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PubMed1983

Further evidence for the protein coding potential of the mouse mammary tumor virus long terminal repeat: nucleotide sequence of an endogenous proviral long terminal repeat.

The 3' half of an endogenous mouse mammary tumor virus from a C3H mouse was cloned in the Charon 4A vector phage. A comparison of the proviral clone with previously published endogenous mouse mammary tumor virus restriction maps identified it as endogenous unit II (J. Cohen and H. Varmus, Nature [London] 278:418-423, 1979), which is present in all inbred mouse strains derived from the original Bagg albino x DBA cross. The nucleotide sequence of the unit II long terminal redundancy (LTR) was determined and compared with the sequence previously determined for the exogenous C3H virus LTR (Donehower et al., J. Virol. 37:226-238, 1981). Virtually all sequence differences between the two LTRs were base substitutions. The total amount of sequence divergence was 6.6%. The large open reading frame reported previously in the exogenous LTR was preserved in the endogenous LTR. In addition, the pattern of sequence divergence was highly nonrandom with respect to the putative amino acid codons of the two open reading frames. Most of the base substitutions in this region resulted in silent or conservative amino acid codon changes. The nonrandom divergence pattern indicates that selective forces are operating on this segment of DNA and argues that the putative protein is functional in the life cycle of mouse mammary tumor virus. Possible roles for the protein and its mode of expression are discussed.

Amino Acid Sequence↗

PubMed1980

Subgenomic fragment of molecular cloned Friend murine leukemia virus DNA contains the gene(s) responsible for Friend murine leukemia virus-induced disease.

Friend murine leukemia virus (G-MuLV) is a helper-independent, type C retrovirus isolated from stocks of Friend virus complex (spleen focus-forming virus plus MuLV). In cell culture, F-MuLV has an ecotropic and NB-tropic host range and causes XC cells to fuse. When injected into newborn NIH Swiss mice, F-MuLV produces hepatosplenomegaly, severe anemia, and numerous circulating hematopoietic precursors in the peripheral blood with normal thymus and lymph nodes after 3 to 6 weeks. Recently, we molecularly cloned an 8.5-kilobase pair (kbp) form of F-MuLV DNA from which we could recover the pathogenic F-MuLV virus by DNA transfection of NIH 3T3 cells. From this molecularly cloned F-MuLV DNA, we have now subcloned in pBR322 a 4.1-kbp HindIII fragment which contains in continuity 3.0 kbp from the 3' terminus (env and c region), 0.6 kbp of the terminal repeat sequences, and 0.5 kbp from the 5'terminus of the viral RNA (genome). NIH 3T3 fibroblasts were transfected with this DNA fragment an then infected with the wild mouse amphotropic retrovirus (cl 1504-A). In cell culture, 1504-A is a helper-independent type C virus which has an N-tropic host range and does not cause fusion of XC cells. When injected into newborn NIH Swiss mice, 1504-A does not produce splenomegaly or thymic enlargement in mice held for up to 8 months. The transfection with the F-MuLV fragment and the infection with 1504-A consistently yielded virus preparations that were XC positive. From such virus stocks we were able to isolate both helper-independent and replication-defective XC-positive viruses. The helper-independent virus was shown to be a recombinant virus since it contains a gp70 molecule derived at least in part from F-MuLV and a specific gag precursor derived from 1504-A as determined by radioactive immune precipitation assays. When injected into newborn Swiss mice, the recombinant helper-independent virus caused hepatosplenomegaly in approximately 50% of the mice in 6 to 8 weeks. The histology of the diseased splenic tissue was indistinguishable from that seen in the disease caused by the whole F-MuLV. The replication-defective virus could be pseudotyped with new 1504-A virus, and this viral complex also caused the F-MuLV disease picture when the complex was injected into newborn Swiss mice. We conclude that the genetic information responsible for the pathogenicity of F-MuLV is contained within the 4.1-kbp DNA fragment, which includes env gene sequences, the terminal repeat sequences, and the c region sequences of the F-MuLV genome.

Animals↗

PubMed2000

Tnr8, a foldback transposable element from rice.

