Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA389720 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5659450_1.fastq.gz | Fastqsanger.gz | |||
| SRR5659450_2.fastq.gz | Fastqsanger.gz | |||
| SRR5659460_1.fastq.gz | Fastqsanger.gz | |||
| SRR5659460_2.fastq.gz | Fastqsanger.gz | |||
| SRR5659470.fastq.gz | Fastqsanger.gz |
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Project description:We profiled retinal progenitor cells by integrating next generation sequencing methods and interrogating changes in chromatin accessibility at embryonic and post-natal murine stages. We identified putative factors involved in the developmental progression of the retinal progenitors epigenome and we report Lhx2 role in the regulation of chromatin accessibility by coordinated action of developmentally regulated pioneer factors
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Project description:Lhx2 is a retinal progenitor cell transcription factor critical for eye development. We previously reported that conditional inactivation of Lhx2 at the start of mouse retinal neurogenesis disrupted retinal progenitor cell (RPC) proliferation, greatly reduced the RPC pool and altered neurogenic output as indicated by changes in the production of multiple fated precursor populations. To identify genes whose expression levels are dependent on Lhx2 at this stage of development, Lhx2 conditional inactivation was initiated at E11.5 in RPCs with the progenitor Cre driver Hes1CreERT2 and retinal tissue was collected at E15.5 for RNA sequencing. The gene expression profiles of Lhx2 CKO retinas were compared to control (Lhx2 conditional heterozygotes) were compared. Downregulated and upregulated gene expression was observed, with some likely due to direct and indirect regulation by Lhx2 within RPCs and others due to changes in differentiation and the altered neurogenic output.
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Project description:Transitions in competence underlie the ability of CNS progenitors to generate a diversity of neurons and glia. Retinal progenitor cells in mouse generate early-born cell types embryonically and late-born cell types largely postnatally. We find that the transition from early to late progenitor competence is regulated by Jarid2. Loss of Jarid2 results in extended production of early cell types and extended expression of early progenitor genes. Jarid2 can regulate histone modifications, and we find reduction of repressive mark H3K27me3 on a subset of early progenitor genes with loss of Jarid2, most notably Foxp1. We show that Foxp1 regulates the competence to generate early-born retinal cell types, promotes early and represses late progenitor gene expression, and is required for extending early retinal cell production after loss of Jarid2. We conclude Jarid2 facilitates progression of retinal progenitor temporal identity by repressing Foxp1, which is a primary regulator of early temporal patterning.
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Project description:Transitions in competence underlie the ability of CNS progenitors to generate a diversity of neurons and glia. Retinal progenitor cells in mouse generate early-born cell types embryonically and late-born cell types largely postnatally. We find that the transition from early to late progenitor competence is regulated by Jarid2. Loss of Jarid2 results in extended production of early cell types and extended expression of early progenitor genes. Jarid2 can regulate histone modifications, and we find reduction of repressive mark H3K27me3 on a subset of early progenitor genes with loss of Jarid2, most notably Foxp1. We show that Foxp1 regulates the competence to generate early-born retinal cell types, promotes early and represses late progenitor gene expression, and is required for extending early retinal cell production after loss of Jarid2. We conclude Jarid2 facilitates progression of retinal progenitor temporal identity by repressing Foxp1, which is a primary regulator of early temporal patterning.
2023-02-15 | GSE222955 | GEO
Project description:Transitions in competence underlie the ability of CNS progenitors to generate a diversity of neurons and glia. Retinal progenitor cells in mouse generate early-born cell types embryonically and late-born cell types largely postnatally. We find that the transition from early to late progenitor competence is regulated by Jarid2. Loss of Jarid2 results in extended production of early cell types and extended expression of early progenitor genes. Jarid2 can regulate histone modifications, and we find reduction of repressive mark H3K27me3 on a subset of early progenitor genes with loss of Jarid2, most notably Foxp1. We show that Foxp1 regulates the competence to generate early-born retinal cell types, promotes early and represses late progenitor gene expression, and is required for extending early retinal cell production after loss of Jarid2. We conclude Jarid2 facilitates progression of retinal progenitor temporal identity by repressing Foxp1, which is a primary regulator of early temporal patterning.
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Project description:Transitions in competence underlie the ability of CNS progenitors to generate a diversity of neurons and glia. Retinal progenitor cells in mouse generate early-born cell types embryonically and late-born cell types largely postnatally. We find that the transition from early to late progenitor competence is regulated by Jarid2. Loss of Jarid2 results in extended production of early cell types and extended expression of early progenitor genes. Jarid2 can regulate histone modifications, and we find reduction of repressive mark H3K27me3 on a subset of early progenitor genes with loss of Jarid2, most notably Foxp1. We show that Foxp1 regulates the competence to generate early-born retinal cell types, promotes early and represses late progenitor gene expression, and is required for extending early retinal cell production after loss of Jarid2. We conclude Jarid2 facilitates progression of retinal progenitor temporal identity by repressing Foxp1, which is a primary regulator of early temporal patterning.
