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J. Exp. Med.
© The Rockefeller University Press
0022-1007/96/12/2423/06 $2.00
Volume 184 December 1996 2423-2428

BRIEF DEFINITIVE REPORT:
The V-J Recombination of  T Cell Receptor-gamma Genes Is Blocked in Interleukin-7 Receptor-deficient Mice

By Kazushige Maki,* Shinji Sunaga,* and Koichi Ikuta*Dagger

From the * Department of Disease-related Gene Regulation Research (Sandoz), Faculty of Medicine, The University of  Tokyo, Tokyo 113, Japan; and the Dagger  Department of Medical Chemistry, Faculty of Medicine, Kyoto University, Kyoto 606, Japan

IL-7R-deficient mice have severely impaired expansion of early lymphocytes and lack gamma delta T cells. To elucidate the role of IL-7R on gamma delta T cell development, we analyzed the rearrangements of TCR-alpha , beta , gamma , and delta  genes in the thymus of the IL-7R-deficient mice. Southern blot analysis with a Jgamma 1 probe revealed that more than 70% of Jgamma 1 and Jgamma 2 alleles are recombined to form distinct Vgamma 1.2-Jgamma 2 and Vgamma 2-Jgamma 1 fragments in control mice. On the contrary, no such recombination was detected in the mutant mice. The rearrangements in the TCR-alpha , beta , and delta  loci were comparably observed in control and mutant mice. PCR analysis indicated that the V-J recombination of all the Vgamma 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 gamma  genes is specifically blocked in the IL-7R-deficient mice and suggested the presence of highly specific regulation for TCR gamma  gene rearrangement.


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