An insertion sequence 418 bp in length was found in one member of rice retroposon p-SINE1 in Oryza glaberrima. This sequence had long terminal inverted repeats (TIRs) and is flanked by direct repeats of a 9-bp sequence at the target site, indicative that the insertion sequence is a rice transposable element, which we named Tnr8. Interestingly, each TIR sequence consisted of a unique 9-bp terminal sequence and six tandem repeats of a sequence about 30 bp in length, like the foldback transposable element first identified in Drosophila. A homology search of databases and analysis by PCR revealed that a large number of Tnr8 members with sequence variations were present in the rice genome. Some of these members were not present at given loci in several rice species with the AA genome. These findings suggest that the Tnr8 family members transposed long ago, but some appear to have mobilized after rice strains with the AA genome diverged. The Tnr8 members are thought to be involved in rearrangements of the rice genome.

Base Sequence↗

PubMed1984

Long terminal repeat nucleotide sequence and specific insertion of the gypsy transposon.

We have determined the nucleotide sequences of the long terminal repeats of the transposable element gypsy from the cloned mutant alleles sc1, bx3, and bx34e. These mutations are suppressible by the suppressor of Hairy-wing, su(Hw). The long terminal repeats are 482 base pairs long and are highly conserved. In each case, gypsy is inserted into the sequence T-A-C-A-T-A and generates a duplication of the sequence T-A-C-A. This was verified by sequencing an empty site in the wild-type bx gene. Consideration of the sequence of the long terminal repeats and their surroundings limits the possible explanations for the mechanism of mutation by these gypsy insertions and for their suppression by su(Hw).

Animals↗

PubMed1985

Expression of long terminal repeat (LTR) sequences in carcinogen-induced murine skin carcinomas.

RNA sequences homologous to the Long Terminal Repeat (LTR) sequence of Moloney Murine Leukemia Virus proviral DNA are expressed in murine squamous cell carcinomas of the skin induced by chemical carcinogens. These transcripts range in size from 8.2 to less than 2.4 kb but their size profile varies between individual tumors. These RNAs are not detected in the poly A+ RNA fraction obtained from the epidermis of control mice or carcinogen induced skin papillomas. The poly A+ RNAs from the livers and spleens of some of the mice with skin carcinomas also revealed LTR related sequences, whereas these RNAs were not detected in the livers and spleens of control mice or of carcinogen-treated mice that did not develop carcinomas. Thus, chemical carcinogenesis in mouse skin is associated with constitutive expression of endogenous retrovirus related sequences in the carcinomas as well as in certain apparently normal host tissues.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed2000

A developmentally regulated deletion element with long terminal repeats has cis-acting sequences in the flanking DNA.

Approximately 6000 specific DNA deletion events occur during development of the somatic macro-nucleus of the ciliate Tetrahymena. The eliminated Tlr1 element is 13 kb or more in length and has an 825 bp inverted repeat near the rearrangement junctions. A functional analysis of the cis -acting sequences required for Tlr1 rearrangement was performed. A construct consisting of the entire inverted repeat and several hundred base pairs of flanking DNA on each side was rearranged accurately in vivo and displayed junctional variability similar to the chromosomal Tlr1 rearrangement. Thus, 11 kb or more of internal element DNA is not required in cis for DNA rearrangement. A second construct with only 51 bp of Tetra-hymena DNA flanking the right junction underwent aberrant rearrangement. Thus, a signal for determination of the Tlr1 junction is located in the flanking DNA, 51 bp or more from the right junction. Within the Tlr1 inverted repeat are 19 bp tandem repeats. A construct with the 19mer repeat region deleted from the right half of the inverted repeat utilized normal rearrangement junctions. Thus, despite its transposon-like structure, Tlr1 is similar to other DNA rearrangements in Tetrahymena in possessing cis -acting sequences outside the deleted DNA.

Animals↗

PubMed1982

Nucleotide sequence analysis of the long terminal repeat of integrated simian sarcoma virus: evolutionary relationship with other mammalian retroviral long terminal repeats.

