Ontology highlight
ABSTRACT:
PROVIDER: PRJNA523455 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8599610.fastq.gz | Fastqsanger.gz | |||
| SRR8599610_1.fastq.gz | Fastqsanger.gz | |||
| SRR8599610_2.fastq.gz | Fastqsanger.gz | |||
| SRR8599611.fastq.gz | Fastqsanger.gz | |||
| SRR8599611_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 36 |
Similar Datasets
Project description:Study the role of the LIM-homeodomain transcription factor LHX4 in the development of retinal bipolar cell subtypes
2019-03-05 | GSE127771 | GEO
Project description:Study the role of the LIM-homeodomain transcription factor LHX4 in the development of retinal bipolar cell subtypes
2019-02-23 | GSE126942 | GEO
Project description:Bhlhe23 is a transcription factor that is required for the maturation and survival of retinal rod bipolar cells in mice. In the adult Bhlhe23-/- retina, rod bipolar cells are almost completely absent. We identified genes that were likely to be important to rod bipolar cell maintenance and function by identifying genes that were significantly down-regulated in the transcriptome of adult Bhlhe23-/- mouse retina compared with wild type retina.
2017-09-20 | E-MTAB-6069 | biostudies-arrayexpress
Project description:Bhlhe23 is a transcription factor that is required for the maturation and survival of retinal rod bipolar cells in mice. In the Bhlhe23-/- retina, rod bipolar cells are born in normal numbers, then die by apoptosis from postnatal day 8. We identified genes that were likely to be important to rod bipolar cell development and survival by identifying genes that were significantly differentially expressed in the transcriptome of the Bhlhe23-/- mouse retina compared with wild type retina at postnatal day 7. just before the onset of rob bipolar cell death.
2017-09-20 | E-MTAB-6071 | biostudies-arrayexpress
Project description:To comprehensively profile cell types in the human retina, we performed single cell RNA-sequencing on 20,009 cells obtained post-mortem from three donors and compiled a reference transcriptome atlas. Using unsupervised clustering analysis, we identified 18 transcriptionally distinct clusters representing all known retinal cells: rod photoreceptors, cone photoreceptors, Müller glia cells, bipolar cells, amacrine cells, retinal ganglion cells, horizontal cells, retinal astrocytes and microglia.
2019-08-21 | E-MTAB-7316 | biostudies-arrayexpress
Project description:Multicellular organisms evolved via repeated functional divergence of transcriptionally related sister cell types, but the mechanisms underlying sister cell type divergence are not well understood. Here, we study a canonical pair of sister cell types, retinal photoreceptors and bipolar cells, to identify key cis-regulatory features that mediate the transcriptomic and functional differences between them. We generated open chromatin maps and transcriptome profiles of mouse ON and OFF bipolar cells isolated by fluorescence-activated cell sorting (FACS) and compared them to similar data from rod and cone photoreceptors. We found that photoreceptors and bipolar cells have divergent transcriptional profiles, and yet share remarkably similar cis-regulatory grammars. The predominant cis-regulatory motifs in the enhancers of both cell classes are K50 homeodomain binding sites, which are required for activity. These motifs are bound by two transcription factors (TFs), CRX and OTX2, which are expressed in both photoreceptors and bipolar cells. In contrast, cell type-specific open chromatin regions are distinguished by enrichment of E-box motifs in bipolar cells, and Q50 homeodomain motifs in photoreceptors. In bipolar cells, Q50 motifs are thought to mediate repression of photoreceptor-specific genes through the bipolar-specific TF VSX2. We show that converting selected K50 motifs to Q50 motifs represses reporter expression in bipolar cells, while photoreceptor expression is maintained. These findings suggest that partitioning of Q50 motifs within cell type-specific CREs was likely a critical step in the divergence of the bipolar transcriptome from that of photoreceptors, facilitating the emergence of the complex interneuronal circuitry of the vertebrate retina.
