Unknown,Transcriptomics,Genomics,Proteomics

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Identification of genes regulated by XOct-25 overexpression in Xenopus ectoderm

ABSTRACT: The Xenopus POU class V transcription factor XOct-25 has been shown to inhibit BMP-dependent epidermal differentiation and promote neural induction in the ectoderm during early embryogenesis. In order to identify genes that act downstream of XOct-25, transcriptional profile of Xenopus ectodermal cells overexpressing XOct-25 was compared with control cells by using a DNA microarray method. Two independent experiments. Each experiment contains ectodermal cells overexpressing XOct-25 and corresponding control cells. Xenopus embryos were injected at the 8-cell stage with mRNA encoding GR-XOct-25, a hormone-inducible version of XOct-25. Explants from stage 9 embryos were treated with or without dexamethazone (DEX) until the sibling embryos reached stage 10.5, when they were used for RNA extraction. The explants cultured without DEX was used as a control sample. biological replicates: Sample name XOct-exp 1, Sample name XOct-exp 2

ORGANISM(S): Xenopus laevis

SUBMITTER: Atsushi Suzuki

PROVIDER: E-GEOD-24562 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Transcriptional targets of neurogenin (Ngnr1) were identified by over-expression of an inducible form of neurogenin in Xenopus ectodermal explants. The effects of co-expressing the nucleoprotein geminin on Ngnr1-dependent target gene transactivation were defined. Regulating the transition from lineage-restricted progenitors to terminally differentiated cells is a central aspect of nervous system development. Here, we investigated the role of the nucleoprotein geminin in regulating neurogenesis at a mechanistic level during both Xenopus primary neurogenesis and mammalian neuronal differentiation in vitro. The latter work utilized both neural cells derived from embryonic stem and embryonal carcinoma cells in vitro and neural stem cells from mouse forebrain. In all of these contexts, geminin antagonized the ability of neural bHLH transcription factors to activate transcriptional programs promoting neurogenesis. Furthermore, geminin promoted a bivalent chromatin state, characterized by the presence of both activating and repressive histone modifications, at genes encoding transcription factors that promote neurogenesis. This epigenetic state restrains the expression of genes that regulate commitment of undifferentiated stem and neuronal precursor cells to neuronal lineages. Geminin is highly expressed in undifferentiated neuronal precursor cells but is downregulated prior to differentiation. Therefore, these data support a model whereby geminin promotes the neuronal precursor cell state by modulating both the epigenetic status and expression of genes encoding neurogenesis-promoting factors. Additional developmental signals acting in these cells can then control their transition toward terminal neuronal or glial differentiation during mammalian neurogenesis. A dexamethasone-inducible (GR ligand binding domain fused) form of Xenopus neurogenin-related 1, NgnrGR, was over-expressed in Xenopus embryonic ectodermal explants, in the presence or absence of over-expressed geminin. Induction of Ngnr1 activity was used to define direct targets as previously described (EMBO J. 26(24): 5093-5108). The ability of geminin to suppress Ngnr1-dependent transactivation of its target gene programs was determined.

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Identification of genes regulated by XOct-25 overexpression in Xenopus ectoderm

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