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Blood, 1 May 2005, Vol. 105, No. 9, pp. 3538-3541.
Prepublished online as a Blood First Edition Paper on January 11, 2005; DOI 10.1182/blood-2004-05-2021.
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HEMATOPOIESIS
Brief report
K-Ras is essential for normal fetal liver erythropoiesis
Waleed F. Khalaf,
Hilary White,
Mary Jo Wenning,
Attilio Orazi,
Reuben Kapur, and
David A. Ingram
From the Department of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN; and Departments of Microbiology and Immunology, Hematology/Pathology, and Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN.
In vitro studies suggest that Ras activation is necessary for erythroid cell development. However, genetic inactivation of the Ras isoforms H-Ras, N-Ras, and K-Ras in mice reportedly did not affect adult or fetal erythropoiesis, though K-Ras-/- embryos were anemic. Given these discrepancies, we performed a more detailed analysis of fetal erythropoiesis in K-Ras-/- embryos. Day-13.5 K-Ras-/- embryos were pale with a marked reduction of mature erythrocytes in their fetal livers. The frequency and number of both early (erythroid burst-forming unit [BFU-E]) and late erythroid progenitors (erythroid colony-forming unit [CFU-E]) were reduced in K-Ras-/- fetal livers compared with wild-type controls and displayed a delay in terminal erythroid cell maturation. Further, K-Ras-/- hematopoietic progenitors had reduced proliferation in response to erythropoietin and Kit ligand compared with control cells. Thus, these studies identify K-Ras as a unique Ras isoform that is essential for regulating fetal erythropoiesis in vivo.
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