Abstract
Abstract The transcription factor HEBAlt is derived from the HEB gene locus, which also encodes the E2A-related factor HEBCan (Can=canonical). HEBAlt is expressed in early lymphocyte precursors. HEBAlt is synergistically upregulated in T cell precursors by Delta-Notch signaling and HEBCan activity, and ectopic expression of HEBAlt in uncommitted precursors enhances entry into the T cell lineage. By contrast, HEBAlt is only expressed in committed B cell precursors, and expression prior to commitment blocks B cell development. A role for HEBAlt in the repression of CD8alpha transcription at the pro-T cell stage of development is suggested by loss of CD8 in the presence of HEBAlt, and upregulation of CD8 in pro-T cells by an HEBAlt-engrailed repressor construct. HEBAlt can also influence the fate choice between the gamma-delta T cell lineage and the alpha-beta T cell lineage. These results suggest that HEBAlt is important in multiple aspects of early T cell development, including locking in the T/B lineage choice downstream of Notch signaling, repressing T cell-specific genes poised for expression past TCRbeta selection, and influencing an early T cell lineage decision.
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