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 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.
Raines
M A
MA
Lewis
W G
WG
Crittenden
L B
LB
Kung
H J
HJ
D000483:Alleles; D000818:Animals; D001287:Attachment Sites, Microbiological; D001353:Avian Leukosis / Q000235:genetics*; D001354:Avian Leukosis Virus / Q000235:genetics*; D001483:Base Sequence; D002645:Chickens; D066246:ErbB Receptors; D005814:Genes, Viral; D009857:Oncogenes; D009876:Operon; D011956:Receptors, Cell Surface / Q000235:genetics
D011956:Receptors, Cell Surface; D066246:ErbB Receptors