A far downstream enhancer for murine Bcl11b controls its T-cell specific expression

Li, Long; Zhang, Jingli A.; Dose, Marei; Kueh, Hao Yuan; Mosadeghi, Ruzbeh; Gounari, Fotini; Rothenberg, Ellen V.

doi:10.1182/blood-2012-08-447839

Cited by 114 publications

(133 citation statements)

References 47 publications

(81 reference statements)

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“…This updated model incorporates recent data on functional impacts of E2A (22), on PU.1 and its interactions with Notch, Myb, and GATA-3 (21,23,24), on Notch blockade of the myeloid program via Hes1 against Cebpa (25, 26), on GATA-3 and its mutual antagonism with the B-cell program (27)(28)(29)(30), and on positive regulators of Bcl11b itself (1,31). Discussed in detail in SI Appendix, Supplementary Text, these results reveal two major switch circuits.…”

Section: T-cell Specification Grn Transitions At Commitment: a Distinctmentioning

confidence: 99%

Bcl11b and combinatorial resolution of cell fate in the T-cell gene regulatory network

Longabaugh

Zeng

Zhang

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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148

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T-cell development from hematopoietic progenitors depends on multiple transcription factors, mobilized and modulated by intrathymic Notch signaling. Key aspects of T-cell specification network architecture have been illuminated through recent reports defining roles of transcription factors PU.1, GATA-3, and E2A, their interactions with Notch signaling, and roles of Runx1, TCF-1, and Hes1, providing bases for a comprehensively updated model of the T-cell specification gene regulatory network presented herein. However, the role of lineage commitment factor Bcl11b has been unclear. We use self-organizing maps on 63 RNA-seq datasets from normal and perturbed T-cell development to identify functional targets of Bcl11b during commitment and relate them to other regulomes. We show that both activation and repression target genes can be bound by Bcl11b in vivo, and that Bcl11b effects overlap with E2A-dependent effects. The newly clarified role of Bcl11b distinguishes discrete components of commitment, resolving how innate lymphoid, myeloid, and dendritic, and B-cell fate alternatives are excluded by different mechanisms.

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Section: T-cell Specification Grn Transitions At Commitment: a Distinctmentioning

confidence: 99%

Bcl11b and combinatorial resolution of cell fate in the T-cell gene regulatory network

Longabaugh

Zeng

Zhang

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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148

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“…ChIP-seq for T cell factor 1 (TCF-1) (a kind gift of Dr Kawamoto), RNApII CTD phospho Ser2 (ab5095), and the unphosphorylated form of RNApII (8WG16) was performed as previously described. 10,17,18 ChIP-seq data for runt-related transcription factor 1 (Runx1) 19 were obtained from the Gene Expression Omnibus database under accession number SRR364255. ChIP-seq for E26 avian leukemia oncogene 1, 59 domain (Ets-1), myelocytomatosis oncogene (c-Myc), GATA binding protein 1 (GATA-1), GATA binding protein 2 (GATA-2), and T cell acute lymphocytic leukemia 1 (Tal-1) were obtained from the Encyclopedia of DNA Elements (ENCODE) project (supplemental Table 7).…”

Section: Chromatin Immunoprecipitation Sequencing Analysismentioning

confidence: 99%

Transcriptional regulation of the Ikzf1 locus

Yoshida

Landhuis

Dose

et al. 2013

Blood

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“…Ce gène a été principalement étudié dans les leucémies lymphoblastiques T (LAL-T). En effet, des translocations faisant intervenir un super-enhancer de BCL11B, entraînant ainsi l'hyperexpression du gène partenaire [73][74][75], et des inactivations monoalléliques de BCL11B (par délétion ou mutation) ont été décrites [76]. L'observation de translocations impliquant le gène BCL11B et la diminution de l'expression de la protéine BCL11B chez certains patients ATL suggère que l'inactivation de ce gène pourrait jouer un rôle important dans la pathogenèse [77,78].…”

Section: Anomalies Moléculairesunclassified