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Context-Dependent Regulation of Hematopoietic Lineage Choice by HEBAlt
Sunnybrook Research Institute.
Sunnybrook Research Institute.
Sunnybrook Research Institute.
Sunnybrook Research Institute.
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2010 (English)In: Journal of Immunology, ISSN 0022-1767, E-ISSN 1550-6606, Vol. 185, no 7, 4109-4117 p.Article in journal (Refereed) Published
Abstract [en]

Hematopoietic development is controlled by combinatorial interactions between E-protein transcription factors and other lineage regulators that operate in the context of gene-regulatory networks. The E-proteins HEB and E2A are critical for T cell and B cell development, but the mechanisms by which their activities are directed to different genes in each lineage are unclear. We found that a short form of HEB, HEBAlt, acts downstream of Delta-like (DL)-Notch signaling to promote T cell development. In this paper, we show that forced expression of HEBAlt in mouse hematopoietic progenitors inhibited B cell development, but it allowed them to adopt a myeloid fate. HEBAlt interfered with the activity of E2A homodimers and with the expression of the transcription factor Pax5, both of which are critical for B cell development. However, when combined with DL-Notch signaling, HEBAlt enhanced the generation of T cell progenitors at the expense of myeloid cells. The longer form of HEB, HEBCan, also inhibited E47 activity and Pax5 expression, but it did not collaborate with DL-Notch signaling to suppress myeloid potential. Therefore, HEBAlt can suppress B cell or myeloid potential in a context-specific manner, which suggests a role for this factor in maintaining T lineage priming prior to commitment.

Place, publisher, year, edition, pages
2010. Vol. 185, no 7, 4109-4117 p.
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-67287DOI: 10.4049/jimmunol.0901783ISI: 000282059500037OAI: diva2:409209
Available from: 2011-04-07 Created: 2011-04-07 Last updated: 2014-09-26

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Sigvardsson, Mikael
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Experimental HematologyFaculty of Health Sciences
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