ATAC-seq in Xenopus laevis gastrula stage
The hypothesis being tested is that loss of competence to respond to inductive signals is mediated by loss of chromatin accessibility. This dataset describes analysis of an Assay for Transposase-Accessible Chromatin followed by sequencing (ATAC-Seq) approach to evaluate genome-wide changes in chromatin accessibility in Xenopus laevis. ATAC-seq identifies ~70,000 accessible regions at early and late gastrula stage; normalized read counts from 3 biological replicates at early (stage 10) and late (stage 12) gastrula stage are presented here. Genome wide distribution of accessible peaks, list of promoters with changes in accessibility between stage 10 and stage 12, comparison with previously published p300 ChIP-seq data to identify putative cis-regulatory modules (pCRMs), comparison of promoter accessibility and gene expression, identification of transcription factor binding motifs associated with pCRMs, and functional gene annotation analyses are presented. Promoters for dorsal genes (Sia and Xnr3) that have lost competence to respond to Wnt signaling are not accessible at the early gastrula stage but competence can be maintained by inhibiting HDACs and increasing histone acetylation at these promoters. Promoters for regulators of mesoderm and neural crest induction maintain accessibility throughout gastrulation despite the loss of competence to respond to their respective inductive signals, suggesting context-dependent regulation of competence. However, 279 promoters lose accessibility at stage 12 and are associated with transcription factors that regulate early development. Accessibility at ≥ 1800 promoter-distal pCRMs is also reduced by the end the gastrula stage, and these pCRMs are frequently near promoters for transcription factors that regulate early development, including homeobox genes. Motif analysis (HOMER) shows marked enrichment for binding sites for pluripotency factors of the Sox, Oct, and KLF transcription factor families, as well as for Fox, Grainyhead-like, and Zic transcription factors.