Organization of chicken DNA sequences homologous to the transforming gene of avian myeloblastosis virus. II. Isolation and characterization of lambda proto-amv DNA recombinant clones from a library of leukemic chicken DNA

Infection of young chickens with RAV-1, a subgroup A isolate of avian leukosis virus, results in the development of lymphoid leukosis, a B-cell lymphoma characterized by provirus insertion into the c-myc locus. We report here that when 12to 13-day-old embryos rather than 1-day-old chickens were infected with RAV-1, a novel B-cell lymphoma developed in which proviral insertions had activated expression of the c-myb gene. These tumors expressed elevated levels of a 4.5-kilobase myb-containing mRNA transcript that contained c-myb sequences not found in v-myb. The c-myc locus in these tumors appeared normal. The biological properties of the activated myb lymphoma were distinct from those of lymphoid leukosis. Metastatic disease developed within 7 weeks of infection. Distinct intermediate pathogenic stages with preneoplastic and primary neoplastic lesions were not detected. Although bursal tissues appeared to be nonmalignant on gross examination, Southern analyses of bursal DNA revealed the presence of tumor with the same clonal origin as abdominal lymphoma masses. The dependence on embryonic infection for development of activated myb lymphoma suggests that the target cells in which c-myb is activated are found only in embryos and are distinct from those cells that give rise to lymphoid leukosis.

Section: Resultsmentioning

confidence: 68%

“…Of 13 sites examined in this study, all were confirmed in SC strain chicken DNA by Southern analysis with v-myb-derived probes. Additional restriction sites were mapped in clone X121, provided by M. Baluda (31). v-myb-homologous exons are indicated by open boxes.…”

Section: Resultsmentioning

confidence: 99%

RAV-1 insertional mutagenesis: disruption of the c-myb locus and development of avian B-cell lymphomas

Pizer

Humphries

1989

“…Of 13 sites examined in this study, all were confirmed in SC strain chicken DNA by Southern analysis with v-myb-derived probes. Additional restriction sites were mapped in clone 121 provided by M. Baluda (37). v-myb homologous exons are indicated by shaded boxes; c-myb exons 5' of v-myb homologous sequences are indicated by open boxes.…”

mentioning

confidence: 99%

Activation of the c-myb locus is insufficient for the rapid induction of disseminated avian B-cell lymphoma

Pizer

Baba

Humphries

1992

“…Avian myeloblastosis virus (AMV) is a replication-defective retrovirus that transforms hematopoietic cells in vitro (3, 39) and induces myeloblastic leukemia in vivo (6,39,55). The tumorigenicity of AMV has been attributed to a nucleotide sequence, designated v-myb (16), which is located at the 3' end of the viral genome (18,31,49,58) and probably arose by the integration of several exons of a cellular gene known as c-myb (4, 20,30,[46][47][48]58). Expression of v-myb proceeds through a spliced subgenomic messenger RNA of 2.0 kilobases (kb) (14,22) which is translated into a 45,000to 48,000-Mr protein (13,32).…”

mentioning

confidence: 99%

Transformation of Brown Leghorn chicken embryo fibroblasts by avian myeloblastosis virus proviral DNA

Soret¹,

Krycève-Martinerie²,

Crochet³

et al. 1985

Self Cite

Brown Leghorn chicken embryo fibroblasts were transfected with a mixture of avian myeloblastosis virus (AMV) and myeloblastosis-associated virus type 1 (MAV1) proviral DNA purified from X-Charon 4A recombinant clones. A transformed cell line (TlAM) able to grow without anchorage in semisolid medium was obtained. The presence of both proviral AMV and MAV sequences was detected in TlAM DNA by hybridization with v-myband MAV1-specific probes. Altered AMV and MAVI proviral genomes were found in TlAM genome. Characterization of the RNA species expressed in transformed cells showed that in addition to a 2.5-kilobase (kb) putative subgenomic v-myb-specific RNA, three other myb-containing RNAs (9.4, 8.4, and 7.0 kb) were present in TlAM cells. No AMV genomic RNA was detected. Also, a new 5.0-kb MAV1-specific RNA species was expressed in transformed cells in addition to MAV1 genomic RNA species (7.8 kb). No infectious AMV virions are released by TlAM cells. Chicken embryo fibroblasts infected by TlAM-released virions contained and expressed all MAV1 sequences detected in TlAM transformed cells but did not express any transformation parameter. These results indicated that the presence of AMV proviral sequences in TlAM cells is responsible for their transformed phenotype.