The Journal of Experimental Medicine · 1996 · 131 citations · 29 references
Life SciencesGeneticsImmunologyCellular ImmunologyDevelopmental ImmunologyImmunogeneticsAntigen Receptor Gene RearrangementLymphocyte DevelopmentT Cell BiologyT Cell DevelopmentT Cell DifferentiationThymic DevelopmentGamma Delta T Cell DifferentiationGamma-delta T Cell DevelopmentGene Rearrangement AnalysisT Cell Receptor Alpha Chain RearrangementT Cell Receptor RearrangementT-cell Receptor Gene SegmentsT-cell Receptor Locus RearrangementThymic T-cell Receptor Gene Rearrangement
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 J gamma 1 probe revealed that more than 70% of J gamma 1 and J gamma 2 alleles are recombined to form distinct V gamma 1.2-J gamma 2 and V gamma 2-J gamma 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 V gamma 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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RAG-1 and RAG-2, Adjacent Genes That Synergistically Activate V(D)J Recombination
Marjorie A. Oettinger, David G. Schatz, Carolyn Gorka et al. · Science · 1990 · 1.5K citations