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Science 7 December 1990: Vol. 250. no. 4986, pp. 1426 - 1429 DOI: 10.1126/science.2255914
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Articles
Science, Vol 250, Issue 4986, 1426-1429
Copyright © 1990 by American Association for the Advancement of Science
Disruption of the human SCL locus by "illegitimate" V-(D)-J recombinase activity
PD Aplan,
DP Lombardi,
AM Ginsberg,
J Cossman,
VL Bertness,
and
IR Kirsch
National Cancer Institute-Navy Medical Oncology Branch, Naval Hospital, Bethesda, MD 20889-5105.
A fusion complementary DNA in the T cell line HSB-2 elucidates a provocative mechanism for the disruption of the putative hematopoietic transcription factor SCL. The fusion cDNA results from an interstitial deletion between a previously unknown locus, SIL (SCL interrupting locus), and the 5' untranslated region of SCL. Similar to 1;14 translocations, this deletion disrupts the SCL 5' regulatory region. This event is probably mediated by V-(D)-J recombinase activity, although neither locus is an immunoglobulin or a T cell receptor. Two other T cell lines, CEM and RPMI 8402, have essentially identical deletions. Thus, in lymphocytes, growth-affecting genes other than immune receptors risk rearrangements.
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