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Molecular and Cellular Biology, September 2000, p. 6195-6200, Vol. 20, No. 17
Division of Immunogenetics, Kumamoto
University Graduate School of Medical
Sciences,1 and Department of
Surgical Pathology2 and Department of
Morphogenesis, Institute of Molecular Embryology and
Genetics,3 Kumamoto University School of
Medicine, Kumamoto 860, Japan
Received 8 May 2000/Accepted 18 May 2000
We previously identified a gene encoding a putative
GTPase, GTPBP1, which is structurally related
to elongation factor 1
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Copyright © 2000, American Society for Microbiology. All rights reserved.
Immunocytochemical Analyses and Targeted Gene Disruption
of GTPBP1
, a key component of protein
biosynthesis machinery. The primary structure of GTPBP1
is highly conserved between human and mouse (97% identical at
the amino acid level). Expression of this gene is
enhanced by gamma interferon in a monocytic cell line, THP-1. Although counterparts of this molecule in Caenorhabditis
elegans and Ascaris suum have also been identified,
the function of this molecule remains to be clarified. In the present
study, our immunohistochemical analyses on mouse tissues revealed that
GTPBP1 is expressed in some neurons and smooth muscle cells
of various organs as well as macrophages. Immunofluorescence analyses
revealed that GTPBP1 is localized exclusively in cytoplasm
and shows a diffuse granular network forming a gradient from
the nucleus to the periphery of the cells in smooth muscle cell lines
and macrophages. To investigate the physiological role of
GTPBP1, we used targeted gene disruption in
embryonic stem cells to generate GTPBP1-deficient
mice. The mutant mice were born at the expected Mendelian frequency,
developed normally, and were fertile. No manifest anatomical or
behavioral abnormality was observed in the mutant mice. Functions of
macrophages, including chemotaxis, phagocytosis, and nitric oxide
production, in mutant mice were equivalent to those seen in wild-type
mice. No significant difference was observed in the immune response to
protein antigen between mutant mice and wild-type mice, suggesting normal function of antigen-presenting cells of the mutant mice. The
absence of an eminent phenotype in GTPBP1-deficient mice may be due to functional compensation by GTPBP2, a molecule we
recently identified which is similar to GTPBP1 in structure
and tissue distribution.
*
Corresponding author. Mailing address: Division of
Immunogenetics, Department of Neuroscience and Immunology, Kumamoto
University Graduate School of Medical Sciences, 2-2-1 Honjo, Kumamoto
860-0811, Japan. Phone: 81-96-373-5310. Fax: 81-96-373-5314. E-mail:
mxnishim{at}gpo.kumamoto-u.ac.jp.
Molecular and Cellular Biology, September 2000, p. 6195-6200, Vol. 20, No. 17
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Copyright © 2000, American Society for Microbiology. All rights reserved.
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