A putative second cell-derived oncogene of the avian leukaemia retrovirus E26

• Published in: Nature (London) 1983-11, Vol.306 (5941), p.395-397
• Main Authors: Leprince, D., Gegonne, A., Coll, J., de Taisne, C., Schneeberger, A., Lagrou, C., Stehelin, D.
• Format: Article
• Language: English
• Subjects: Animals; Avian Leukosis Virus - genetics; Cell Transformation, Viral; Chickens - genetics; Genes, Viral; Humanities and Social Sciences; letter; multidisciplinary; Oncogenes; RNA, Messenger - genetics; RNA, Viral - genetics; Science; Science (multidisciplinary)
• ISSN: 0028-0836; 1476-4687
• DOI: 10.1038/306395a0

The acute avian leukaemia retroviruses AMV and E26 both induce myeloblastosis in vivo and transform myeloblasts in vitro 1–5 . Both viruses contain the oncogene v- myb first described for AMV 6,7 . Unlike AMV, E26 has the additional capacity to induce erythroblastosis in vivo and to transform erythroblasts 4,5 . Previous analyses indicated that the genome of E26 also contained nucleotide sequences distinct from v- myb and unrelated to viral replicative genes 6,8,9 . Using a molecularly cloned E26 provirus, we have now identified a novel nucleotide sequence designated v- ets (for E -twenty-six specific) 10 of ∼1.5 kilobase pairs (kbp) located next to v- myb . v- ets possesses all the structural characteristics of a putative new oncogene: it has a conserved cellular counterpart c- ets which is transcribed in some normal chicken cells as a major 7.5-kb polyadenylated RNA. Although our results now await elucidation of their biological significance, we propose that v- ets could be a new oncogene accounting for the additional transforming properties of E26, or potentiating the transforming properties of the v- myb oncogene.