GEO Series: GSE64551
Summary
V1 interneurons are a class of inhibitory neurons that play an essential role in vertebrate locomotion; however, the factors contributing to their specification are poorly understood. Morphological and molecular evidence suggest that the zinc finger transcription factor Prdm12 may play a role in promoting V1 interneurons while repressing V2 and V0 fates. Here, we performed RNAseq on Xenopus laevis ectoderm converted to posteriorized neural tissue (with noggin and retinoic acid) in the presence or absence of a series of Prdm12 constructs (wild-type Prdm12, Prdm12-VP16, and Prdm12-engrailed-repressor). We also performed ChIPseq on a Prdm12-FLAG in wild-type or posteriorized neuralized (with noggin and retinoic acid) X. laevis ectoderm. Taken together, these data demonstrate Prdm12's genomic targets and their downstream transcription.
Contributors: Ian Quigley, Kristine Henningfeld, Chris Kintner, Eric Bellefroid, Claude Van Campenhout
Experiment Type: X. laevis embryos were injected with mRNAs encoding prdm12 constructs, along with the bmp inhibitor noggin. Presumptive ectoderm (neuralized by noggin) was dissected and treated with retinoic acid. Samples were then processed into RNAseq libraries or prdm12-FLAG was immunoprecipitated and its targets sequenced. Background was input prior to IP.
Experiment Reagents: nog.L, Retinoic acid, Tg(Flag-Mmu.prdm12),
Article: Xenbase, PubMed
Source: NCBI GEO, Xenbase FTP
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