CODING JOINT FORMATION OF ENDOGENOUS T-CELL RECEPTOR GENES IN LYMPHOID-CELLS FROM SCID MICE - UNUSUAL P-NUCLEOTIDE ADDITIONS IN VJ-CODING JOINTS

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 TcR-gamma coding joints each, even though the majority of the multiple TcR-gamma chain gene rearrangements and all TcR-beta 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 TcR gamma 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-gamma-5-J-gamma-3 coding joint was formed. This establishes the transcriptional orientation of J-gamma-3-C-gamma-3 and confirms a previously proposed organization of the TcR gamma genes.