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J. Biol. Chem., Vol. 283, Issue 18, 11897-11904, May 2, 2008

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Splenomegaly and Modified Erythropoiesis in KLF13^–/– Mice^*

Adele R. Gordon¹, Susan V. Outram¹, Mohammad Keramatipour¹, Catherine A. Goddard, William H. Colledge^¶, James C. Metcalfe, Ariadne L. Hager-Theodorides, Tessa Crompton, and Paul R. Kemp^||2

From the Section of Cardiovascular Biology, Department of Biochemistry, University of Cambridge, Downing Site, Cambridge, CB2 1QW, United Kingdom, the Division of Cell and Molecular Biology, Sir Alexander Flemming Building, Imperial College, South Kensington Campus, London SW7 2AZ, United Kingdom, the ^¶Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Site, Cambridge CB2 3EG, United Kingdom, and the ^||National Heart and Lung Institute, Sir Alexander Flemming Building, Imperial College, South Kensington Campus, London, SW7 2AZ, United Kingdom

To study the function of the Krüppel-like transcription factor KLF13 in vivo, we generated mice with a disrupted Klf13 allele. Although Klf13^–/– mice are viable, fewer mice were present at 3 weeks than predicted by Mendelian inheritance. Viable Klf13^–/– mice had reduced numbers of circulating erythrocytes and a larger spleen. The spleen contained an increased number of Ter119^medCD71^hi, Ter119^hiCD71^hi, and Ter119^hiCD71^med cells but not Ter119^hiCD71^– cells, indicating an increase in less mature erythroblasts. A higher proportion of the Ter119^medCD71^hi cells were proliferating, indicating that the mice were under a degree of erythropoietic stress. These data indicate that KLF13 is involved in the normal control of erythropoiesis.

Received for publication, November 21, 2007 , and in revised form, January 31, 2008.

^* This work was supported by British Heart Foundation Grant PG/02/135/14620 (to P. R. K. and J. C. M.). This work was also supported by funds from the Biotechnology and Biological Sciences Research Council (to S. O.), the Wellcome Trust (to A. L. H.-T.), the Medical Research Council (to C. A. G.), and the Ford Physiology Endowment Fund (to W. H. C.). 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 These authors contributed equally to this work.

² To whom correspondence should be addressed: National Heart and Lung Institute, Imperial College, South Kensington Campus, London SW7 2AZ, UK. Tel.: 44-20-7594-1716; Fax: 44-20-7594-3100; E-mail: p.kemp{at}imperial.ac.uk.

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