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Originally published In Press as doi:10.1074/jbc.M201834200 on May 1, 2002

J. Biol. Chem., Vol. 277, Issue 29, 26327-26334, July 19, 2002
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The Effects of the Fanconi Anemia Zinc Finger (FAZF) on Cell Cycle, Apoptosis, and Proliferation Are Differentiation Stage-specific*

Mu-Shui DaiDagger §, Nathalie Chevallier||, Stacie StoneDagger , Michael C. Heinrich**Dagger Dagger , Melanie McConnell||, Tanja ReuterDagger , Hal E. Broxmeyer§, Jonathan D. Licht||, Li Lu§, and Maureen E. HoatlinDagger §§

From the Dagger  Division of Molecular Medicine, Oregon Health and Science University, Portland, Oregon 97201, § Department of Microbiology/Immunology and the Walther Oncology Center, Indiana University School of Medicine and the Walther Cancer Institute, Indianapolis, Indiana 46202, || Derald H. Ruttenberg Cancer Center and Department of Medicine, The Mount Sinai School of Medicine, New York, New York 10029, and ** Division of Hematology and Medical Oncology, Department of Medicine and the Portland Veterans Administration Medical Center, Portland, Oregon 97201

FAZF, a member of the BTB/POZ family of transcriptional repressor proteins, has been shown to bind to FANCC, the protein defective in patients with the bone marrow failure syndrome Fanconi anemia complementation group C. Because bone marrow failure in Fanconi anemia has been attributed to a failure of the hematopoietic stem cell population to produce sufficient progeny, we documented the expression of FAZF in human CD34+ hematopoietic progenitor cells. FAZF was expressed at high levels in early stages of differentiation but declined during subsequent differentiation into erythroid and myeloid lineages. Consistent with its presumed role as a transcriptional repressor, FAZF was found in the nuclear compartment, where it resides in distinct nuclear speckles at or near sites of DNA replication. Using a FAZF-inducible myeloid cell line, we found that enforced expression of FAZF was accompanied by accumulation in the G1 phase of the cell cycle followed later by apoptosis. These results suggest an essential role for FAZF during the proliferative stages of primitive hematopoietic progenitors, possibly acting in concert with (a subset of) the Fanconi anemia proteins.

* This work was supported by grants from the Fanconi Anemia Research Fund and National Institutes of Health (NIH) Grant HL56045 (to M. E. H.), American Chemical Society Grant DHP 160, and NIH Grant CA59936 (to J. D. L.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Current address: Dept. of Biochemistry and Molecular Biology, Oregon Health and Science University, Portland, OR 97201.

Dagger Dagger Recipient of a Veterans Affair Merit Review Grant.

§§ To whom correspondence should be addressed: Div. of Molecular Medicine, Oregon Health and Science University, 3181 S. W. Sam Jackson Park Rd., Portland, OR 97201. Tel.: 503-494-1123; Fax: 503-494-7368; E-mail: hoatlinm@OHSU.edu.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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