c-erbB Activation in Avian Leukosis Virus-Induced Erythroblastosis: Clustered Integration Sites and the Arrangement of Provirus in the c-erbB Alleles

There is considerable evidence that links the activation of cellular genes to oncogenesis. We previously reported that structural rearrangements in the cellular oncogene c-erbB correlate with the development of erythroblastosis induced by avian leukosis virus (ALV). c-erbB recently has been shown to...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1985-04, Vol.82 (8), p.2287-2291
Main Authors: Raines, Maribeth A., Lewis, Wynne G., Crittenden, Lyman B., Kung, Hsing-Jien
Format: Article
Language:English
Subjects:
Alleles
Animals
Attachment Sites, Microbiological
Avian Leukosis - genetics
avian leukosis virus
Avian Leukosis Virus - genetics
Base Sequence
Biological and medical sciences
Cell physiology
Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
Chickens
DNA probes
ErbB Receptors
Exons
Fundamental and applied biological sciences. Psychology
Genes, Viral
Introns
Molecular and cellular biology
Oncogenes
Operon
Promoter regions
Proviruses
Receptors, Cell Surface - genetics
Region of integration
Viruses
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Summary:There is considerable evidence that links the activation of cellular genes to oncogenesis. We previously reported that structural rearrangements in the cellular oncogene c-erbB correlate with the development of erythroblastosis induced by avian leukosis virus (ALV). c-erbB recently has been shown to be related to the gene encoding epidermal growth factor receptor. We now have characterized the detailed mechanisms of c-erbB activation by ALV proviruses. We report here that the ALV proviral integration sites are clustered 5′to the region where homology to v-erbB starts, suggesting that interruption in this region of c-erbB is important for its activation. The proviruses are oriented in the same transcriptional direction as c-erbB and usually are full-size. The latter finding is in contrast to the frequent deletions observed within the c-myc-linked proviruses in B-cell lymphomas. We have also identified a second c-erbB allele, which differs from the previously known allele primarily by a deletion in an intron region. This allele is also oncogenic upon mutation by an ALV provirus.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.82.8.2287