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Active DNA demethylation is upstream of rod photoreceptor fate determination and required for retinal development [RNA-Seq]

ABSTRACT: Active DNA demethylation is upstream of rod photoreceptor fate determination and required for retinal development [RNA-Seq]

PROVIDER: PRJNA1216196 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32136467_1.fastq.gz	Fastqsanger.gz
	SRR32136467_2.fastq.gz	Fastqsanger.gz
	SRR32136468_1.fastq.gz	Fastqsanger.gz
	SRR32136468_2.fastq.gz	Fastqsanger.gz
	SRR32136469_1.fastq.gz	Fastqsanger.gz

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Active DNA demethylation is upstream of rod photoreceptor fate determination and required for retinal development [Bisulfite-Seq]

Project description:Active DNA demethylation is upstream of rod photoreceptor fate determination and required for retinal development [Bisulfite-Seq]

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Active DNA demethylation is upstream of rod photoreceptor fate determination and required for retinal development [snRNA-seq]

Project description:Active DNA demethylation is upstream of rod photoreceptor fate determination and required for retinal development [snRNA-seq]

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Active DNA demethylation is upstream of rod photoreceptor fate determination and required for retinal development [Bisulfite-Seq]

Project description:The goal of this study is to investigate the role of TET enzyme-mediated DNA demethylation on retinal development and cell fate specification. We utilized an allelic series of TET enzyme retinal conditional mouse mutants using the Chx10-Cre-GFP transgene, removing the TET enzymes from retinal progenitor cells. We observe that inhibition of DNA demethylation results in abnormal retinal development and a loss of visual function. Immunohistological and genomic profiling (RNA-seq, scRNA-seq, WGBS, and bACE-seq) indicate that rod photoreceptor gene regulatory networks are inhibited when DNA demethylation is lost, indicating that DNA demethylation is required for NRL and NR2E3 expression, resulting in a retina with increased specification of cone photoreceptors.

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Active DNA demethylation is upstream of rod photoreceptor fate determination and required for retinal development [snRNA-seq]

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Active DNA demethylation is upstream of rod photoreceptor fate determination and required for retinal development [RNA-Seq]

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Active DNA demethylation is upstream of rod photoreceptor fate determination and required for retinal development [Human RNA-Seq]

Project description:Active DNA demethylation is upstream of rod photoreceptor fate determination and required for retinal development [Human RNA-Seq]

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The orphan nuclear hormone receptor ERR-beta controls rod photoreceptor survival.

Project description:Mutation of rod photoreceptor-enriched transcription factors is a major cause of inherited blindness. We identified the orphan nuclear hormone receptor ERRÎ² as selectively expressed in rod photoreceptors. Overexpression of ERRÎ² induces expression of rod-specific genes in retinas of both wildtype and in Nrl-/- mice, which lack rod photoreceptors. Mutation of ERRÎ² results in dysfunction and degeneration of rods, while inverse agonists of ERRÎ² trigger rapid rod degeneration, which is rescued by constitutively active mutants of ERRÎ². ERRÎ² coordinates expression of multiple genes that are rate-limiting regulators of ATP generation and consumption in photoreceptors. Furthermore, enhancing ERRÎ² activity rescues photoreceptor defects that result from loss of the photoreceptor-specific transcription factor Crx. Our findings demonstrate that ERRÎ² is a critical regulator of rod photoreceptor function and survival, and suggest that ERRÎ² agonists may be useful in the treatment of certain retinal dystrophies. Affymetrix MOE430 microarrays were used to analyze the expression patterns of P21 mouse retinal tissues. The results were compared across the variable of Genotype, specifically ERRÎ² knockout versus wildtype.

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The orphan nuclear hormone receptor ERRβ controls rod photoreceptor survival.

Project description:Mutation of rod photoreceptor-enriched transcription factors is a major cause of inherited blindness. We identified the orphan nuclear hormone receptor ERRβ as selectively expressed in rod photoreceptors. Overexpression of ERRβ induces expression of rod-specific genes in retinas of both wildtype and in Nrl-/- mice, which lack rod photoreceptors. Mutation of ERRβ results in dysfunction and degeneration of rods, while inverse agonists of ERRβ trigger rapid rod degeneration, which is rescued by constitutively active mutants of ERRβ. ERRβ coordinates expression of multiple genes that are rate-limiting regulators of ATP generation and consumption in photoreceptors. Furthermore, enhancing ERRβ activity rescues photoreceptor defects that result from loss of the photoreceptor-specific transcription factor Crx. Our findings demonstrate that ERRβ is a critical regulator of rod photoreceptor function and survival, and suggest that ERRβ agonists may be useful in the treatment of certain retinal dystrophies.

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Active DNA demethylation is upstream of rod photoreceptor fate determination and required for retinal development [Human RNA-Seq]

Project description:The goal of this study is to investigate the role of TET enzyme-mediated DNA demethylation on retinal development and cell fate specification. We utilized an allelic series of TET enzyme retinal conditional mouse mutants using the Chx10-Cre-GFP transgene, removing the TET enzymes from retinal progenitor cells. We observe that inhibition of DNA demethylation results in abnormal retinal development and a loss of visual function. As human retinoblastoma displays reduced TET3 protein expression and a reduction in 5hmC similar to our TET mutant models, we compare the RNA expression changes across human retinoblastoma and TET mutant retinas to identify common pathways that are altered when 5hmC is lost.

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