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Blood, 15 August 2008, Vol. 112, No. 4, pp. 1068-1077.
Prepublished online as a Blood First Edition Paper on June 3, 2008; DOI 10.1182/blood-2008-01-133504.
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Submitted January 11, 2008
Accepted May 12, 2008
Id2 intrinsically regulates lymphoid and erythroid development via interaction with different target proteins
Ming Ji, Huajie Li, Hyung Chan Suh, Kimberly D. Klarmann, Yoshifumi Yokota, and Jonathan R. Keller*
Basic Research Program, SAIC-Frederick, Center for Cancer Research, National Cancer Institute, Frederick, Maryland, United States
Department of Biochemistry, Fukui Medical University, Fukui, Japan
* Corresponding author; email: kellerj{at}ncifcrf.gov.
Inhibitors of DNA binding (Id) family members are key regulators of cellular differentiation and proliferation. These activities are related to the ability of Id proteins to antagonize E proteins and other transcription factors. As negative regulators of E proteins, Id proteins have been implicated in lymphocyte development. Over expression of Id1, Id2 or Id3 has similar effects on lymphocyte development. However which Id protein plays a physiological role during lymphocyte development is not clear. By analyzing Id2 knock-out mice and retroviral transduced hematopoietic progenitors, we demonstrated that Id2 is an intrinsic negative regulator of B cell development. Hematopoietic progenitor cells over expressing Id2 did not reconstitute B cell development in vivo, which resembled the phenotype of E2A null mice. The B cell population in bone marrow was significantly expanded in Id2 knock-out mice compared to their wild type littermates. Knock-down of Id2 by shRNA in hematopoietic progenitor cells promoted B cell differentiation and induced the expression of B cell lineage-specific genes. These data identified Id2 as a physiologically relevant regulator of E2A during B lymphopoiesis. Furthermore, we identified novel Id2 function in erythroid development. Over expression of Id2 enhanced erythroid development, and decreased level of Id2 impaired normal erythroid development. Id2 regulation of erythroid development is mediated via interacting with transcription factor PU.1 and modulating PU.1 and GATA-1 activities. We conclude that Id2 regulates lymphoid and erythroid development via interaction with different target proteins.
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