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J. Biochem, 2003, Vol. 134, No. 2 203-210
© 2003 Japanese Biochemical Society


MOLECULAR BIOLOGY

The Mouse mafB 5'-Upstream Fragment Directs Gene Expression in Myelomonocytic Cells, Differentiated Macrophages and the Ventral Spinal Cord in Transgenic Mice

Michito Hamada*, Takashi Moriguchi*, Tomomasa Yokomizo, Naoki Morito, Chuan Zhang and Satoru Takahashi§

Departments of Anatomy and Embryology, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba 305-8575

The b-Zip transcription factor MafB is an essential determinant of neural development and an inducer of monocytic differentiation. The MafB protein is expressed in a variety of tissues including the developing spinal cord, retina, myelomonocytic lineages of hematopoietic cells, and peritoneal macrophages. However, the tissue-specific regulatory mechanism of mafB gene expression and its biological relevance have not been examined in detail. Here, we report, for the first time, analysis of the regulatory mechanism and tissue-specific expression of the mafB gene in vivo using transgenic mice. A transgene, containing the 8.2-kb sequence flanking the 5' end of the mafB exon, directed the expression of a GFP reporter gene specifically in the retina, myelomonocytic lineages of hematopoietic cells, peritoneal macrophages and the ventral spinal cord. In situ hybridization analysis showed that the reporter gene expression specifically recapitulates the endogenous expression profile of mafB in the retina and spinal cord. FACS analysis revealed that the Gr-1, Mac-1 and F4/80 antigens were present on most of the GFP-positive hematopoietic cells from transgenic adult bone marrow and spleen. On the other hand, B220 CD4, 8, and Ter119 cells were almost absent from among the GFP-positive cells examined. These observations suggest that gene regulatory regions located in the 8.2-kb upstream region of mafB are responsible for directing mafB expression in the retina, myelomonocytic lineages, peritoneal macrophages and the ventral spinal cord.

* These authors contributed equally to this work.

§ To whom correspondence should be addressed. Phone: +81-29-853-7516, Fax: +81-29-853-6965, E-mail: satoruta{at}md.tsukuba.ac.jp


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