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J. Biol. Chem., Vol. 281, Issue 43, 32820-32830, October 27, 2006

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GATA-4 Incompletely Substitutes for GATA-1 in Promoting Both Primitive and Definitive Erythropoiesis in Vivo^*

From the Graduate School of Comprehensive Human Sciences, Center for Tsukuba Advanced Research Alliance, and Environmental Response Project, Exploratory Research for Advanced Technology, Japan Science and Technology Corporation, University of Tsukuba, Tsukuba 305-8577, Japan

Vertebrate GATA transcription factors have been classified into two subgroups; GATA-1, GATA-2, and GATA-3 are expressed in hematopoietic cells, whereas GATA-4, GATA-5, and GATA-6 are expressed in mesoendoderm-derived tissues. We previously discovered that expression of GATA-2 or GATA-3 under the transcriptional control for the Gata1 gene eliminates lethal anemia in Gata1 germ line mutant mice (Gata1.05/Y). Here, we show that the GATA-4 expression by the same regulatory cassette prolongs the life span of Gata1.05/Y embryos from embryonic day 12.5 to 15.5 but fails to abrogate its embryonic lethality. Gata1.05/Y mice bearing the GATA-4 transgene showed impaired maturation of both primitive and definitive erythroid cells and defective erythroid cell expansion in fetal liver. Moreover, the incidence of apoptosis was observed prominently in primitive erythroid cells. In contrast, a GATA-4-GATA-1 chimeric protein prepared by linking the N-terminal region of GATA-4 to the C-terminal region of GATA-1 significantly promoted the differentiation and survival of primitive erythroid cells, although this protein is still insufficient for rescuing Gata1.05/Y embryos from lethal anemia. These data thus show a functional incompatibility between hematopoietic and endodermal GATA factors in vivo and provide evidence indicating specific roles of the C-terminal region of GATA-1 in primitive erythropoiesis.

Received for publication, June 15, 2006 , and in revised form, August 29, 2006.

^* This work was supported by grants from the Japan Science and Technology Corporation-ERATO Environmental Response Project (to M. Y.) and Ministry of Education, Science, Sports, and Culture Grant 17390088 (to M. Y.) and Grant 17590237 (to K. O.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ To whom correspondence may be addressed: Dept. of Pharmacy, Faculty of Pharmacy, Takasaki University of Health and Welfare, 60 Nalaorui-machi, Takasaki-shi, Gunma 370-0033, Japan. Tel.: 81-273-52-1180; Fax: 81-273-52-1118; E-mail: kohneda{at}takasaki-u.ac.jp.

² To whom correspondence may be addressed: Center for TARA, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba 305-8577, Japan. Tel.: 81-29-853-6158; Fax: 81-29-853-7318; E-mail: masi{at}tara.tsukuba.ac.jp.

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