The V–J Recombination of T Cell Receptor-γ Genes Is Blocked in Interleukin-7 Receptor–deficient Mice |
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| Authors: | Kazushige Maki Shinji Sunaga Koichi Ikuta |
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| Affiliation: | From the *Department of Disease-related Gene Regulation Research (Sandoz), Faculty of Medicine, The University of Tokyo, Tokyo 113, Japan; and the ‡Department of Medical Chemistry, Faculty of Medicine, Kyoto University, Kyoto 606, Japan |
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| Abstract: | IL-7R-deficient mice have severely impaired expansion of early lymphocytes and lack γδ T cells. To elucidate the role of IL-7R on γδ T cell development, we analyzed the rearrangements of TCR-α, β, γ, and δ genes in the thymus of the IL-7R-deficient mice. Southern blot analysis with a Jγ1 probe revealed that more than 70% of Jγ1 and Jγ2 alleles are recombined to form distinct Vγ1.2–Jγ2 and Vγ2–Jγ1 fragments in control mice. On the contrary, no such recombination was detected in the mutant mice. The rearrangements in the TCR-α, β, and δ loci were comparably observed in control and mutant mice. PCR analysis indicated that the V–J recombination of all the Vγ genes is severely hampered in the mutant mice. The mRNA of RAG-1, RAG-2, Ku-80, and terminal deoxynucleotidyl transferase (TdT) genes was equally detected between control and mutant thymi, suggesting that the expression of common recombination machinery is not affected. These data demonstrated that the V–J recombination of the TCR γ genes is specifically blocked in the IL-7R-deficient mice and suggested the presence of highly specific regulation for TCR γ gene rearrangement. |
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