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Loss of FOXC1 contributes to the corneal epithelial fate switch and pathogenesis

ABSTRACT: Loss of FOXC1 contributes to the corneal epithelial fate switch and pathogenesis

PROVIDER: PRJNA655547 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12396749_1.fastq.gz	Fastqsanger.gz
	SRR12396749_2.fastq.gz	Fastqsanger.gz
	SRR12396750_1.fastq.gz	Fastqsanger.gz
	SRR12396750_2.fastq.gz	Fastqsanger.gz
	SRR12396751_1.fastq.gz	Fastqsanger.gz

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Loss of FOXC1 contributes to the corneal epithelial fate switch and pathogenesis

Project description:Forkhead box C1 (FOXC1) is required for neural crest and ocular development, and mutations in FOXC1 lead to inherited Axenfeld–Rieger syndrome. Here, we find that FOXC1 and paired box 6 (PAX6) are co-expressed in the human limbus and central corneal epithelium. Deficiency of FOXC1 and alternation in epithelial features occur in patients with corneal ulcers. FOXC1 governs the fate of the corneal epithelium by directly binding to lineage-specific open promoters or enhancers marked by H3K4me2. FOXC1 depletion not only activates the keratinization pathway and reprograms corneal epithelial cells into skin-like epithelial cells but also disrupts the collagen metabolic process and interferon signaling pathways. Loss of interferon regulatory factor 1 (IRF1) and PAX6 induced by FOXC1 dysfunction is linked to the corneal ulcer. Collectively, our results reveal a FOXC1-mediated regulatory network responsible for corneal epithelial homeostasis and provide a potential therapeutic target for corneal ulcer.

2021-07-22 | GSE155773 | GEO

Loss of FOXC1 contributes to the corneal epithelial fate switch and pathogenesis.

Project description:Forkhead box C1 (FOXC1) is required for neural crest and ocular development, and mutations in FOXC1 lead to inherited Axenfeld-Rieger syndrome. Here, we find that FOXC1 and paired box 6 (PAX6) are co-expressed in the human limbus and central corneal epithelium. Deficiency of FOXC1 and alternation in epithelial features occur in patients with corneal ulcers. FOXC1 governs the fate of the corneal epithelium by directly binding to lineage-specific open promoters or enhancers marked by H3K4me2. FOXC1 depletion not only activates the keratinization pathway and reprograms corneal epithelial cells into skin-like epithelial cells, but also disrupts the collagen metabolic process and interferon signaling pathways. Loss of interferon regulatory factor 1 and PAX6 induced by FOXC1 dysfunction is linked to the corneal ulcer. Collectively, our results reveal a FOXC1-mediated regulatory network responsible for corneal epithelial homeostasis and provide a potential therapeutic target for corneal ulcer.

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Foxc1 IIBA ChIP-seq

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Project description:Foxc1 has been identified to participate in regulating genes expression directly by binding their promoters as well as playing various roles in signal transduction within the cells. In this study, we found that, in F9 Embryonal Carcinoma cells, Foxc1 repressed the promoter’s transcription activity by binding the region of 1Kb upstream of Transcription Start Site within Nanog promoter.To understand more functions of Foxc1, streptavidin-biotin affinity purification combined with Liquid chromatography electrospray ionization tandem mass spectrometry (LC-ESI-MS/MS) analysis was carried out.Bioinformatic analysis identified 360 proteins which may act as Foxc1 interactors.

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