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Series GSE138905 Query DataSets for GSE138905
Status Public on Feb 26, 2020
Title ATAC-seq identifies accessible chromatin domains in gastrula stage Xenopus laevis
Organism Xenopus laevis
Experiment type Genome binding/occupancy profiling by high throughput sequencing
Summary In the embryo, inductive cues are interpreted by competent tissues in a spatially and temporally restricted manner, and the mechanisms for the loss of responsiveness are not well understood. To test the hypothesis that loss of competence is associated with changes in chromatin accessibility, we adapted the assay for transposase-accessible chromatin with high throughput sequencing (ATAC-seq) for use in Xenopus laevis to evaluate genome-wide changes in chromatin accessibility in early and late gastrula stages. ATAC-seq was performed on presumptive ectoderm (animal caps) explanted at the blastula stage and cultured until siblings reached early (stage 10) or late (stage 12) gastrula stage. Approximately 70,000 accessible regions were identified at intergenic regions, introns, promoters, and transcription termination sites at both stages. Accessibility decreased from stage 10 to stage 12 at 279 promoters, including developmental regulators such as Foxh1, chordin, and VegT. Accessible chromatin domains overlap extensively with previously reported p300 binding sites, consistent with putative cis-regulatory modules (pCRMs), and these pCRMs are enriched for binding motifs for pluripotency factors, including Sox, Oct/Pou, and KLF binding motifs. Dorsal Wnt target gene promoters are not accessible after the loss of competence, but inhibition of histone deacetylases increases acetylation at these promoters and extends competence for dorsal gene induction by Wnt signaling. In contrast, the promoters for genes involved in mesoderm and neural crest development remain open through gastrulation, and histone deacetylase inhibition does not extend competence for mesoderm or neural crest induction. These data suggest that chromatin state regulates the loss of competence to inductive signals in a context-dependent manner.
 
Overall design ATAC-seq performed on ectodermal explants from stage 10 (early gastrula) and stage 12 (late gastrula).
 
Contributor(s) Yang J, Zhang K, Esmaeili M, Klein P
Citation(s) 32119833
NIH grant(s)
Grant ID Grant title Affiliation Name
R01 GM115517 An unexpected signaling output for the tumor suppressor APC UNIVERSITY OF PENNSYLVANIA PETER S KLEIN
Submission date Oct 15, 2019
Last update date May 27, 2020
Contact name Peter S Klein
E-mail(s) pklein@pennmedicine.upenn.edu
Organization name University of Pennsylvania School of Medicine
Department Medicine
Street address 3400 Civic Center Blvd
City Philadelphia
State/province PA
ZIP/Postal code 19104
Country USA
 
Platforms (1)
GPL22393 Illumina HiSeq 4000 (Xenopus laevis)
Samples (6)
GSM4121478 stage 10 ectodermal explant rep1
GSM4121479 stage 10 ectodermal explant rep2
GSM4121480 stage 10 ectodermal explant rep3
Relations
BioProject PRJNA577715
SRA SRP225796

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Supplementary file Size Download File type/resource
GSE138905_s10_sort.bed.gz 2.5 Mb (ftp)(http) BED
GSE138905_s12_sort.bed.gz 3.5 Mb (ftp)(http) BED
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Raw data are available in SRA
Processed data are available on Series record

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