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Inversion of chromosome 7 in ataxia telangiectasia is generated by a
rearrangement between T-cell receptor beta and T-cell receptor gamma genes
MH Stern, S Lipkowitz, A Aurias, C Griscelli, G Thomas and IR Kirsch
NCI-NMOB, Naval Hospital, Bethesda, MD 20814.
Specific and recurrent chromosomal rearrangements are often observed in the
karyotypes of phytohemagglutinin-stimulated lymphocytes. The percentage of
cells demonstrating these rearrangements is dramatically increased in the
genetic disease ataxia telangiectasia. Inversion of chromosome 7 represents
approximately half of the chromosomal rearrangements in this disease.
Because the chromosomal locations of the inv(7) breakpoints coincide
precisely with those of the T-cell antigen receptor (TCR) beta and gamma
genes, it has been hypothesized that this rearrangement may occur by
recombination between those two loci. Here, we present direct evidence that
inversion of chromosome 7 in ataxia telangiectasia is generated by
site-specific recombination between a TCR gamma variable segment and a TCR
beta joining segment.
Volume 74,
Issue 6,
pp. 2076-2080,
11/01/1989
Copyright © 1989 by The American Society of Hematology
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