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Journal of Experimental Medicine, Vol 174, 769-773, Copyright © 1991 by Rockefeller University Press
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LJ Kienker, WA Kuziel and PW Tucker
Department of Microbiology, University of Texas Southwestern Medical Center, Dallas 75235.
The severe combined immunodeficiency (SCID) mutation has been postulated to affect a V(D)J recombinase activity involved in coding joint formation. Analysis of 38 joints from 34 distinct sequences of normally rearranged T cell receptor (TCR) gamma and delta genes from adult, SCID thymocytes reveals coding joints with an increased number of P nucleotides. One-third of P sequences are greater than or equal to 4 nucleotides in length and P elements of up to 15 bases are observed. This suggests that the SCID defect deregulates P nucleotide addition. Consequently, essential V(D)J recombination intermediates may seldom be generated.
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