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IL-4 drastically decreases deuterosomal and multiciliated cells via alteration in progenitor cell differentiation

ABSTRACT: IL-4 drastically decreases deuterosomal and multiciliated cells via alteration in progenitor cell differentiation

PROVIDER: PRJNA1028120 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26386513.fastq.gz	Fastqsanger.gz
	SRR26386514.fastq.gz	Fastqsanger.gz
	SRR26386515.fastq.gz	Fastqsanger.gz
	SRR26386516.fastq.gz	Fastqsanger.gz

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IL-4 drastically decreases deuterosomal and multiciliated cells via alteration in progenitor cell differentiation

Project description:Allergic inflammation affects the epithelial cell populations resulting in goblet cell hyperplasia and decreased ciliated cells. In this study, we aimed to investigate the effect of allergic inflammation in nasal epithelial cell transcriptomes at the single-cell level. We performed scRNAseq in cultured primary human nasal epithelial (HNE) cells and in vivo nasal epithelium. The transcriptomic features and epithelial cell subtypes were determined under IL-4 stimulation, and cell-specific marker genes and proteins were identified. We confirmed that cultured HNE cells were similar to in vivo epithelial cells through scRNAseq. Cell-specific marker genes were utilized to cluster the cell subtypes, and FOXJ1+ -ciliated cells were sub-classified into multiciliated and deuterosomal cells. PLK4 and CDC20B were specific for deuterosomal cells, and SNTN, CPASL, and GSTA2 were specific for multiciliated cells. IL-4 altered the proportions of cell subtypes, resulting in a decrease in multiciliated cells and loss of deuterosomal cells. The trajectory analysis revealed deuterosomal cells as precursor cells of multiciliated cells and deuterosomal cells function as a bridge between club and multiciliated cells. A decrease in deuterosomal cell marker genes was observed in nasal tissue samples with type 2 inflammation.The effects of IL-4 appear to be mediated through the loss of the deuterosomal population, resulting in the reduction in multiciliated cells. This study also newly suggests cell-specific markers that might be pivotal for investigating respiratory inflammatory diseases.

2023-11-21 | GSE245392 | GEO

RNAseq profiling of multiciliated cells

Project description:To determine what genes are upregulated in multiciliated cells, we manipulated Xenopus laevis ectoderm to either make more or fewer of this cell type with multiple approaches across multiple timepoints. By finding differentially expressed genes in common across all comparisons in which multiciliated cell number changed, we obtained a robust, but conservative, core group of multiciliated cell genes.

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RNAseq and ChIPseq profiling of Foxn4 and Foxj1 in multiciliated cells

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Edf1 control multiciliated ependymel cell associated genes expression

Project description:Edf1 control multiciliated ependymel cell associated genes expression

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Project description:Multiciliated cells (MCCs) are essential for generating directional fluid flow across specialized epithelia in various vertebrate organs. MCC differentiation involves a unique, tightly regulated program characterized by massive centriole amplification, independently of DNA replication. Although much is known about the transcriptional control of MCC development, insights into proteome dynamics have been limited due to the lack of suitable models. In this study, we report the generation of a stable inducible MCC line, derived from Xenopus laevis A6 kidney epithelial cells. Upon induction of the MCC master regulator Multicilin (MCI), most A6-MCI cells synchronously differentiate into mature MCCs in 48 hours. Using this novel resource, custom antibodies and super-resolution imaging, we could characterize Xenopus deuterosomes, the platforms that allow massive centriole synthesis in vertebrate MCCs. We performed a detailed proteomic profiling throughout MCC differentiation, and uncovered previously uncharacterized regulators. Notably, we highlight a critical role for CDK7 in MCC differentiation in both Xenopus and human systems. Our work provides a valuable resource for mechanistic studies of MCC biology and opens avenues to identify novel therapeutic targets for motile ciliopathies.

2026-02-06 | PXD064476 | Pride

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