Nucleotide sequence analysis of the long terminal repeat (LTR) of the integrated simian sarcoma virus showed that the simian sarcoma virus LTR comprised 504 nucleotides with an inverted repeat of seven bases at its 5' and 3' termini. At the site of simian sarcoma virus integration, cellular flanking sequences adjacent to the proviral LTR contained a direct repeat of four bases. A 13-base sequence after the 5' LTR was found to be complementary to prolyl tRNA, suggesting that tRNAPro may serve as the primer for reverse transcription of simian sarcoma virus RNA. The U5 and R regions, derived respectively from the 5' end and terminally redundant sequences of the viral RNA, were found to have similar organization and sequence homology close to that of Moloney murine sarcoma virus or Moloney murine leukemia virus. These results indicate that regions within LTRs with known functionally important sequences have been most well conserved during retrovirus evolution.

Biological Evolution↗

PubMed1980

Frequent site-specific deletion of coliphage lambda murine sarcoma virus recombinants and its use in the identification of a retrovirus integration site.

Stocks of hybrid lambda phages carrying the complete integrated provirus of either m1 or HT1 Moloney murine sarcoma virus, as well as flanking host sequences, frequently contain significant numbers of phages carrying a specific deletion. This deletion arises from a recombination event between the terminally repeated sequences in the provirus that deletes the unique Moloney murine sarcoma virus sequences bracketed by the terminally repeated sequences. Physical mapping has shown that the deletion phage retains one complete copy of the terminally repeated sequence and the flanking mink host sequences. One such deletion, lambdaHT1r+, was used to characterize a mink genomic DNA sequence that contains an HT1 Moloney murine sarcoma virus integration site. This integration site sequence from normal mink cells was also cloned into phage lambda. An analysis of the heteroduplexes between the integration site and the lambdaHT1r+ deletion indicated that no major rearrangement of host sequences occurred upon integration of the Moloney murine sarcoma provirus.

Animals↗

PubMed1992

Interaction of SEWA sarcoma cell proteins with the intracisternal A-type particle long terminal repeat DNA sequence.

Intracisternal A-type particle (IAP) transcripts are endogenous retrovirus-like sequences expressed during specific stages of normal development and in a variety of murine tumors. In this study, we have analyzed two cell lines derived originally from the SEWA murine osteosarcoma and grown either as ascites or as solid tumors, for proteins that might regulate IAP expression. We found that subline AA7-NA, originally derived from the ascites tumor, expressed about five times more IAP RNA than the AS12-AD subline, which was derived from a solid tumor. In view of this finding, we examined the binding of cellular proteins from the two cell lines to the 5' end of an IAP long terminal repeat sequence. Gel retardation assays of DNA-protein complexes and DNase I footprinting assays identified several DNA sequences within the long terminal repeat fragment that were protected by protein extracts from both SEWA sublines. Gel retardation assays using specific synthetic oligonucleotide sequences that correspond to two of these protected regions revealed different patterns of DNA-protein complexes with extracts from the two SEWA sublines. These data suggest that expression of IAP sequences is regulated by complex mechanisms involving several proteins that appear to differ between the two sublines.

Animals↗

PubMed1983

A unique sequence in murine leukemia virus long terminal repeat functions as a termination signal for transcription in Escherichia coli.

Moloney murine leukemia virus DNA fragments were subcloned into two plasmids downstream of active promoters to detect termination sequences for transcription initiated at these promoters. Two of the viral DNA fragments (2,050 and 595 base pairs) were able to block transcription when inserted in one orientation but not when inserted in the other. These two viral DNA fragments contained long terminal repeat sequences. Deletion of 84 base pairs from the U-3 and R regions in the long terminal repeat removed the transcription termination activity.

Cloning, Molecular↗

PubMed2000

In vivo genomic footprinting of the human T-cell leukemia virus type 1 (HTLV-1) long terminal repeat enhancer sequences in HTLV-1-infected human T-cell lines with different levels of Tax I activity.

