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Expression data of kidney multiciliated cells from zebrafish embryos

ABSTRACT: Multiciliated cells (MCCs) possess multiple motile cilia on the cell surface and are widely distributed throughout the vertebrate body to perform important physiological functions by regulating fluid movement in the intercellular space. However, neither their function during organ development nor the molecular mechanisms underlying multiciliogenesis are yet well understood. We aim to study the function of miR-34b in multiciliogenesis. We used microarrays to study the global gene expression change in multiciliated cells after miR-34b knockdown.

ORGANISM(S): Danio rerio

PROVIDER: GSE46844 | GEO | 2013/05/11

SECONDARY ACCESSION(S): PRJNA202452

REPOSITORIES: GEO

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Expression data of kidney multiciliated cells from zebrafish embryos

Project description:Multiciliated cells (MCCs) possess multiple motile cilia on the cell surface and are widely distributed throughout the vertebrate body to perform important physiological functions by regulating fluid movement in the intercellular space. However, neither their function during organ development nor the molecular mechanisms underlying multiciliogenesis are yet well understood. We aim to study the function of miR-34b in multiciliogenesis. We used microarrays to study the global gene expression change in multiciliated cells after miR-34b knockdown. Multiciliated cells were isolated from 3 dpf control embryos (injected with control morpholino) and miR-34b morphants (injected with miR-34b morpholino) for RNA extraction and hybridization on Affymetrix microarrays. Two independent sets of biological replicates were used.

2013-05-11 | E-GEOD-46844 | biostudies-arrayexpress

MiR-34b regulates multiciliogenesis during organ formation in zebrafish

Project description:Multiciliated cells possess multiple motile cilia on the cell surface and are widely distributed throughout the vertebrate body to perform important physiological functions by regulating fluid movement in the intercellular space. However the molecular mechanisms underlying multiciliogenesis are not well understood. Although dysregulation of members of the miR-34 family plays a critical role in the progression of various cancers, the physiological function of miR-34b, especially in regulating multiciliogenesis, is largely unknown. Here we focus on the multiciliated cells in the zebrafish kidney to study whether and how miR-34b regulate multiciliogenesis. We performed genome-wide gene expression profiling of zebrafish kidney multiciliated cells in the absence (miR-34b morpholino) or presence of miR-34b (control morpholino). RNA samples for microarray gene expression profiling were collected at 3 days post fertilization.

2013-06-14 | E-MEXP-3893 | biostudies-arrayexpress

GEMC1 and MCIDAS interactions with SWI/SNF complexes regulate the multiciliated cell-specific transcriptional program

Project description:Multiciliated cells (MCCs) project dozens to hundreds of motile cilia from their apical surface to promote the movement of fluids or gametes in the mammalian brain, airway or reproductive organs. Differentiation of MCCs requires the sequential action of the Geminin family transcriptional activators, GEMC1 and MCIDAS, that both interact with E2F4/5-DP1. How these factors activate transcription and the extent to which they play redundant functions remains poorly understood. Here, we carried out a transcriptomic analysis to compare the relative influence of GEMC1 and MCIDAS on gene expression.

2023-02-27 | GSE161197 | GEO

Edf1 control multiciliated ependymel cell associated genes expression

Project description:The development and differentiation of Multiciliated ependymal cells are crucial for brain development, with defects leading to conditions such as congenital hydrocephalus. The differentiation of MCCs depends on a unique transcriptional program. Our study shows that Edf1, previously implicated as a transcriptional co-factor, is consistently expressed during MCC development and positively regulates key genes involved in multiciliogenesis and physiological functions.

2023-12-31 | GSE244940 | GEO

RNAseq analysis of Xenopus laevis wildtype and emi2 mutant multiciliated cells during and post differentiation

Project description:Multiciliated cells (MCCs) form when progenitors massively expand centriole number, yielding the hundreds of basal bodies required to extend multiple motile cilia. This organelle biogenesis is promoted transcriptionally by Multicilin acting in a complex with the E2F transcription factors, which activates the expression of genes known to be involved required to form centrioles during the cell cycle, but also requires a cell cycle state required for the centrosome cycle. Multicilin also activates the expression of Emi2 (fbxo43) an inhibitor of the APC/C ubiquitin ligase. In Emi2 mutants, basal body formation during MCCl differentiation is blocked. RNAseq analysis is used to show that gene expression associated with MCC differentiation is upregulated normally in Emi2 mutants, but surprisingly is not downregulated when MCC differentiation is complete. Emi2 is required to promote the centrosomal cycle during MCC differentiation, but then also acts to turn off gene expression associated with centriole biogenesis in differentiated cells.

