Transcriptome regulation and chromatin occupancy by E2F3 and MYC in mice

E2F3 and MYC are transcription factors that control cellular proliferation. To study their mechanism of action in the context of a regenerating tissue, we isolated both proliferating (crypts) and non-dividing (villi) cells from wild-type and Rb depleted small intestines of mice and performed ChIP-ex...

Full description

Saved in:
Bibliographic Details
Published inScientific data Vol. 3; no. 1; p. 160008
Main Authors Tang, Xing, Liu, Huayang, Srivastava, Arunima, Pécot, Thierry, Chen, Zhong, Wang, Qianben, Huang, Kun, Sáenz-Robles, Maria Teresa, Cantalupo, Paul, Pipas, James, Leone, Gustavo
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 16.02.2016
Nature Publishing Group
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:E2F3 and MYC are transcription factors that control cellular proliferation. To study their mechanism of action in the context of a regenerating tissue, we isolated both proliferating (crypts) and non-dividing (villi) cells from wild-type and Rb depleted small intestines of mice and performed ChIP-exo-seq (chromatin immunoprecipitation combined with lambda exonuclease digestion followed by high-throughput sequencing). The genome-wide chromatin occupancy of E2F3 and MYC was determined by mapping sequence reads to the genome and predicting preferred binding sites (peaks). Binding sites could be accurately identified within small regions of only 24 bp-28 bp long, highlighting the precision to which binding peaks can be identified by ChIP-exo-seq. Forty randomly selected E2F3- and MYC-specific binding sites were validated by ChIP-PCR. In addition, we also presented gene expression data sets from wild type, Rb-, E2f3- and Myc -depleted crypts and villi within this manuscript. These represent comprehensive and validated datasets that can be integrated to identify putative direct targets of E2F3 and MYC involved in the control of cellular proliferation in normal and Rb -deficient small intestines. Design Type(s) parallel group design • genetic modification design Measurement Type(s) chromatin binding • transcription profiling assay Technology Type(s) transcription factor binding site identification by ChIP-Seq assay • DNA microarray Factor Type(s) Genetic Variation Sample Characteristic(s) Mus musculus • small intestine Machine-accessible metadata file describing the reported data (ISA-Tab format)
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ObjectType-Undefined-3
PMCID: PMC4755127
H.L. and G.L. designed the experiments. H.L. performed the wet-lab experiments. X.T., A.S., T.P., P.C., performed the bioinformatics and statistical analysis of gene expression and ChIP-exo-seq data sets with supervision from K.H., R.M. and G.L. Z.C. and Q.W. provided guidance on the ChIP-exo-seq experiments. J.M.P. and G.L. supervised the overall study. X.T., H.L. and G.L. wrote the manuscript with inputs from all authors.
ISSN:2052-4463
2052-4463
DOI:10.1038/sdata.2016.8