Chicken leukosis virus genome sequences in DNA from normal chick cells and virus-induced bursal lymphomas

Nelman, Paul E.; Purchase, H. G.; Okazaki, W.

doi:10.1016/0092-8674(75)90151-8

Cited by 38 publications

(30 citation statements)

References 27 publications

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“…The amount of viral RNA in the cell may increase as much as 5000-to 20,000-fold after virus infection of chf-cells, but viral DNA content increases only slightly, perhaps two-fold (26,(38)(39)(40). It is clear, therefore, that regulation occurs at some step controlling viral RNA content, but we cannot determine whether this process affects the synthesis or the breakdown of RNA, since the hybridization assay used in these experiments measures only the steady state RNA level.…”

Section: This Results Is Consistent With the Location Of The Env Gene mentioning

confidence: 99%

Independent regulation of endogenous and exogenous avian RNA tumor virus genes.

Hayward¹,

Hanafusa²

1976

Proc. Natl. Acad. Sci. U.S.A.

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Uninfected fibroblasts from chicken embryos contain avian leukosis-sarcoma virus genetic information in the form of DNA (1-3), which may exist in a latent unexpressed state or may be at least partially expressed, as shown by the presence of viral specific RNA, structural proteins, and the envelope glycoprotein (4)(5)(6)(7)(8)(9)(10)(11)(12). The last mentioned product complements a defect of the Bryan strain of Rous sarcoma virus (BH-RSV) and is thus known as chicken helper factor (chf) (8). The regulatory function which controls the expression of the endogenous virus-related genes (9, 13) appears to act at some step controlling the amount of viral RNA in the cell, either by altering the rate of transcription or by affecting the stability of the RNA (4, 5). Certain cell types, in particular those derived from line 7 or related chicken lines, spontaneously release an infectious virus, RAV-O. Virus production in these cells is genetically controlled (14,15), and appears to correlate with the presence or absence of viral RNA (unpublished results). However, most types of uninfected cells, including those used in the present study, do not produce virus particles even though viral RNA and proteins may be synthesized. This lack of virus production suggests either that certain viral genes are unexpressed in these cells, or that the endogenous viral genome is incomplete or defective.Infection of chicken cells with avian leukosis-sarcoma viruses results in substantial increases in the amounts of viral RNA and in production of progeny virus. The amounts of RNA and virus in infected cells are essentially the same in both endogenous chicken helper factor positive (chf+) and chicken helper factor negative (chf-) cells (4, 16 (13,20). Two classes of chf+ chicken embryos have been described, which contain high levels (hH) and extremely high levels (hE) of helper activity (4, 13). Where necessary, they are designated as chf+ (hH) and chf+ (hE). The Schmidt-Ruppin strain RSV, subgroup A (SR-RSV-A), SR-RSV-B (21), and SR-RSV-N8 (22) were kindly provided by S. Kawai of this laboratory; RAV-0 was spontaneously released from Line 100 chicken cells (kindly supplied by L. B. Crittenden, U.S. Dept. of Agriculture, East Lansing, Mich.). Other viruses used in this study were Rous associated virus-2 (RAV-2), RAV-7, and BH-RSV(-). Their preparation has been described before (6,21). BH-RSV-infected cell cultures were prepared by infection of chf-cells with BH-RSV(-) in the presence of ultraviolet light-inactivated Sendai virus (6, 16) and were fully transformed after several cell transfers.Nucleic Acid Extraction. Cellular and viral RNAs were extracted as described previously (4). Cell DNA was purified by the methods of Marmur (23) and Berns and Thomas (24) as modified by Schincariol and Joklik (25). For annealing experiments, the DNA was cleaved by acid hydrolysis to an average length of approximately 150 nucleotides (26).

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Section: This Results Is Consistent With the Location Of The Env Gene mentioning

confidence: 99%

Independent regulation of endogenous and exogenous avian RNA tumor virus genes.

Hayward¹,

Hanafusa²

1976

Proc. Natl. Acad. Sci. U.S.A.

