Immunocytochemical Analyses and Targeted Gene Disruption of GTPBP1

Author:

Senju Satoru1,Iyama Ken-ichi2,Kudo Hironori1,Aizawa Shinichi3,Nishimura Yasuharu1

Affiliation:

1. Division of Immunogenetics, Kumamoto University Graduate School of Medical Sciences,1 and

2. Department of Surgical Pathology2 and

3. Department of Morphogenesis, Institute of Molecular Embryology and Genetics,3 Kumamoto University School of Medicine, Kumamoto 860, Japan

Abstract

ABSTRACT We previously identified a gene encoding a putative GTPase, GTPBP1, which is structurally related to elongation factor 1α, 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.

Publisher

American Society for Microbiology

Subject

Cell Biology,Molecular Biology

Reference32 articles.

1. cDNA structures and regulation of two interferon-induced human Mx proteins

2. Requirement of endogenous interferon-gamma production for resolution of Listeria monocytogenes infection;Buchmeier N. A.;Proc. Natl. Acad. Sci. USA,1985

3. Mouse immune interferon enhances fibronectin production of elicited macrophages;Cofano F.;J. Immunol.,1984

4. Altered nociception, analgesia and aggression in mice lacking the receptor for substance P;De Felipe C.;Nature,1998

5. The molecular cell biology of interferon-gamma and its receptor;Farrar M. A.;Annu. Rev. Immunol.,1993

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