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Blood, Vol. 93 No. 9 (May 1), 1999:
pp. 2771-2779
RAPID COMMUNICATION
Mice Homozygous for a Truncated Form of CREB-Binding Protein Exhibit
Defects in Hematopoiesis and Vasculo-angiogenesis
Yuichi Oike,
Nobuyuki Takakura,
Akira Hata,
Tadashi Kaname,
Miwa Akizuki,
Yuji Yamaguchi,
Hirofumi Yasue,
Kimi Araki,
Ken-ichi Yamamura, and
Toshio Suda
From the Department of Developmental Genetics, the Department of Cell
Differentiation, Institute of Molecular Embryology and Genetics and the
Department of Cardiovascular Medicine, Kumamoto University School of
Medicine, Kumamoto; and the Department of Public Health, Asahikawa
Medical College, Asahikawa, Japan.
CREB-binding protein (CBP) and the closely related adenovirus
E1A-associated 300-kD protein (p300) function as coactivators of
transcription factors such as CREB, c-Fos, c-Jun, c-Myb, and several
nuclear receptors. To study the roles of CBP in embryonic development,
we generated CBP homozygous mutant mouse embryos that expressed a
truncated form of CBP protein (1-1084 out of 2441 residues). The
embryos died between embryonic days 9.5 (E9.5) and E10.5 and exhibited
a defect in neural tube closure. They appeared pale and showed
decreases in erythroid cells and colony-forming cells (CFCs) in the
yolk sac, suggesting defects in primitive hematopoiesis.
Immunohistochemistry with an anti-PECAM antibody showed a lack of
vascular network formation. Organ culture of para-aortic
splanchnopleural mesoderm (P-Sp) with stromal cells (OP9) showed an
autonomous abnormality of putative endothelial precursors, which may
induce the microenvironmental defect in hematopoiesis. In addition,
these defects were partially rescued by the addition of VEGF to this
culture. Our analyses demonstrate that CBP plays an essential role in
hematopoiesis and vasculo-angiogenesis.
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