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Blood, 1 October 2007, Vol. 110, No. 7, pp. 2351-2360. Prepublished online as a Blood First Edition Paper on July 10, 2007; DOI 10.1182/blood-2007-01-069914. This Article Full Text (PDF) Supplemental Methods and Figures All Versions of this Article: blood-2007-01-069914v1 110/7/2351    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Perry, S. S. Articles by Sun, X.-H. Search for Related Content PubMed PubMed Citation Articles by Perry, S. S. Articles by Sun, X.-H. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted January 24, 2007 Accepted July 7, 2007 Id1, but not Id3, directs long-term repopulating hematopoietic stem cell maintenance S. Scott Perry, Ying Zhao, Lei Nie, Shawn W. Cochrane, Zhong Huang, and Xiao-Hong Sun* Immunobiology and Cancer Reserch Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, United States * Corresponding author; email: sunx{at}omrf.ouhsc.edu. E-proteins are widely-expressed basic helix-loop-helix (HLH) transcription factors that regulate differentiation in many cell lineages, including lymphoid, muscle and neuronal cells. E-protein function is controlled by HLH inhibitors such as Id and SCL/TAL1 proteins, which have recently been suggested to play a role in hematopoietic stem cell (HSC) differentiation. However, the precise stages when these proteins are expressed and their specific functions are not entirely clear. Using a knock-in mouse model, where the sequence for the enhanced green fluorescent protein (GFP) was inserted downstream of the Id1 promoter, we were able to track Id1 expression on an individual cell basis and detected Id1 expression in long-term repopulating HSC (LT-HSC). Functional assays showed that the Id1/GFP+Lin-Sca1+c-kitHi population was highly enriched for LT-HSC. Consistent with this expression pattern, Id1-deficiency led to a two-fold reduction in the number of LT-HSC defined as Lin-Sca1+c-kitHiCD48-CD150+. Primary bone marrow transplantation studies revealed that Id1 is dispensable for short-term engraftment. In contrast, both Id1-/- whole bone marrow and Lin-Sca1+c-kitHiThy1.1Lo enriched HSC, but not Id3-/- marrow, displayed impaired engraftment relative to wild-type controls in secondary transplantation assays. These findings suggest a unique role for Id1 in LT-HSC maintenance and hematopoietic development. 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