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Series GSE89847 Query DataSets for GSE89847
Status Public on Jan 23, 2018
Title Id proteins suppress E2A-driven iNKT cell development prior to TCR selection [ChIP-seq]
Organism Mus musculus
Experiment type Genome binding/occupancy profiling by high throughput sequencing
Summary Id proteins have been shown to promote the differentiation of conventional αβ and γδT cells, and to suppress the expansion of invariant Natural Killer T (iNKT) cells and innate-like γδNKT within their respective cell lineages. However, it remains to be determined whether Id proteins regulate lineage specification in developing T cells that give rise to these distinct cell fates. Here we report that in the absence of Id2 and Id3 proteins, E2A prematurely activates genes critical for the iNKT cell lineage prior to TCR expression. Lack of Id proteins also promotes a biased TCR rearrangement in favor of iNKT cell fate prior to selection at the CD4+CD8+ double positive (DP) stage. Enhanced iNKT development in Id3-deficient mice lacking γδNKT cells suggests that Id3 regulates the lineage competition between these populations. RNA-Seq analysis establishes E2A as the transcriptional regulator of both iNKT and γδNKT development. In the absence of pre-TCR signaling, Id2/Id3 deletion gives rise to a large population of iNKT cells and a unique innate-like DP population, despite the block in conventional αβ T cell development. The transcriptional profile of these unique DP cells reflects enrichment of innate-like signature genes, including PLZF (Zbtb16) and Granzyme A (Gzma). Results from these genetic models and genome-wide analyses suggest that Id proteins suppress E2A-driven innate-like T cell programs prior to TCR selection to enforce predominance of conventional T cells.
Overall design The ChIP-Seq experiment included E2A ChIP-Seq of DP and iNKT cells from L-DKO mice (deficient in Id2 and Id3). Each sample consisted of pooled cells from 3-4 mice. Input controls (i.e. not immunoprecipitated with E2A antibody) were included for each sample.
The mouse strains for these experiments were either C57BL/6, or C57BL/6 and 129 hybrids.
Web link
Contributor(s) Roy S, Moore AJ, Love C, Reddy A, Rajagopalan D, Dave S, Li L, Murre C, Zhuang Y
Citation(s) 29416542
Submission date Nov 15, 2016
Last update date May 15, 2019
Contact name Yuan Zhuang
Phone 919-613-7824
Organization name Duke University
Department Immunology
Lab Zhuang lab
Street address 207 Research Drive
City Durham
State/province NC
ZIP/Postal code 27705
Country USA
Platforms (1)
GPL21103 Illumina HiSeq 4000 (Mus musculus)
Samples (4)
GSM2391480 L-DKO DP E2A
GSM2391481 L-DKO DP Input
GSM2391482 L-DKO NKT E2A
This SubSeries is part of SuperSeries:
GSE89849 Id proteins suppress E2A-driven iNKT cell development prior to TCR selection
BioProject PRJNA354281
SRA SRP096040

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Supplementary file Size Download File type/resource
GSE89847_RAW.tar 1.4 Gb (http)(custom) TAR (of BED, WIG, XLSX)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

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