2024-03-20 | GSE195635 | GEO

Identification of CDC20/CDC20B partners in HEK cells demonstrates that CDC20, but not CDC20B, interacts with multiple APC/C components

Project description:Multiciliated cells (MCCs) harbour dozens to hundreds of motile cilia, which beat in a synchronized and directional manner, thus generating hydrodynamic forces important in animal physiology. In vertebrates, MCC differentiation critically depends on the synthesis and release of numerous centrioles by specialized structures called deuterosomes. Little is known about the composition, organization and regulation of deuterosomes. Here, single-cell RNA sequencing reveals that human deuterosome-stage MCCs are characterized by the expression of many cell cycle-related genes. We further investigated the uncharacterized vertebrate specific cell division cycle 20B (CDC20B) gene, the host gene of microRNA-449abc. We show that the CDC20B protein associates to deuterosomes and is required for the release of centrioles and the subsequent production of cilia in mouse and Xenopus MCCs. CDC20B interacts with PLK1, which has been shown to coordinate centriole disengagement with the protease Separase in mitotic cells. Strikingly, over-expression of Separase rescued centriole disengagement and cilia production in CDC20B-deficient MCCs. This work reveals the shaping of a new biological function, deuterosome-mediated centriole production in vertebrate MCCs, by adaptation of canonical and recently evolved cell cycle-related molecules. A specific aim of this mass spectrometry experiment was to verify on immunoprecipitated protein complexes from CDC20 or CDC20B transfected HEK cells that CDC20, but not CDC20B, interacts with multiple APC/C components.

2019-04-03 | PXD010629 | Pride

Gene expression changes in the respiratory epithelium of miR-34/449 knockout mice

Project description:MicroRNA ablation prevents multiciliogenesis via cell cycle deregulation MicroRNAs (miRNAs) have been implicated in various biological processes but have been most frequently described to inhibit proliferation and tumorigenesis. Here we describe an essential function of the miR-34/449 family during differentiation of multiciliated cells that is mediated by their well-described suppression of cell cycle progression. Constitutive deletion of all six members of this miRNA family triggers a derepression of multiple cell cycle-promoting proteins, thereby preventing epithelial cells from exiting the cell cycle and to maintain in a quiescent state. As a result, formation of motile multicilia is strongly inhibited in several tissues including the respiratory epithelium and the fallopian tube. Consequently, mice lacking miR-34/449 genes display infertility as well as severe chronic airway disease leading to postnatal death. These results show how miRNA-mediated repression of the cell cycle is required to allow multiciliogenesis to proceed during epithelial differentiation.

2017-09-12 | GSE92296 | GEO

Schizophrenia-related microdeletion causes progressive brain ventricle enlargement through microRNA-dependent deceleration of motile cilia beating

Project description:Progressive ventricular enlargement is one of the most reproducible and recognizable structural abnormalities in schizophrenia, and is associated with more severe symptoms and poorer clinical outcome. The mechanisms of ventricular enlargement in schizophrenia is unknown. We identified that progressive ventricular enlargement is associated with deceleration of motile cilia beating in ependymal cells lining ventricular walls in murine models of schizophrenia-associated 22q11 deletion syndrome (22q11DS). The cilia beating deficit is caused by an aberrant elevation of Drd1, which is highly enriched in the motile cilia. Haploinsufficiency of the microRNA-processing gene Dgcr8 is responsible for the Drd1 elevation in ependymal cells of 22q11DS mice, and is mediated by reduction of Drd1-targeting microRNAs miR-674-3p and miR-382-3p. Replenishing miR-674-3p or miR-382-3p in 22q11DS mice rescued the motile cilia beating abnormalities and normalized the ventricular size. Knockdown of these microRNA mimicked cilia beating and ventricular deficits. Ventricular enlargement was also caused by Crispr/cas9-mediated deletion of the Drd1 seed site for miR-674-3p/miR-382-3p. This suggests that Dgcr8-miR-674-3p/miR-382-3p-Drd1–dependent disruption of cilia motility in ependymal cells is a pathogenic event underlying schizophrenia-associated ventricular enlargement.

2019-12-07 | GSE123560 | 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.

2015-12-25 | GSE76342 | GEO

Influenza defective interfering virus promotes multiciliated cell differentiation and reduces the inflammatory response in mice

Project description:Influenza defective interfering (DI) viruses have long been considered promising antiviral candidates because of their ability to interfere with replication-competent viruses and to induce antiviral immunity. However, the mechanisms underlying DI-mediated antiviral immunity have not been extensively explored. Here, we demonstrated interferon (IFN) independent protection conferred by influenza DI virus against homologous virus infection in mice deficient in type I and III IFN signaling. By integrating transcriptional and post-transcriptional regulatory data we identified unique host signatures in response to DI co-infection. DI-treated mice exhibited reduced viral transcription, less intense inflammatory and innate immune responses, and primed multiciliated cell differentiation in their lungs at an early stage of infection, even in the absence of type I or III IFNs. This increased multiciliogenesis could also be detected at the protein level by immunofluorescence staining of lung tissue from DI-treated mice. Overall, our study provides mechanistic insight into the protection mediated by DIs, implying a unifying theme involving inflammation and multiciliogenesis in maintaining respiratory homeostasis, and reveals their IFN-independent antiviral activity.

2023-05-15 | GSE188122 | GEO

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