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ASH2L mediates epidermal differentiation and hair follicle morphogenesis via the regulation of the Notch signaling pathway activity [CUT&Tag]

ABSTRACT: ASH2L mediates epidermal differentiation and hair follicle morphogenesis via the regulation of the Notch signaling pathway activity [CUT&Tag]

PROVIDER: PRJNA1029952 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26439111_1.fastq.gz	Fastqsanger.gz
	SRR26439111_2.fastq.gz	Fastqsanger.gz
	SRR26439112_1.fastq.gz	Fastqsanger.gz
	SRR26439112_2.fastq.gz	Fastqsanger.gz

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ASH2L mediates epidermal differentiation and hair follicle morphogenesis via the regulation of the Notch signaling pathway activity

Project description:ASH2L mediates epidermal differentiation and hair follicle morphogenesis via the regulation of the Notch signaling pathway activity

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ASH2L mediates epidermal differentiation and hair follicle morphogenesis via the regulation of the Notch signaling pathway activity [RNA-Seq]

Project description:ASH2L mediates epidermal differentiation and hair follicle morphogenesis via the regulation of the Notch signaling pathway activity [RNA-Seq]

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ASH2L mediates epidermal differentiation and hair follicle morphogenesis via the regulation of the Notch signaling pathway activity [CUT&Tag]

Project description:To elucidate the role of H3K4 methylation in epidermal development, we conditionally knocked out ASH2L, the core subunit of the COMPASS complex, in mouse epidermal progenitor (EP) cells. Then, we performed H3K4me3 modification profiling of FACS-sorted integrin α6-positive epidermal progenitor cells in P0 control mice (K14Cre,Ash2lF/+) by CUT&Tag-seq.

2024-03-18 | GSE245773 | GEO

ASH2L mediates epidermal differentiation and hair follicle morphogenesis via the regulation of the Notch signaling pathway activity [RNA-Seq]

Project description:To elucidate the role of H3K4 methylation in epidermal development, we conditionally knocked out the core subunit ASH2L of the COMPASS complex in mouse epidermal progenitor cells (eps). Then, we performed RNA-seq analysis on FACS-classified integrin α6 positive epidermal progenitor cells from P0 control mice (K14Cre,Ash2lF/+) and cKO mice (K14Cre,Ash2lF/ F).

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ASH2L mediates epidermal differentiation and hair follicle morphogenesis via the regulation of the Notch signaling pathway activity

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2024-03-18 | GSE245774 | GEO

Single cell ATAC-seq of mouse hair follicle morphogenesis

Project description:Single cell ATAC-seq of mouse hair follicle morphogenesis

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A single-cell transcriptome atlas during Cashmere goat hair follicle morphogenesis

Project description:Cashmere, also known as soft gold, is produced from secondary hair follicles in Cashmere goats and it’s therefore of significance to investigate the molecular profiles during Cashmere goat hair follicle development. However, our current understanding of the machinery underlying Cashmere goat hair follicle remains largely unexplored and researches regarding hair follicle development mainly used the mouse as a research model. To provides comprehensively understanding on the cellular heterogeneity and cell lineage cell fate decisions, we performed single-cell RNA sequencing on 19,705 single cells from induction (embryonic day 60), organogenesis (embryonic day 90) and cytodifferentiation (embryonic day 120) stage fetus Cashmere goat dorsal skin. Unsupervised clustering analysis identified 16 cell clusters and their corresponding cell types were also successfully characterized. Based on cell lineage inference, we revealed detailed transcriptional gene expression profiles during dermal and epidermal lineage cell fate decisions. These works together delineate unparalleled molecular profiles of different cell populations during Cashmere goat hair follicle morphogenesis and provide a valuable resource for identifying biomarkers during Cashmere goat hair follicle development.

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Less invasive diagnostics for cancer using hair follicle

Project description:Primary outcome(s): Comparison of the gene expression profile in hair follicle between cancer patients and healthy volunteer

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Integrin-linked kinase is required for epidermal and hair follicle morphogenesis.

Project description:Integrin-linked kinase (ILK) links integrins to the actin cytoskeleton and is believed to phosphorylate several target proteins. We report that a keratinocyte-restricted deletion of the ILK gene leads to epidermal defects and hair loss. ILK-deficient epidermal keratinocytes exhibited a pronounced integrin-mediated adhesion defect leading to epidermal detachment and blister formation, disruption of the epidermal-dermal basement membrane, and the translocation of proliferating, integrin-expressing keratinocytes to suprabasal epidermal cell layers. The mutant hair follicles were capable of producing hair shaft and inner root sheath cells and contained stem cells and generated proliferating progenitor cells, which were impaired in their downward migration and hence accumulated in the outer root sheath and failed to replenish the hair matrix. In vitro studies with primary ILK-deficient keratinocytes attributed the migration defect to a reduced migration velocity and an impaired stabilization of the leading-edge lamellipodia, which compromised directional and persistent migration. We conclude that ILK plays important roles for epidermis and hair follicle morphogenesis by modulating integrin-mediated adhesion, actin reorganization, and plasma membrane dynamics in keratinocytes.

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?-parvin is required for epidermal morphogenesis, hair follicle development and basal keratinocyte polarity.

Project description:Epidermal morphogenesis and hair follicle (HF) development depend on the ability of keratinocytes to adhere to the basement membrane (BM) and migrate along the extracellular matrix. Integrins are cell-matrix receptors that control keratinocyte adhesion and migration, and are recognized as major regulators of epidermal homeostasis. How integrins regulate the behavior of keratinocytes during epidermal morphogenesis remains insufficiently understood. Here, we show that ?-parvin (?-pv), a focal adhesion protein that couples integrins to actin cytoskeleton, is indispensable for epidermal morphogenesis and HF development. Inactivation of the murine ?-pv gene in basal keratinocytes results in keratinocyte-BM detachment, epidermal thickening, ectopic keratinocyte proliferation and altered actin cytoskeleton polarization. In vitro, ?-pv-null keratinocytes display reduced adhesion to BM matrix components, aberrant spreading and stress fibers formation, and impaired directed migration. Together, our data demonstrate that ?-pv controls epidermal homeostasis by facilitating integrin-mediated adhesion and actin cytoskeleton organization in keratinocytes.

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