Abstract

The developmental regulation of antigen receptor gene transcription and recombination are mediated by cis regulatory elements. At the T cell receptor β chain locus ( TCRβ), two DNase I hypersensitive sites within the Jβ2–Cβ2 intron contained binding sites for NF-κB and additional nuclear factors and were postulated to be involved in controlling TCRβ transcription and V(D)J recombination. To test this possibility, we deleted these elements from the mouse genome by homologous recombination and assayed the effect on transcription of both the germline and rearranged TCRβ locus, and on TCRβ rearrangement in T and B lymphocytes. We found that TCRβ transcription and V(D)J recombination and T cell development were normal in these mutant mice. Therefore, the Jβ2–Cβ2 intronic elements are dispensable for TCRβ assembly and function.

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