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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.

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