Rearrangement of the oncogene c-mos in mouse myeloma NSI and hybridomas

Justus B. Cohen*, Tamar Unger, Gideon Rechavi, Eli Canaani, David Givol

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

67 Scopus citations

Abstract

The activity and products of cellular oncogenes can be altered by various processes, such as the nearby integration of a retroviral genome, point mutation within the oncogene coding region, gene amplification, and chromosomal translocation (reviewed in ref. 1). Our work has provided an example of oncogene activation by yet a different process; the integration of an endogenous retrovirus-like DNA element (identified as an intracisternal A particle or IAP genome2) within the coding region of the oncogene c-mos in a mouse plasmacytoma, XRPC 243,4. The rearranged c-mos gene of XRPC24 is actively transcribed and has transforming activity3, suggesting some role for activated c-mos in the progression of the XRPC24 tumour. In this report we describe rearrangement of c-mos in a second mouse plasmacytoma, NSI, and in two hybridomas. In this case, as in XRPC24, c-mos was split by the insertion of a IAP genome. The rearranged c-mos genes (rc-mos) of NSI and XRPC24 differ in three major aspects: (1) The site of IAP integration in c-mos is in codon 30 in NSI but in codon 88 in XRPC24; (2) The orientation of the integrated IAP relative to c-mos is 'tail-to-head' in NSI and 'head-to-head' in XRPC24; and (3) transcriptional activity of rc-mos in NSI is much lower than in XRPC24. The two latter points suggest a correlation between the orientation of the long terminal repeat (LTR) of IAP relative to c-mos and its activity upon IAP integration.

Original languageEnglish
Pages (from-to)797-799
Number of pages3
JournalNature
Volume306
Issue number5945
DOIs
StatePublished - 1983
Externally publishedYes

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