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“…Amplified RNA was prepared with a MessageAmp kit (Ambion, Austin, TX, USA) as per the manufacturer's instructions. DNA was prepared as described (Neiman et al, 1975).…”

Section: Methodsmentioning

confidence: 99%

Genomic instability during Myc-induced lymphomagenesis in the bursa of Fabricius

Kimmel

Icreverzi

et al. 2006

Oncogene

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Retroviral vector-mediated overexpression of c-myc in embryonic bursal precursors induces multi-staged tumorigenesis beginning with preneoplastic-transformed follicles (TF) and progressing to clonal metastatic B-cell lymphomas. Using a 13K chicken cDNA microarray, specifically enriched for chicken immune system expressed sequence tagged (ESTs), we carried out array-based comparative genomic hybridization (array-CGH) and detected significant DNA copy number change at many loci on most or all chromosomes in both early TF and end-stage lymphomas. Formation of long palindromes, through breakage-fusion-bridge cycles, is thought to play an early role in gene amplification. Employing genome-wide analysis of palindrome formation (GAPF), we detected extensive palindrome formation in early TF and end-stage lymphomas. The population of loci showing amplification by array-CGH was enriched for palindromes detected by GAPF providing strong evidence for genetic instability early in Myc-induced tumorigenesis and further support for the role of palindromes in gene amplification. Comparing gene copy number change and RNA expression changes profiled on the same cDNA array, we detected very little consistent contribution of gene copy number change to RNA expression changes. Palindromic loci in TF and tumors, however, were expressed, many at high levels, suggesting an abundance of RNA species with long double-stranded segments generated during tumorigenesis.

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“…The nephroblastoma and neoplastic bursal nodule were derived from the progeny of Line 151 x brown leghorn crosses infected with a previously characterized field isolate, ALV 5938 (3,4). The development of tumors in these chickens, characterization of ALV DNA in various tissues by using a representative cDNA probe, and detection of activated transforming genes in the tumor DNA have been described elsewhere (5,6).…”

Section: Methodsmentioning

confidence: 99%

Independent recombination between avian leukosis virus terminal sequences and host DNA in virus-induced proliferative disease.

Neiman¹,

Beemon²,

Luce³

1981

Proc. Natl. Acad. Sci. U.S.A.

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A cDNA transcript of Rous sarcoma virus, which contained the long terminal repeat (LTR) and some additional 3'-terminal sequences, was inserted into the plasmid pBR322. This recombinant plasmid, p53, was then used as a hybridization probe to detect viral terminal sequences in DNA from a number of tissues of birds with a variety of avian leukosis virus (ALV)-induced proliferative diseases. Using restriction endonuclease digestion and blot hybridization analysis, we detected, in addition to standard ALV genomes, viral terminal sequences linked to host DNA and not to viral genes. In DNA from bursal lymphomas and nephroblastomas, we observed small numbers of integration sites occupied by sequences in p53 and lacking most or all of the remainder of the viral genome. In DNA from osteopetrosis, we observed apparently multiple copies of molecules containing host DNA linked to viral LTR sequences. Some of these structures were contained in discrete, probably unintegrated, DNA molecules. We concluded that viral LTR sequences can be inserted as independent elements during recombination with host DNA in some forms of interaction between exogenous retroviruses and host cells. Because the LTRs have been implicated in integration and transcription of viral genes, the possibility that translocation or activation, or both, of host genes may occur as a consequence of viral infection is reinforced by these observations. The DNA copies of avian leukosis virus (ALV) genomes in infected cells are bounded by long terminal repeat (LTR) sequences composed of 101 base pairs (bp) from the 5' end and about 200 bp from the 3' end of genomic viral RNA (1, 2). These structures have been implicated in viral functions such as integration and transcription and bear a striking resemblance to nonviral transposable elements detected in lower organisms. We have investigated the possibility that LTR sequences derived from exogenous avian retroviruses might behave as independent elements in some host cells. The organization of viral sequences in DNA from a variety of normal, preneoplastic, and neoplastic tissues of ALV-infected chickens was compared by restriction endonuclease digestion and blot hybridization analysis. Two hybridization probes were used: one that detects the bulk of the viral genome but not the LTR and another that detects primarily the LTR. We report here that LTR sequences linked to host and not viral DNA were detected in several proliferative diseases induced by ALV.

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Chicken leukosis virus genome sequences in DNA from normal chick cells and virus-induced bursal lymphomas

Cited by 38 publications

References 27 publications

Independent regulation of endogenous and exogenous avian RNA tumor virus genes.

Independent regulation of endogenous and exogenous avian RNA tumor virus genes.

Genomic instability during Myc-induced lymphomagenesis in the bursa of Fabricius

Independent recombination between avian leukosis virus terminal sequences and host DNA in virus-induced proliferative disease.

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