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OTX2 regulatory network and maturation-associated gene programs are inherent barriers to RPE neural competency

ABSTRACT: OTX2 regulatory network and maturation-associated gene programs are inherent barriers to RPE neural competency

PROVIDER: PRJNA812904 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18230016_1.fastq.gz	Fastqsanger.gz
	SRR18230016_2.fastq.gz	Fastqsanger.gz
	SRR18230017_1.fastq.gz	Fastqsanger.gz
	SRR18230017_2.fastq.gz	Fastqsanger.gz
	SRR18230018_1.fastq.gz	Fastqsanger.gz

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Otx2 ChIP-seq in the adult mouse Retinal Pigmented Epithelium (RPE) and neural retina

Project description:Otx2 has been shown to be non cell autonomously required for photoreceptor cell survival in the adult mouse RPE. This study aims to identify Otx2 DNA binding profile in both RPE and neural retina to i) identify direct targets of Otx2 in the RPE ii) compare Otx2 binding profile in neural retina and RPE to unveil hidden functions in the neural retina. WT and GFP antibodies were used to perform two independent ChIP-seq experiments using Illumina GAIIx.

2014-01-15 | E-GEOD-54084 | biostudies-arrayexpress

ChIP-seq analysis of OTX2 in hES-RPE cells

Project description:OTX2 binding sites were profiled in RPE cells generated from human embryonic stem cells (hES-RPE)

2022-11-21 | GSE178165 | GEO

Otx2 ChIP-seq in the adult mouse Retinal Pigmented Epithelium (RPE) and neural retina

2014-01-15 | GSE54084 | GEO

A Stage-Specific OTX2 Regulatory Network and Maturation-Associated Gene Programs Are Inherent Barriers to RPE Neural Competency.

Project description:The retinal pigment epithelium (RPE) exhibits a diverse range of plasticity across vertebrates and is a potential source of cells for the regeneration of retinal neurons. Embryonic amniotes possess a transitory ability to regenerate neural retina through the reprogramming of RPE cells in an FGF-dependent manner. Chicken RPE can regenerate neural retina at embryonic day 4 (E4), but RPE neural competence is lost by embryonic day 5 (E5). To identify mechanisms that underlie loss of regenerative competence, we performed RNA and ATAC sequencing using E4 and E5 chicken RPE, as well as at both stages following retinectomy and FGF2 treatment. We find that genes associated with neural retina fate remain FGF2-inducible in the non-regenerative E5 RPE. Coinciding with fate restriction, RPE cells stably exit the cell cycle and dampen the expression of cell cycle progression genes normally expressed during regeneration, including E2F1. E5 RPE exhibits progressive activation of gene pathways associated with mature function independently of retinectomy or FGF2 treatment, including retinal metabolism, pigmentation synthesis, and ion transport. Moreover, the E5 RPE fails to efficiently repress OTX2 expression in response to FGF2. Predicted OTX2 binding motifs undergo robust accessibility increases in E5 RPE, many of which coincide with putative regulatory elements for genes known to facilitate RPE differentiation and maturation. Together, these results uncover widespread alterations in gene regulation that culminate in the loss of RPE neural competence and implicate OTX2 as a key determinant in solidifying the RPE fate. These results yield valuable insight to the basis of RPE lineage restriction during early development and will be of importance in understanding the varying capacities for RPE-derived retinal regeneration observed among vertebrates.

| S-EPMC9062105 | biostudies-literature

OTX2 regulatory network and maturation-associated gene programs are inherent barriers to RPE neural competency

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

2022-05-11 | GSE197938 | GEO

The LHX2-OTX2 regulatory module controls RPE differentiation and underlies a causal regulatory risk-SNP in age-related macular degeneration

Project description:Tissue-specific transcription factors control the transcriptome through an association with noncoding regulatory regions (cistromes). Identifying the combination of transcription factors that dictate specific cell fate, their specific cistromes and examining their involvement in complex human traits remain a major challenge. Here we focus on the retinal pigmented epithelium (RPE), an essential lineage for retinal development and function and the primary tissue affected in age-related macular degeneration (AMD), a leading cause of blindness. By combining mechanistic findings in stem-cell-derived human RPE, in- vivo functional studies in mice and global transcriptomic and proteomic analyses, we revealed that the key developmental transcription factors LHX2 and OTX2 function together in transcriptional module containing LDB1 and SWI/SNF (BAF) to regulate the RPE transcriptome. Importantly, the intersection between the identified LHX2-OTX2 cistrome with published expression quantitative trait loci, ATAC-seq data from human RPE, and AMD GWAS data, followed by functional validation using a reporter assay, revealed a causal genetic variant that affects AMD risk by altering TRPM1 expression in the RPE through modulation of LHX2 transcriptional activity on its promoter. Taken together, the reported cistrome of LHX2 and OTX2, the identified downstream genes and interacting co-factors reveal the RPE transcription module and uncover a causal regulatory risk SNP in the multifactorial common blinding disease AMD.

2023-03-11 | PXD038485 | Pride

ChIP-seq analysis of OTX2 in hES-RPE cells

Project description:ChIP-seq analysis of OTX2 in hES-RPE cells

| PRJNA737497 | ENA

Adult mouse choroid plexus OTX2 Co-IP

Project description:To analyze OTX2 function in adult choroid plexus, we performed several OTX2 co-immunoprecipitation (co-IP) experiments with mass spectrometry analysis to identify potential protein partners. We previously discovered that OTX2 protein also accumulates non-cell autonomously in subventricular zone (SVZ) and rostral migratory stream (RMS) astrocytes and in visual cortex (VCx) parvalbumin cells. The identification of alternate protein partners in cell-autonomous and non-cell-autonomous contexts would suggest OTX2 takes on specific roles after transferring between cells. In order to test this hypothesis, and to reinforce choroid plexus analysis, we also performed OTX2 co-IP on lysates from adult mouse SVZ, RMS and VCx.

2021-08-23 | PXD021244 | Pride

O-GlcNAcylation and chaperonin CCT5 protect OTX2 from aggregation in medulloblastoma cellsO-GlcNAcylation andanalysis of OTX2 O-GlcNac sites and dependent interactions

Project description:In this study, we demonstrated that OTX2 was transcriptionally and post-transcriptionally regulated by O-GlcNAcylation. We describe the modes of degradation of this essential homeobox protein involving both the proteasome and macroautophagy. While the proteasome remains the canonical degradation pathway, we demonstrated that OTX2 forms oligomers and/or aggregates that are resistant to proteasomal degradation and require macroautophagy. Furthermore, elevated cellular concentration of OTX2 promoted aggregation, OTX2 could either interact with the chaperonin CCT5 or be O-GlcNAcylated at the key residues (S1135/S136/T137) to prevent its oligomerization, suggesting a protective role of O-GlcNAcylation in OTX2 turnover.

2024-01-22 | PXD040353 | Pride

Photoreceptor Otx2 cKO

Project description:Homeobox transcription factor Otx2 is a key actor in retinal development, but in adult stage its function is not yet elucidated. In order to elucidate it we induced Otx2 KO specifically in MATURE PHOTORECEPTORS. Here, we report RNA seq data, that were produced in order to investigate on the effect of Otx2 ablation on its regulatoy network. Post natal day 30 (P30) is the time of KO induction. KO mice were collected 2, 4 and 8 days after Otx2 ablation.

2019-09-28 | GSE138097 | GEO

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