Coding joint formation of endogenous T cell receptor genes in lymphoid cells from scid mice: unusual P‐nucleotide additions in VJ‐coding joints

Abstract

The mouse mutation scid adversely affects the process of VDJ recombination. Attempts to form coding joints, that is, to join V or D to J gene segments generally fail in developing scid lymphocytes. It has been proposed that the scid mutation results a defective VDJ recombinase system. Here we describe five scid T cell lymphomas containing one or two TcRγ coding joints each, even though the majority of the multiple TcRγ chain gene rearrangements and all TcRβ rearrangements in these cells were abnormal with the deletions typically found in scid lymphoid cells. One of the five T cell lymphomas was shown to have an active VDJ recombinase system; however, this activity was defective indicating that the scid phenotype has been retained. We conclude that the scid VDJ recombinase system has not completely lost the ability to form coding joints. P‐nucleotide additions of unusual length or composition were found at the junctional border in five of the eight TcRγ coding joints. This might reflect a defect in the activity of a component of the VDJ recombinase system involved in the generation of P‐nucleotide additions. In one of the observed rearrangements, a V_γ5‐J_γ3 coding joint was formed. This establishes the transcriptional orientation of J_γ3‐Cγ3 and confirms a previously proposed organization of the TcR_γ genes.