-cell analysis on lesional and non-lesional skin of mice lacking OTULIN in keratinocytes, we could identify signalling pathways through which these inflammatory lesions appear, allowing us to get new insights on the molecular events that regulate skin homeostasis and mediate skin inflammation.

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Analysis of LPS-induced gene expression of OTULIN-deficient murine macrophages by RNA sequencing

Project description:In order to unravel the role of the linear deubiquitinase OTULIN in LPS-induced gene expression in macrophages, we performed RNA-sequencing on primary bone marrow-derived macrophages of mice lacking OTULIN selectively in myeloid cells. Myeloid cell-specific OTULIN knock-out mice develop an auto-inflammatory phenotype and macrophages derived from these mice display increased LPS-induced inflammasome activation and cell death. Through analysing LPS-induced gene expression analyses on OTULIN-deficient macrophages we aimed to identify signalling pathways and genes that regulate inflammasome activation and cell death in these cells, in order to get new insights on the molecular events that regulate the development of autoinflammation in myeloid cell specific OTULIN-deficient mice.

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Project description:We conducted RNA sequencing analysis on skin tissues obtained from spontaneous inflammatory skin lesions in keratinocyte-specific Mettl3 knockout (K14CreERT2;Mettl3fl/fl) mice and their controls (Mettl3fl/fl). In brief, we observed spontaneous skin inflammation in the tail of K14CreERT2;Mettl3fl/fl mice 2-3 weeks following tamoxifen injection. The objective of this study was to investigate the impact and underlying mechanism of Mettl3 in epidermal keratinocytes regarding skin inflammation

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Expression data from keratinocyte-specific Zfp36-deficient mouse skin treated with imiquimod

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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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RNASeq analysis of skin from mice with keratinocyte-specific loss of MCPIP3.

Project description:RNASeq analysis of skin from mice with keratinocyte-specific loss of MCPIP3.

| PRJNA1223806 | ENA