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Differential expression in Zebrafish retinal muller glia under injured and knockout

ABSTRACT: Differential expression in Zebrafish retinal muller glia under injured and knockout

PROVIDER: PRJNA1047494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27010839_1.fastq.gz	Fastqsanger.gz
	SRR27010839_2.fastq.gz	Fastqsanger.gz
	SRR27010840_1.fastq.gz	Fastqsanger.gz
	SRR27010840_2.fastq.gz	Fastqsanger.gz
	SRR27010841_1.fastq.gz	Fastqsanger.gz

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Differential expression in Muller glia of injured zebrafish in a mycb-/- context

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Transcriptome analysis of the uninjured Muller glia (MG) and MG derived retinal progenitors at 4 day post injured zebrafish retina

Project description:The study was aimed at comparing the transcriptome of MG cells of the retina with the progenitors derived from them after an injury. This information will help in the identification of factors that are responsible for the retinal regeneration. Muller glia were isolated by fluorescent activated cell sorting (FACS) using uninjured retinas from transgenice zebrafish (gfap:gfp) where green florescent protein (GFP) is under the control of the glial fibrillary acidic protein (gfap) promoter. MG-derived retinal progenitors were isolated by FACS at 4 days post retinal injury from 1016 tuba1a:gfp transgenic fish where GFP is driven by the tuba1a promoter which is specifically activated in these progenitors. Total RNA was isolated from these cell populations and subjected to microarray analysis to compare their transcriptomes. Samples were prepared in duplicate.

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Differential expression in Muller glia of injured zebrafish in a mycb-/- context

Project description:Differential expression in Muller glia of injured zebrafish in a mycb-/- context

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Project description:In this work we identify genes differentially expressed in Muller glia form uninjured and injured retina with and without apobec2a knockdown

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Project description:In mammals, loss of retinal cells due to disease or trauma is an irreversible process which can lead to blindness. Interestingly, regeneration of retinal neurons is a well-established process in some non-mammalian vertebrates and is driven by the Muller glia (MG), which are able to re-enter the cell cycle and reprogram into neurogenic progenitors upon retinal injury or disease. Progress has been made to restore this mechanism in mammals to promote retinal regeneration: MG can be stimulated to generate new neurons in vivo in the adult mouse retina after the over-expression of the pro-neural transcription factor Ascl1. In this study, we applied the same strategy to reprogram human MG derived from fetal retina and retinal organoids into neurons. Combining scRNA-seq, scATAC-seq, Immunofluorescence, and electrophysiology we demonstrate that human MG can be reprogrammed into neurogenic cells in vitro.

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Differential expression in Zebrafish retinal muller glia under injured and knockout

Project description:This SuperSeries is composed of the SubSeries listed below.

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