Steep Cone Geyser Living, Silicified, and Lithified Biomat
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ABSTRACT:
PROVIDER: PRJNA946768 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: The goals of this study are to evaluate the impact of the removal of the key circadian clock component BMAL1 on the transcriptome of cone photoreceptors Methods: Cone mRNA profiles of adult wild-type (WT, HRGPcre;Bmal1f/+) and cone-specific BMAL1 (HRGPcre;Bmal1f/f or cone-Bmal1−/−) mice were generated by deep sequencing, in triplicate, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays Results: Comparison of the cone transcriptome between cone-Bmal1-/- and wild-type littermates at a single time point (middle of the light phase) revealed 88 genes differentially expressed (P < 0.05, fold change > 2). As expected, these 88 genes included known clock components but also genes known to be involved in a wide range of functions: gene regulation, neuron development and structure, protein binding, and transport. Conclusions: Our study represents the first detailed analysis of cone-BMAL1 transcriptomes, with biologic replicates, generated by RNA-seq technology. These data are consistent with the view that the cone clock controls many aspects of the development, maintenance, and function of the cones through its control of the transcriptome.
2020-08-03 | GSE155550 | GEO
Project description:We determined the accessible genome of postmitotic cone photoreceptors in the central region of the mouse retina on postnatal days P3, P6, and P10. At eachtimepoint we isolated GFP-labeled cells from three different Chrnb4-GFP mice (biological triplicates) using fluorescence-activated cell sorting. We then acquired reads of regions of accessible DNA of the sorted cones using ATAC sequencing. Our data set contained 9 samples.
2017-11-07 | GSE97535 | GEO
Project description:Inherited retinal diseases (IRDs) are a heterogeneous group of blinding disorders, which result in dysfunction or death of the light-sensing cone and rod photoreceptors. Despite individual IRDs being rare, collectively they affect up to 1:2000 people worldwide, causing a significant socioeconomic burden, especially when cone-mediated central vision is affected. This study uses the Pde6ccpfl1 mouse model of achromatopsia, a cone-specific vision loss IRD, to investigate the potential gene-independent therapeutic benefits of a histone demethylase inhibitor GSK-J4 on cone cell survival. We investigated the effects of GSK-J4 treatment on cone cell survival in vivo and ex vivo and changes in cone-specific gene expression via single-cell RNA sequencing. A single intravitreal GSK-J4 injection led to transcriptional changes in pathways involved in mitochondrial dysfunction, endoplasmic reticulum stress, among other key epigenetic pathways, highlighting the complex interplay between methylation and acetylation in healthy and diseased cones. Furthermore, continuous administration of GSK-J4 in retinal explants increased cone survival. Our results suggest that IRD-affected cones respond positively to epigenetic modulation of histones, indicating the potential of this approach in the development of a broad class of novel therapies to slow cone degeneration.
2022-07-20 | GSE195895 | 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:The mechanisms that specify cone photoreceptor cell-fate to short-wave-sensitive (S) versus medium-wave-sensitive (M) cones and maintain their nature are not fully understood. Here we report the importance of the GTF2IRD1 transcription factor in maintaining M cone cell identity and function. In the mouse, GTF2IRD1 is expressed in cell-fate determined photoreceptors at postnatal day 10. GTF2IRD1 binds to the enhancer and promoter regions of mouse M and S opsin genes, but regulates their expression differentially, suppressing S opsin expression and, through interaction with the transcription factors CRX and TR2, enhancing M opsin expression. Null mutation of Gtf2ird1 leads to altered topology of cone opsin expression in the retina, with aberrant S opsin over-expression and M opsin under-expression in M cones. Gtf2ird1 null mice also demonstrate abnormal M cone electrophysiological responses. These findings indicate a dual and specific regulatory role of GTF2IRD1 in maintaining normal M cone-specific gene expression and function.
2014-12-31 | GSE54164 | 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:Retinoblastoma is a childhood retinal tumor that initiates in response to biallelic RB1 inactivation. We show that post-mitotic human cone precursors are uniquely sensitive to the oncogenic effects of Rb depletion. Rb knockdown induced cone precursor proliferation in prospectively isolated populations. SNP-array analysis of two Rb/p130-depleted cone precursor cell lines, revealing no megabase-size loss of heterozygosity (LOH) or copy number alterations (CNAs). SNP-array analysis of one Rb/p130-depleted (tumor 1) or one Rb-depleted (tumor 2) cone precursor-derived tumors, revealing no megabase-size LOH or CNAs, consistent with the lack of DNA copy number alterations in some retinoblastomas. Thus, the cone precursor tumors resembled human retinoblastomas at the molecular cytogenetic level. High resolution SNP-array DNA copy number analyses were performed using CytoScan® HD (Affymetrix, 901835) according to the manufacturer's directions. Data were analyzed using Chromosome Analysis Suite 2.0 (Affymetrix). DNA was extracted from two Rb/p130 depleted cone precursor cell lines and two cryopreserved mouse retinoblastoma samples from eyes xenograted with Rb/p130 or Rb depleted cone precursors. Affymetrix SNP analysis on retinoblastoma cell lines Y79, RB176, and WERI were used as control. Normal human genome 19 was used as reference.
2014-08-25 | E-GEOD-60720 | biostudies-arrayexpress