Low-molecular-weight RNAs and initiation of RNA-directed DNA synthesis in avian reticuloendotheliosis virus

Self Cite

Section: Cpsupporting

confidence: 86%

mentioning

confidence: 99%

See 1 more Smart Citation

tRNA's and priming of RNA-directed DNA synthesis in mouse mammary tumor virus

Peters¹,

Glover²

1980

Self Cite

“…REV-A REV-T c-re/ (turkey) primer associated with virion RNA of reticuloendotheliosis viruses and murine leukemia viruses (15,33). In contrast, avian leukosis-sarcoma viruses have tRNATTrp primers (7).…”

Section: Rev-mentioning

confidence: 99%

Nucleic acid sequences of the oncogene v-rel in reticuloendotheliosis virus strain T and its cellular homolog, the proto-oncogene c-rel

Wilhelmsen¹,

Eggleton²,

Temin³

1984

275

Reticuloendotheliosis virus strain T (Rev-T) is a highly oncogenic replication-defective retrovirus which contains the oncogene v-rel. It is thought that Rev-T arose when a virus similar to Rev-A, the helper virus of Rev-T, infected a turkey and recombined with c-rel from that turkey. There is one large c-rel locus in the turkey genome which contains all of the sequences homologous to v-rel (K. C. Wilhelmsen and H. M. Temin, J. Virol. 49:521-529, 1984). We have sequenced v-rel and its flanking sequences, each of the regions of the c-rel locus from turkey that are homologous to v-rel and their flanking sequences, and the coding sequence for env and part of pol of Rev-A. The v-rel coding sequences can be translated into a 503-amino acid env-v-rel-out-offrame-env fusion polypeptide. We have not detected any sequences in the Los Alamos or University of California-San Diego data bases that are more significantly related to the amino acid or nucleic acid sequence of v-rel than to the randomized sequence of v-rel. Comparison of Rev-A, Rev-T, and c-rel indicates that the v-rel sequences may have been transduced from the c-rel (turkey) locus by a novel mechanism. There are sequences in Rev-A and c-rel that are similar to splicing signals, indicating that the 5' virus-rel junction of Rev-T may have been formed by cellular RNA splicing machinery. Eight presumed introns have presumably been spliced out of c-rel to generate v-rel. There are also short imperfect regions of homology between sequences at the boundaries of v-rel and sequences in Rev-A and c-rel (turkey), indicating that c-rel may have been transduced by homologous recombination. There are many differences between the amino acid sequences of the predicted translational products of v-rel and c-rel which may account for their difference in transformation potential. These sequence differences between v-rel and c-rel include 10 missense transitions, four missense transversions, and three places where Rev-T has a small in-frame deletion of sequences relative to c-rel. Most of the coding sequence differences between c-rel and v-rel are nonconservative amino acid changes. * Corresponding author. 172 gene appears to be the result of a quantitative difference in the level of their expression (13, 30). We have been studying the highly oncogenic retrovirus reticuloendotheliosis virus strain T (Rev-T), which contains the oncogene v-rel. Rev-T was first isolated from a turkey (28). It is thought that Rev-T arose when a virus similar to Rev-A infected a turkey and recombined with c-rel from that turkey. Analysis of molecular clones of proviruses of Rev-T and Rev-A (Rev-A is the nondefective helper virus of Rev-T) shows that in Rev-T, v-rel is substituted for most of env in Rev-A (see Fig. 1) (3, 8, 18). Rev-T also has a large deletion of sequences which encode much of gag and pol in Rev-A. This deletion is necessary for transformation of cells by v-rel (4). In Rev-T-infected cells, there are two viral RNA transcripts that contain v-rel sequences: a full-length genomic size tran...

“…The taxonomical position of the REV group within the Retroviridae is uncertain (10,51). However, there is evidence that the REVs are related to mammalian retroviruses, all of which use tRNA Pro to initiate reverse transcription (38). The capsid and reverse transcriptase proteins share antigenic similarity (1, 3-5, 8, 18, 36).…”

Section: Discussionmentioning

confidence: 99%

The Secondary Structure of the R Region of a Murine Leukemia Virus Is Important for Stimulation of Long Terminal Repeat-Driven Gene Expression

Cupelli

Okenquist

Trubetskoy

et al. 1998

In addition to their role in reverse transcription, the R-region sequences of some retroviruses affect viral transcription. The first 28 nucleotides of the R region within the long terminal repeat (LTR) of the murine type C retrovirus SL3 were predicted to form a stem-loop structure. We tested whether this structure affected the transcriptional activity of the viral LTR. Mutations that altered either side of the stem and thus disrupted base pairing were generated. These decreased the level of expression of a reporter gene under the control of viral LTR sequences about 5-fold in transient expression assays and 10-fold in cells stably transformed with the LTR-reporter plasmids. We also generated a compensatory mutant in which both the ascending and descending sides of the stem were mutated such that the nucleotide sequence was different but the predicted secondary structure was maintained. Most of the activity of the wild-type SL3 element was restored in this mutant. Thus, the stem-loop structure was important for the maximum activity of the SL3 LTR. Primer extension analysis indicated that the stem-loop structure affected the levels of cytoplasmic RNA. Nuclear run-on assays indicated that deletion of the R region had a small effect on transcriptional initiation and no effect on RNA polymerase processivity. Thus, the main effect of the R-region element was on one or more steps that occurred after the template was transcribed by RNA polymerase. This finding implied that the main function of the R-region element involved RNA processing. R-region sequences of human immunodeficiency virus type 1 or mouse mammary tumor virus could not replace the SL3 element. R-region sequences from an avian reticuloendotheliosis virus partially substituted for the SL3 sequences. R-region sequences from Moloney murine leukemia virus or feline leukemia virus did function in place of the SL3 element. Thus, the R region element appears to be a general feature of the mammalian type C genus of retroviruses.