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A global network of transcription factors, involving E2A, EBF1 and FOXO1, that orchestrates the B cell fate

ABSTRACT: It is now established that the transcription factors E2A, EBF1 and Foxo 1 play critical roles in B cell development. Here we show that E2A and EBF1 bound regulatory elements present in the Foxo1 locus. E2A and EBF1 as well as E2A and Foxo1, in turn, were wired together by a vast spectrum of cis-regulatory codes. These associations were dynamic during developmental progression. Occupancy by the E2A isoform, E47, directly elevated the abundance as well as the pattern of histone H3K4 monomethylation across putative enhancer regions. Finally, the pro-B cell epigenome was divided into clusters of loci that show E2A, EBF and Foxo1 occupancy. From this analysis a global network consisting of transcriptional regulators, signaling and survival factors, was constructed that we propose orchestrates the B cell fate.

ORGANISM(S): Mus musculus

PROVIDER: GSE21978 | GEO | 2010/06/13

SECONDARY ACCESSION(S): PRJNA127185

REPOSITORIES: GEO

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A global network of transcription factors, involving E2A, EBF1 and FOXO1, that orchestrates the B cell fate

Project description:It is now established that the transcription factors E2A, EBF1 and FoxoM-BM- 1 play critical roles in B cell development. Here we show that E2A and EBF1 bound regulatory elements present in the Foxo1 locus. E2A and EBF1 as well as E2A and Foxo1, in turn, were wired together by a vast spectrum of cis-regulatory codes. These associations were dynamic during developmental progression. Occupancy by the E2A isoform, E47, directly elevated the abundance as well as the pattern of histone H3K4 monomethylation across putative enhancer regions. Finally, the pro-B cell epigenome was divided into clusters of loci that show E2A, EBF and Foxo1 occupancy. From this analysis a global network consisting of transcriptional regulators, signaling and survival factors, was constructed that we propose orchestrates the B cell fate. ChIP-Seq and gene expression profiling was performed in a variety of genetically modified primary B cell populations and cell lines approximating developmental stages of B cell development.

2010-06-12 | E-GEOD-21978 | biostudies-arrayexpress

Microarray analysis of E2a-/- and E2a/-Lef1F/F leukemia lines after retroviral Cre expression

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Transcriptional function of E2A, Ebf1, Pax5, Ikaros and Aiolos analyzed by in vivo acute protein degradation in early B cell development [CUT&RUN]

Project description:Early B-lymphopoiesis depends on E2A, Ebf1, Pax5 and Ikaros family members. Here, we used acute protein degradation in vivo to identify direct target genes of these transcription factors in pro-B, small pre-B and immature B-cells. E2A, Ebf1 and Pax5 predominantly function as transcriptional activators by inducing open chromatin at their target genes, have largely unique functions and maintain cell viability in vivo by activating Bcl2l1. Ikaros and Aiolos cooperatively control early B-cell development and act as dedicated repressors to suppress open chromatin at their target genes. The surrogate light-chain genes Igll1 and Vpreb1 are directly activated by Ebf1 and Pax5 in pro-B cells and directly repressed by Ikaros and Aiolos in small pre-B cells. Pax5 and E2A contribute to V(D)J recombination by activating Rag1, Rag2, Dntt, Irf4 and Irf8. Like Pax5, Ebf1 also represses the cohesin-release factor gene Wapl to mediate prolonged loop extrusion across the Igh locus. In summary, in vivo protein degradation has provided unprecedented insight into the control of early B-lymphopoiesis by five transcription factors.

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Opposing roles of E2A and Id3 that orchestrate and enforce the naive T cell fate

Project description:It is established that E2A and its antagonist, Id3, modulate developmental progression at the pre-TCR and TCR checkpoints. Here we show at a global scale how E2A promotes commitment to the T cell lineage and how pre-TCR mediated signalling affects E2A genome-wide occupancy. We find aberrant development of CD4 memory-like and TFH-like cells, T-B cell conjugates and, remarkably, B cell follicles in Id3-/-thymi. We also find that Id3-/-CD4 splenocytes exhibit increased numbers of TFH-like cells. We propose a model in which Id3 modulates the naive versus effector/memory cell fate. Collectively, these data show how E2A acts globally to orchestrate T-lineage development and that Id3 antagonizes E2A activity beyond the pre-TCR checkpoint to enforce the naive T cell fate.

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