The Tax protein of human T-cell leukemia virus type 1 (HTLV-1) enhances viral gene expression through sequences in the U3 region of the viral long terminal repeat. These sequences consist of three imperfect 21-bp repeats (TRE-1s) and a region between the promoter-central and promoter-proximal 21-bp repeats (TRE-2). The TRE-1s contain a core cyclic AMP response element (CRE) motif and can be bound by CREB, ATF-1, ATF-2, and other members of the CREB-ATF superfamily of transcription factors. Tax enhances CREB binding to TRE-1 in vitro, and it promotes dimerization of CREB as well as other bZIP proteins. Using ligation-mediated PCR on in vivo dimethyl sulfate-treated HTLV-1-infected cell lines MT-2 and MT-4, we have compiled a profile of protein occupancy in the HTLV-1 enhancer sequences in the presence of high (MT-2) and low (MT-4) levels of biologically active Tax I. The in vivo footprinting showed that all three TRE-1s were bound by protein(s), but only in MT-2 cells. In MT-2 cells, all TRE-1s showed strong protection of the G residues in the central CRE, and the footprints extended to differing degrees into the GC-rich flanking sequences. This indicated Tax I-dependent loading of transcription factors onto the HTLV-1 TRE-1s in vivo. In vivo footprinting on TRE-2 indicated that this region was bound by proteins regardless of the Tax I status of the cell line. However, the presence of Tax I increased the extent and altered the profile of proteins binding TRE-2 in vivo.

Base Sequence↗

PubMed2006

Emergence of a new human adenovirus type 4 (Ad4) genotype: identification of a novel inverted terminal repeated (ITR) sequence from majority of Ad4 isolates from US military recruits.

BACKGROUND: Ad4 is the principal etiological agent of acute respiratory disease (ARD) in the US military. Discovery of the novel 208bp inverted terminal repeated (ITR) sequence from a recent Ad4 Jax78 field isolate was totally distinct from the analogous 116bp ITR of Ad4 prototype. OBJECTIVES: To investigate the origin and distribution of the novel Ad4 ITR sequence from ARD infections. STUDY DESIGN: Direct sequencing of ligated Ad ITR termini. RESULTS: The new Ad4 ITR was highly homologous with the ITRs of human Ad subgroup B. The left post-ITR region of Ad4 Jax78 was found to be highly homologous to the corresponding region of subgroup B Ads: 81% for Ad11 and 98% for Ad3 and Ad7. The right post-ITR region of Ad4 Jax78 contained a truncated classic ITR of the Ad4 prototype. CONCLUSIONS: The Ad4 Jax78 ITR most likely evolved from Ad4 prototype by substituting the Ad4 prototype ITR with the subgroup B Ads ITR. The ITR-based PCR assays developed from this study can be used to distinguish the new Ad4 genotype from the classical Ad4 prototype. The new Ad4 genotype was first detected in 1976 from Georgia, USA, and is the main causative agent of ARD infections in US military population.

Adenovirus Infections, Human↗

PubMed2000

Retrotransposition of the I factor, a non-long terminal repeat retrotransposon of Drosophila, generates tandem repeats at the 3' end.

Non-long terminal repeat (LTR) retrotransposons or LINEs transpose by reverse transcription of an RNA intermediate and are thought to use the 3' hydroxyl of a chromosomal cleavage to initiate synthesis of the first strand of the cDNA. Many of them terminate in a poly(dA) sequence at the 3' end of the coding strand although some, like the I factor of Drosophila melanogaster, have 3' ends formed by repeats of the trinucleotide TAA. We report results showing that I factor transcripts end a few nucleotides downstream of the TAA repeats and that these extra nucleotides are not integrated into chromosomal DNA during retrotransposition. We also show that the TAA repeats are not required for transposition and that I elements containing mutations affecting the TAA sequences generate transposed copies ending with tandem repeats of various types. Our results suggest that during integration the 3' end of the I factor RNA template can pair with nucleotides at the target site and that tandem duplications are generated by the reverse transcriptase of the I factor in a manner that is reminiscent of the activity of the reverse transcriptases of telomerases. Reverse transcriptases of other non-LTR retrotransposons may function in a similar way.

