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Prepublished online as a Blood First Edition Paper on August 1, 2002; DOI 10.1182/blood-2002-04-1131.

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Blood, 1 January 2003, Vol. 101, No. 1, pp. 318-324

RED CELLS

Ribosomal protein S19 expression during erythroid differentiation

Lydie Da Costa, Goutham Narla, Thiébaut-Noel Willig, Luanne L. Peters, Marilyn Parra, Jason Fixler, Gil Tchernia, and Narla Mohandas

From the New York Blood Center and Mount Sinaï Medical Center, NY; the Lawrence Berkeley National Laboratory, Life Sciences Division, Berkeley, CA; The Jackson Laboratory, Bar Harbor, ME; and the Laboratoire d'Hématologie, AP-HP, Faculté de Médecine Paris XI, INSERM U473, Hôpital de Bicêtre, Le Kremlin Bicêtre, France.

The gene encoding ribosomal protein S19 (RPS19) has been shown to be mutated in 25% of the patients affected by Diamond-Blackfan anemia (DBA), a congenital erythroblastopenia. As the role of RPS19 in erythropoiesis is still to be defined, we performed studies on RPS19 expression during terminal erythroid differentiation. Comparative analysis of the genomic sequences of human and mouse RPS19 genes enabled the identification of 4 conserved sequence elements in the 5' region. Characterization of transcriptional elements allowed the identification of the promoter in the human RPS19 gene and the localization of a strong regulatory element in the third conserved sequence element. By Northern blot and Western blot analyses of murine splenic erythroblasts infected with the anemia-inducing strain Friend virus (FAV cells), RPS19 mRNA and protein expression were shown to decrease during terminal erythroid differentiation. We anticipate that these findings will contribute to further development of our understanding of the contribution of RPS19 to erythropoiesis.

© 2003 by The American Society of Hematology.
 

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