Multiple immunoglobulin heavy-chain gene transcripts in Abelson murine leukemia virus-transformed lymphoid cell lines
Abstract
Lymphoid cells transformed by Abelson murine leukemia virus (A-MuLV) contain three classes of RNA transcripts from immunoglobulin mu genes. P mu-mRNAs (productive) correspond to the normal 2.7-kilobase (kb) membrane (mu m) and 2.4-kb secreted (mu s) mu mRNA species both in size and coding capacity and occur at approximately equal abundance in most mu-positive (pre-B-like) A-MuLV transformants. A mu-mRNAs (aberrant) generally fall into one of two categories--aberrantly small 2.3-kb mu m and 2.0-kb mu s mRNAs which encode aberrantly small mu polypeptide chains, or normal-sized, V H-containing mu RNAs which do not encode immunologically identifiable mu polypeptide chains. In one case, the latter type of A mu-mRNA was demonstrated to result from an in-phase termination codon in the D segment of the mu mRNA. Also, most, if not all, A-MuLV transformants express members of a 3.0 to 1.9-kb set of C mu-containing, but V H-negative S mu-RNAs (for sterile), the expression of which may occur simultaneously with but independently of P mu-mRNAs or A mu-mRNAs. The S mu-RNA sequences do not encode immunologically identifiable mu chains and can be produced by cells with unrearranged heavy-chain alleles, such as T-lymphocytes, although the structure of the S mu-RNAs from T-lymphoid cells appears to be different from that of B-lymphoid cell S mu-RNAs. Certain A-MuLV transformants also express gamma-RNA sequences that are probably analogous to the three different forms of mu RNA. These data support the concept that heavy-chain allelic exclusion, like that of light chains, is not mediated by control at the DNA or RNA levels but is probably a consequence of feedback control from cytoplasmic mu chains.
Additional Information
Copyright © 1982 by the American Society for Microbiology. Received 11 December 1981/Accepted 22 January 1982 We thank Margaret Woo, Elise Thomas, and Michael Paskind for assistance with aspects of this work, and Michael Boss for generously providing Charon 16A DNA arms. This work was supported by grant MV-34M from the American Cancer Society (to D.B.), Public Health Service core grant CA-14051 from the National Cancer Institute (to S.E. Luria), Public Health Service grants CA-24220 and CA-24530 from the National Cancer Institute (to N.R.), and by a contribution from The Whitehead Charitable Foundation (to D.B.). F.W.A. was a Special Fellow of the Leukemia Society of America. N.R. is the recipient of a Research Career Development Award from the National Cancer Institute. D.B. is an American Cancer Society Research Professor.Files
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2007-01-03Created from EPrint's datestamp field
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