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Motile cilia modulate neuronal and astroglial activity in the zebrafish larval brain

ABSTRACT: Motile cilia modulate neuronal and astroglial activity in the zebrafish larval brain

PROVIDER: PRJNA1068100 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27700027_1.fastq.gz	Fastqsanger.gz
	SRR27700027_2.fastq.gz	Fastqsanger.gz
	SRR27700029_1.fastq.gz	Fastqsanger.gz
	SRR27700029_2.fastq.gz	Fastqsanger.gz
	SRR27700030_1.fastq.gz	Fastqsanger.gz

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Motile cilia modulate neuronal and astroglial activity in the zebrafish larval brain

Project description:The brain uses a specialized system to transport cerebrospinal fluid (CSF), consisting of interconnected ventricles lined by motile ciliated ependymal cells. These cells act jointly with CSF secretion and cardiac pressure gradients to regulate CSF dynamics. To date, the link between cilia-mediated CSF flow and brain function is poorly understood. Using zebrafish larvae as a model system, we identify that loss of ciliary motility does not alter progenitor proliferation, brain morphology, or spontaneous neural activity despite leading to an enlarged telencephalic ventricle. We observe altered neuronal responses to photic stimulations in the optic tectum and hindbrain and brain asymmetry defects in the habenula. Finally, we investigate astroglia since they contact CSF and regulate neuronal activity. Our analyses reveal a reduction in astroglial calcium signals during both spontaneous and light-evoked activity. Our findings highlight a role of motile cilia in regulating brain physiology through the modulation of neural and astroglial networks.

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The Ciliary GTPase ARL13B maintains Ductule Physiology through the Primary and Motile Cilia in Male Reproduction

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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.

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Project description:LC/MS/MS analysis was performed on astroglial exosome samples (3 biological replicates) to identify proteins expressed on the surface of astroglial exosomes. Thes astroglial exosome samples were purified using size-exclusion column from astrocyte conditioned medium (ACM) of primary astrocyte cultures.

2023-08-10 | PXD040650 | Pride

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

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

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