Epidermis Kif3a knockout transcriptome reveals genes involved in skin barrier homeostasis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA637026 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11916710.fastq.gz | Fastqsanger.gz | |||
| SRR11916711.fastq.gz | Fastqsanger.gz | |||
| SRR11916712.fastq.gz | Fastqsanger.gz | |||
| SRR11916713.fastq.gz | Fastqsanger.gz | |||
| SRR11916714.fastq.gz | Fastqsanger.gz |
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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.
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Project description:The cross-linked envelope of the mammalian epidermal corneocyte is important as a scaffold for assembly of the lipid barrier of the epidermis. Illustrating its importance, deficient envelope cross-linking by keratinocyte transglutaminase (TGM1) is a major cause of the autosomal recessive congenital ichthyoses, characterized by barrier defects. Expectations that loss of some of the known envelope protein components would also confer an ichthyosis phenotype have been difficult to demonstrate. To help rationalize this observation with one major component, the protein profile of epidermis from loricrin knockout mice has been compared to that of the wild type. Despite the mild phenotype of the knockout, some 40 proteins have been seen to be incorporated into envelope material to significantly different extents. Nearly half of these proteins were also seen to be incorporated to similarly altered extents into the disulfide bonded keratin network of the corneocyte. The results suggest that loss of loricrin alters their incorporation into envelopes as a consequence of protein-protein interactions during cell maturation. Mass spectrometric protein profiling revealed that keratin 1, keratin 10 and filaggrin are prominent envelope components and that dozens of other proteins are minor components. This finding helps rationalize the potential formation of functional envelopes despite loss of a single component due to availability of many alternative transglutaminase substrates.
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