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Expression data from adult mouse epidermis upon tamoxifen induced inactivation of Alox12b

ABSTRACT: Expression data from adult mouse epidermis upon tamoxifen induced inactivation of Alox12b

PROVIDER: PRJNA524789 | ENA |

REPOSITORIES: ENA

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Expression data from adult mouse epidermis upon tamoxifen induced inactivation of Alox12b

Project description:Autosomal recessive congenital ichthyoses (ARCI) are a group of non-syndromic congenital keratinization disorders including harlequin ichthyosis, lamellar ichthyosis, and congenital ichthyosiform erythroderma with a total prevalence of 1:200,000. Affected individuals who are often born as collodion babies present with generalized scaling of the skin. This reflects a physical compensation for the defective cutaneous permeability barrier underlying all ichthyoses. Inactivity of 12R-lipoxygenase (12R-LOX) is a frequent cause of ARCI. Epidermis-specific conditional knockout of Alox12b encoding 12R-LOX was established in mice using the Cre-Lox system. Tamoxifen-induced Alox12b inactivation in mouse skin caused an ichthyosis-like phenotype. We used microarray to compare the gene expression profile in the epidermis of mice after tamoxifen induced Alox12b inactivation with that of control animals. Inactivation of Alox12b was associated with the upregulation of genes involved in keratinization, cholesterol biosynthesis, and Fc-epsilon receptor signaling.

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Adult zebrafish: cornea vs epidermis

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Effects on the transcriptome of adult mouse pancreas (principally acinar cells) by the inactivation of the Ptf1a gene in vivo

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ΔNp63 controls stemness and inflammation in the adult epidermis

Project description:The p63 transcription factor is critical for epidermis formation in embryonic development, but its role in the adult epidermis is barely investigated. Here we show that acute genetic ablation of ΔNp63, the main p63 isoform, in the adult epidermis disrupts keratinocyte proliferation and self-maintenance and, unexpectedly, triggers an inflammatory psoriasis-like condition. Mechanistically, single-cell RNA sequencing revealed down-regulation of the cell cycle genes, up-regulation of differentiation markers, and induction of several pro-inflammatory pathways in ΔNp63-ablated keratinocytes. Intriguingly, ΔNp63-ablated cells disappear three weeks post-ablation, at the expense of the remaining non-ablated cells. This was not associated with active cell death mechanisms, but rather with reduced stemness and self-maintenance capacity. Indeed, in vivo wound healing assay, a physiological readout of the epidermal stem cell function, was largely impaired in the ablated skin. We found that the Wnt signaling pathway (Wnt5a, Wnt10a, Fzd6, Fzd10) and Col17a1 are the likely ΔNp63 effectors responsible for keratinocyte proliferation and stemness, while AP1 factors are responsible for excessive differentiation, and Il-1a, Il-18, Il-24 and Il-36γ for the suppression of inflammation. These data implicate ΔNp63 as a critical node that coordinates balanced epidermal homeostasis and suppression of inflammation in the adult epidermis, upstream of known regulatory pathways.

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Molecular consequences of Dlx3 deletion by tamoxifen inducible K14 Cre in adult mouse epidermis (P42-P46) as determined by RNASeq analysis

Project description:Molecular consequences of Dlx3 deletion by tamoxifen inducible K14 Cre in adult mouse epidermis (P42-P46) as determined by RNASeq analysis

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ΔNp63 controls stemness and inflammation in the adult epidermis

Project description:ΔNp63 controls stemness and inflammation in the adult epidermis

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Genes regulated by the winged helix transcription factor Rfx6 in adult beta cell in the mouse

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