2019-10-16 | GSE131625 | GEO
Project description:Cone photoreceptors are the primary initiator of visual transduction in the human retina. Dysfunction or death of rod photoreceptors precedes cone loss in many retinal and macular degenerative diseases, suggesting a rod-dependent trophic support for cone survival. Rod differentiation and homeostasis are dependent on the basic motif leucine zipper transcription factor NRL. The loss of Nrl in mice (Nrl-/-) results in a retina with predominantly S-opsin containing cones that exhibit molecular and functional characteristics of WT cones. Here we report that Nrl-/- retina undergoes a rapid but transient period of degeneration in early adulthood, with cone apoptosis, retinal detachment, alterations in retinal vessel structure, and activation and translocation of retinal microglia. However, cone degeneration stabilizes by four months of age, resulting in a thinned but intact outer nuclear layer with residual cones expressing S- and M-opsins and a preserved photopic ERG. At this stage, microglia translocate back to the inner retina and reacquire a quiescent morphology. Gene profiling analysis during the period of transient degeneration reveals misregulation of stress response and inflammation genes, implying their involvement in cone death. The Nrl-/- retina illustrates the long-term viability of cones in the absence of rods and may serve as a model for elucidating mechanisms of cone homeostasis and degeneration that would be relevant to understanding diseases of the cone-dominant human macula. Targets were generated from a pair of retinas (one Nrl-/- mouse) per biological replicate. Four biological replicates were generated for each of the five aging timepoints (1, 2, 4, 6, and 10 months post natal).
2011-11-15 | E-GEOD-33674 | biostudies-arrayexpress
Project description:While dysfunction and/or death of light-detecting photoreceptor cells underlies most inherited retinal dystrophies, knowledge of the species-specific details of human rod and cone photoreceptor cell development remains limited. Here, we generate retinal organoids using induced pluripotent stem cells (iPSC) derived from a patient with genetic photoreceptor disease, an isogenic control, and an unrelated control. Organoids were sampled using single-cell RNA sequencing across the developmental window encompassing photoreceptor specification, emergence, and maturation; up to 260 days of in vitro differentiation. Using single-cell transcriptomics data, we reconstruct the rod photoreceptor developmental lineage and identify a branchpoint in development unique to the disease state that gives rise to a divergent rod photoreceptor cell population. We show that the rod-specific transcription factor NR2E3 is required for the proper expression of genes involved in phototransduction, including expression of the light-sensitive protein rhodopsin, which is absent in divergent rods. NR2E3-null rods additionally misexpress several cone-specific phototransduction genes at both the transcript and protein level. Using joint multimodal single-cell sequencing on late-stage retinal organoids, we further identify the specific putative regulatory sites where rod-specific factors act to steer rod and cone photoreceptor cell development. Importantly, these findings are strikingly different than that observed in rodent models of disease. Together, these data provide a roadmap of human photoreceptor development and leverage patient iPSCs to define the specific roles of rod transcription factors in photoreceptor cell emergence and maturation.
2024-04-01 | GSE236197 | GEO
Project description:Cone photoreceptors are the primary initiator of visual transduction in the human retina. Dysfunction or death of rod photoreceptors precedes cone loss in many retinal and macular degenerative diseases, suggesting a rod-dependent trophic support for cone survival. Rod differentiation and homeostasis are dependent on the basic motif leucine zipper transcription factor NRL. The loss of Nrl in mice (Nrl-/-) results in a retina with predominantly S-opsin containing cones that exhibit molecular and functional characteristics of WT cones. Here we report that Nrl-/- retina undergoes a rapid but transient period of degeneration in early adulthood, with cone apoptosis, retinal detachment, alterations in retinal vessel structure, and activation and translocation of retinal microglia. However, cone degeneration stabilizes by four months of age, resulting in a thinned but intact outer nuclear layer with residual cones expressing S- and M-opsins and a preserved photopic ERG. At this stage, microglia translocate back to the inner retina and reacquire a quiescent morphology. Gene profiling analysis during the period of transient degeneration reveals misregulation of stress response and inflammation genes, implying their involvement in cone death. The Nrl-/- retina illustrates the long-term viability of cones in the absence of rods and may serve as a model for elucidating mechanisms of cone homeostasis and degeneration that would be relevant to understanding diseases of the cone-dominant human macula.
2011-11-15 | GSE33674 | GEO
Project description:In inherited retinal disorders such as retinitis pigmentosa (RP), rod photoreceptor-specific mutations cause primary rod degeneration that is followed by secondary cone death and loss of high-acuity vision. Mechanistic studies of retinal degeneration are challenging because of retinal heterogeneity. Moreover, the detection of early cone responses to rod death is especially difficult due to the paucity of cones in the retina. To resolve heterogeneity in the degenerating retina and investigate events in both types of photoreceptors during primary rod degeneration, we utilized droplet-based single-cell RNA sequencing in an RP mouse model, rd10.
2022-04-13 | GSE183206 | GEO