DNA of avian myeloblastosis-associated virus type 2 integrates at multiple sites in the chicken genome

We analyzed retroviral integration into a host genome by using avian sarcoma virus infection of natural target cells under conditions where secondary integration via virus spread was inhibited. This was accomplished by using the noninfectious polenv-a variant of the Bryan high-titer strain of Rous sarcoma virus. A total of 12 independent Bryan high-titer Rous sarcoma virus-transforned chicken embryo fibroblast clones were obtained and mapped by using restriction endonucleases. Provirus-cell junction fragments were identified with appropriate hybridization probes. We found that expression of the viral genes could occur after proviral integration at many sites on the chicken genome and that there was no apparent preference for specific integration sites.

Section: -mentioning

confidence: 99%

Integration of Rous sarcoma virus DNA into chicken embryo fibroblasts: no preferred proviral acceptor site in the DNA of clones of singly infected transformed chicken cells

Lerner¹,

Skalka²,

Hanafusa³

1981

Developmental and molecular aspects of nephroblastomas induced by avian myeloblastosis-associated virus 2-O

Böni-Schnetzler¹,

Böni²,

Ferdinand³

et al. 1985

Avian myeloblastosis-associated virus-induced nephroblastomas are tumors consisting mainly of mesenchymal and epithelial renal elements with variable degrees of differentiation. The spatial distribution of developmental stages reflects a gradient of differentiation from less differential structures in the periphery towards more differentiated structures in the center of the lobules formed in the nephroblastomas. These heterogenic tumors contain discrete virus-cell DNA junction fragments and are therefore clonal outgrowths of a single transformed cell. These findings support the hypothesis that a mesenchymal, nephrogenic cell residual in the postembryonic kidney is the origin of the tumor, which grows by proliferation and differentiation of this target cell. All the tumors expressed higher levels of viral genomic and env messages than nontransformed tissue from the same kidney. A screening of oncogene expression with 13 different oncogenes revealed enhanced myc levels. There was, however, no rearrangement of c-myc or of the other oncogenes detected with EcoRI-digested tumor DNAs. This suggests that there is no insertion of viral elements adjacent to a c-myc. The levels of myc expression in embryonic kidneys were as high as in the tumors. Therefore, the enhanced myc expression in nephroblastomas is a reflection of the embryonic status of the tumor rather than a newly acquired function. This finding, plus the similarity of development and morphology of nephroblastomas and embryonic kidneys, suggests that the tumors arise as a result of a deficiency in a function which turns the embryonic status off.

Infrequent involvement of c-fos in avian leukosis virus-induced nephroblastoma

Collart

Aurigemma

Smith

et al. 1990

To determine whether c-fos is involved in avian leukosis virus-induced nephroblastoma, 28 tumors from chickens were analyzed for novel fos fragments. DNA from 1 of 16 clonal outgrowths (in chicken 6561) contained novel fos-related EcoRI and KpnI fragments which hybridized to both v-fos and viral probes. Oncogenicity tests using filtered 6561 tumor cell homogenates did not reveal a tumor-inducing transduction of c-fos. We conclude that c-fos is only an occasional target for proviral insertions or new transductions in avian leukosis virus-induced nephroblastoma. The results also identify a polymorphism in c-fos in K28 chickens and demonstrate that unintegrated viral DNA is not a general characteristic of avian leukosis virus-induced nephroblastoma.