Nucleic Acids Research Advance Access originally published online on September 26, 2006
Nucleic Acids Research 2006 34(18):5232-5237; doi:10.1093/nar/gkl680
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Nucleic Acids Research, 2006, Vol. 34, No. 18 5232-5237
© 2006 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Molecular Biology |
BP1 is a negative modulator of definitive erythropoiesis
Molecular Genetics and Development Institut de Recherches Cliniques de Montreal, Faculte de Medecine de l'Universite de Montreal 110 ouest avenue des Pins Montreal, Quebec, Canada H2W 1R7 1 Department of Biochemistry and Molecular Biology, The George Washington University Medical Center Washington DC, USA 2 Department of Pathology, College of Physicians and Surgeons of Columbia University New York, NY, USA
*To whom correspondence should be addressed. Tel: +1 514 987 5712; Fax: +1 514 987 5585; Email: trudelm{at}ircm.qc.ca
Received August 14, 2006. Revised September 1, 2006. Accepted September 5, 2006.
Beta protein 1 (BP1), a human homeotic transcription factor, is expressed during hematopoeisis in the erythroid lineage. To determine the in vivo role of BP1 in erythropoiesis, we have undertaken two complementary approaches using enforced BP1 expression in both transgenic mice and embryonic stem (ES) cells. Despite repeated attempts, only one adult transgenic BP1 founder mouse among 121 mice was obtained. This mouse presumably survived due to transgene mosaicism because the transgene could not be transmitted. This mouse expressed BP1 and displayed splenomegaly, extramedullary erythropoiesis and severe amyloidosis A in the kidney, a phenotype compatible with thalassemia. Consistently, the presence of BP1 transgene in fetuses was associated with paleness and lethality. In ES cells, BP1 expression in primary differentiation appeared to antagonize adult ß-globin expression. In secondary differentiation, BP1 expression reduced significantly ß-globin gene expression in both primitive and definitive erythroid cells, whereas it impaired only the definitive erythroid cell differentiation. These studies showed that BP1 can negatively modulate adult ß-globin gene expression and definitive erythroid cell differentiation, and suggest that BP1 could play a role in thalassemia.
The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors
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