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Project description:During retinal development, neurons and glia are produced in a highly stereotyped and evolutionarily conserved birth order. Landmark studies have demonstrated that the sequence of cell production is temporally encoded. Transcription factors and heterochromatic determinants have been elsewhere implicated in the temporal regulation of progenitor competence states, but the underlying mechanisms are not well understood. Since chromatin remodelling complexes interact with both transcription factors and heterochromatic complexes such as polycomb, we focused on the nucleosome remodeller Chd4. We generated conditional knockouts (cKOs) of Chd4 – a key chromatin remodelling enzyme in neural progenitors. Chd4 cKOs exhibited a marked expansion in early-born retinal ganglion cells. Postnatally, rod photoreceptors were drastically underproduced. As a result, progenitors failed to be exhausted during late phases of development, leading to a striking increase in the production of Müller glia. Clonal retroviral lineaging and histological marker analyses suggest that these effects were independent of alterations in cell death or proliferation. Next, we examined the effect of Chd4 on the genome and transcriptome, focusing on retinal progenitors at P0/P1. Multi-seq single-cell transcriptomics demonstrated that deletion of Chd4 created divergent gene expression profiles and developmental trajectories. ATAC-seq experiments performed on sorted P1 retinal progenitors revealed that chromatin accessibility was significantly increased at ~10 000 enhancer elements and ~4000 genes in the Chd4 cKO, demonstrating that Chd4 is required to repress gene expression and genome accessibility. Finally, to determine whether Chd4 regulates retinal cell-type production by altering competence windows, we performed EdU birthdating. These experiments revealed that cell fates were altered without affecting competence windows. Thus, despite a very strong shift in the production of early-born and late-born cell types, our data suggest that chromatin remodelling does not directly regulate competence windows.
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Project description:The histone methyltransferase complex PRC2 controls key steps in developmental transitions and cell fate choices. However, its roles in vertebrate eye development remain unknown. Here we report that in Xenopus PRC2 regulates the progression of retinal progenitors from proliferation to differentiation. We show that the PRC2 core components are enriched in retinal progenitors and downregulated with differentiation. Knockdown of the PRC2 core component Ezh2 leads to reduced retinal progenitor proliferation in part due to upregulation of the cdk inhibitor p15Ink4b. In addition, while PRC2 knockdown does not alter eye patterning, retinal progenitor gene expression or expression of the neural competence factor Sox2, it does cause suppression of proneural bHLH gene expression, indicating that PRC2 is critical for the initiation of neural differentiation in the retina. Consistent with this, knocking down or blocking PRC2 function constrains the generation of most retinal neural cell types and promotes a Mueller glial cell fate decision. We also show that Wnt/β-catenin signaling acting through the receptor Frizzled 5, but independent of Sox2, regulates expression of key PRC2 subunits in the developing retina. This is consistent with a role for this pathway in coordinating proliferation and the transition to neurogenesis in the Xenopus retina. Our data establishes PRC2 as a regulator of proliferation and differentiation during eye development.
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Project description:The histone methyltransferase complex PRC2 controls key steps in developmental transitions and cell fate choices. However, its roles in vertebrate eye development remain unknown. Here we report that in Xenopus PRC2 regulates the progression of retinal progenitors from proliferation to differentiation. We show that the PRC2 core components are enriched in retinal progenitors and downregulated with differentiation. Knockdown of the PRC2 core component Ezh2 leads to reduced retinal progenitor proliferation in part due to upregulation of the cdk inhibitor p15Ink4b. In addition, while PRC2 knockdown does not alter eye patterning, retinal progenitor gene expression or expression of the neural competence factor Sox2, it does cause suppression of proneural bHLH gene expression, indicating that PRC2 is critical for the initiation of neural differentiation in the retina. Consistent with this, knocking down or blocking PRC2 function constrains the generation of most retinal neural cell types and promotes a Mueller glial cell fate decision. We also show that Wnt/?-catenin signaling acting through the receptor Frizzled 5, but independent of Sox2, regulates expression of key PRC2 subunits in the developing retina. This is consistent with a role for this pathway in coordinating proliferation and the transition to neurogenesis in the Xenopus retina. Our data establishes PRC2 as a regulator of proliferation and differentiation during eye development. Xenopus embryos were injected at the 8-cell stage with 5ng Ezh2 ATG MO or 5ng control MO (scrambled sequence of Ezh2 ATG MO) together with 400 pg mRNA for GFP as a lineage tracer. At stage 27, GFP-positive eyes were isolated by microdissection. Pools of 20-25 eyes were used to prepare total RNA for each sample on the microarray. 4 control and 4 Ezh2 ATG MO samples were hybridized to Agilent 1-color microarrays.
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