The V(D)J Recombination Activating Gene, RAG-1
Abstract
The RAG-1 (recombination activating gene-1) genomic locus, which activates V(D)J recombination when introduced into NIH 3T3 fibroblasts, was isolated by serial genomic transfections of oligonucleotide-tagged DNA. A genomic walk spanning 55 kb yielded a RAG-1 genomic probe that detects a single 6.6–7.0 kb mRNA species in transfectants and pre-B and pre-T cells. RAG-1 genomic and cDNA clones were biologically active when introduced into NIH 3T3 cells. Nucleotide sequencing of human and mouse RAG-1 cDNA clones predicts 119 kd proteins of 1043 and 1040 amino acids, respectively, with 90% sequence identity. RAG-1 has been conserved between species that carry out V(D)J recombination, and its pattern of expression correlates exactly with the pattern of expression of V(D)J recombinase activity. RAG-1 may activate V(D)J recombination indirectly, or it may encode the V(D)J recombinase itself.
Additional Information
© 1989 by Cell Press. Reprinted from Cell 59: 1035–1048, © 1989, with permission from Elsevier. Received October 11, 1989. We are deeply indebted to Carolyn Gorka for her superb technical assistance with many of the aspects of the work described here, and particularly for the construction of the cDNA library from 22D6. We thank P. D'Eustachio for somatic cell hybrid DNAs, W. Dove for the bacterial strain MB408, G. Mardon for the Northern blot containing embryo RNA, R. Mosher and D. Page for the Southern blot containing mammalian DNA, A. Winoto for Northern blots and RNA samples, L. Corcoran for RNA samples, D. Weaver for scid pre-B RNA samples, D. Kaul and A. Bernarda for the Nalm 6 cDNA library, R. Risser for the 2017 and 2052D cell lines. W. Gilbert for assistance with the computer analysis of the RAG-1 sequences, and K. Struhl for many helpful discussions. We are also grateful to S. Smale, D. Black, D. Silver, M. Schlissel, and A. Winoto for critical reading of and many helpful comments on the manuscript. Finally, we gratefully acknowledge the important experimental contributions of the late Dr. Samuel Latt. This work was supported by a grant to D. B. from the American Cancer Society. D. G. S. was supported by fellowships from the Life and Health Insurance Medical Research Fund and the Whitaker Health Sciences Fund. M. A. O. was supported by NIH training grant CA09541-04 and fellowships from the Johnson and Johnson Research Fund and the Whitaker Health Sciences Fund. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to Indicate this fact.Additional details
- Eprint ID
- 102826
- DOI
- 10.1016/0092-8674(89)90760-5
- Resolver ID
- CaltechAUTHORS:20200428-072046193
- American Cancer Society
- Life and Health Insurance Medical Research Fund
- Whitaker Health Sciences Fund
- CA09541-04
- NIH Predoctoral Fellowship
- Johnson and Johnson Research Fund
- Created
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2020-04-28Created from EPrint's datestamp field
- Updated
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2021-11-16Created from EPrint's last_modified field