Xenopus laevis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA205635 | ENA |
REPOSITORIES: ENA
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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.
2013-05-30 | E-GEOD-47456 | biostudies-arrayexpress
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.
2013-05-30 | GSE47456 | GEO
Project description:Genome-wide binding pattern of β-catenin during Xenopus gastrulation
| PRJNA310141 | ENA
Project description:Spemann organizer transcriptome induction by early β-Catenin, Wnt, Nodal and Siamois signals in Xenopus laevis
| PRJNA360282 | ENA
Project description:Geminin cooperates with Polycomb to restrain multi-lineage commitment in the early embryo: Transient maintenance of a pluripotent embryonic cell population followed by the onset of multi-lineage commitment is a fundamental aspect of development. However, molecular regulation of this transition is not well characterized in vivo. Here we demonstrate that the nuclear protein Geminin is required to restrain commitment and spatially restrict mesoderm, endoderm, and non-neural ectoderm to their proper locations in the Xenopus embryo. We used microarray analyses to demonstrate that Geminin overexpression represses many genes associated with cell commitment and differentiation, while elevating expression levels of genes that maintain pluripotent early and immature neurectodermal cell states. We characterized Geminin’s relationship to cell signaling and found that Geminin broadly represses Activin-, FGF-, and BMP-mediated cell commitment. Conversely, Geminin knockdown enhances commitment responses to growth factor signaling and causes ectopic mesodermal, endodermal, and epidermal fate commitment in the embryo. We also characterized Geminin’s functional relationship with transcription factors that had similar activities and found that Geminin represses commitment independent of Oct4 ortholog (Oct25/60) activities, but depends upon intact Polycomb repressor function. Consistent with this, chromatin immunoprecipitation assays directed at mesodermal genes demonstrate that Geminin promotes Polycomb binding and Polycomb-mediated repressive histone modifications, while inhibiting modifications associated with gene activation. This work defines Geminin as an essential regulator of the embryonic transition from pluripotency through early multi-lineage commitment, and demonstrates that functional cooperativity between Geminin and Polycomb contributes to this process.
2010-12-06 | GSE25158 | GEO
Project description:Transcriptome analysis of Wnt knockdown embryos reveals candidate canonical Wnt/β-catenin target genes during Xenopus laevis gastrulation
| PRJNA310139 | ENA
Project description:Wnt/β-catenin in Xenopus laevis gastrulation
| PRJNA310142 | ENA