Animals↗

PubMed1994

Identification of the region that determines the specificity of binding of the transposases encoded by Tn3 and gamma delta to the terminal inverted repeat sequences.

To analyze the region that determines the specificity of binding of the Tn3 transposase to the terminal inverted repeat sequences (IR), we first determined the nucleotide sequence of a Tn3-family transposon, gamma delta, which is supposed to encode a transposase similar to that of Tn3. gamma delta was 5981 bp in length and contained three coding frames: Two were the genes, tnpA and tnpR, encoding transposase (1002 amino acids) and resolvase/repressor (183 amino acids), respectively, and the third, named tnpX, encoding a protein (698 amino acids) of unknown function but containing two NTP-binding motifs. Utilizing the tnpA sequence, we then constructed a series of Tn3-gamma delta hybrid genes encoding chimeric proteins in the N-terminal segments of the transposases (amino acid position 1 to 242 of Tn3 or 1' to 243' of gamma delta), which has been previously shown to be responsible for specific binding of transposase to IR sequences in Tn3. Examination of their DNA-binding activities revealed that the subsegment of the N-terminus from amino acid position 1 to 109 determines the specificity of binding to the IR sequences. The third coding frame found in gamma delta, tnpX, is located downstream of tnpR and is expressed from the tnpR promoter in the absence of the tnpR gene product, resolvase/repressor, to produce a protein that inhibits the growth of the host cells. Possible roles of this protein are discussed.

Amino Acid Sequence↗

PubMed1990

Transcription of human endogenous retroviral long terminal repeat (LTR) sequence in a lung cancer cell line.

The human genome carries several endogenous retroviral sequences. One of them that we named 'HERV-A', carries almost the complete sequence of the long terminal repeat (LTR), and is located in the 5' region of the amylase genes (M.Emi, A.Horii, N.Tomita, T.Nishide, M.Ogawa, T. Mori and K.Matsubara, Gene 62: 229-235, 1988). Using this sequence as a probe, we found a 1.4 kb LTR transcript(s) in a lung cancer cell line. No corresponding transcript was observed in control cells. Two partial, but different cDNA clones were obtained, and each one was found to be a transcript starting within human sequences at 5' upstream from the LTR and ending within the LTR sequence.

Base Sequence↗

PubMed1991

Functional analysis of the two domains in the terminal inverted repeat sequence required for transposition of Tn3.

Bacterial transposon Tn3 has a 38-bp terminal inverted repeat (IR) sequence. The IR sequence has been divided into two domains, A and B, of which domain B is bound by transposase, and domain A is not Here, we defined the two domains more precisely by constructing three IR mutants with a 2-bp substitution at relevant sites within the IR sequence, followed by examination of the binding of transposase to the fragments containing these IR mutants: domain A was located at bp 1-11, whereas domain B was at bp 12-38. To see if the two domains in the IR are functionally distinct, we constructed mini-Tn3 derivatives flanked by two IRs with various 2-bp substitutions within domain A or B, and analyzed their ability to mediate cointegration. The mini-Tn3 derivatives flanked by IR(A+ B+) and IR(A- B+) [or IR(A+ B-)] and those flanked by IR(A-B+) and IR(A+ B-) mediate cointegration more efficiently than the mini-Tn3 derivatives flanked by two IR(A- B+)s or by two IR(A+ B-)s. These results and others presented here indicate that the two domains of IR are functionally distinct in promoting cointegration.

Base Sequence↗

PubMed1987

Phylogenetic relationships between adenoviruses as inferred from nucleotide sequences of inverted terminal repeats.

The nucleotide (nt) sequences of inverted terminal repeats (ITR) from human adenovirus (Ad) 19, bovine Ad1 (BAd1), bovine Ad3 (BAd3), canine Ad2 (CAd2) and an avian Ad, EDS-76, were determined. The length of the ITR sequence was 160 bp in Ad19, 159 bp in BAd1, 195 bp in BAd3, 196 bp in CAd2 and 52 bp in EDS-76. CAd2 had the longest ITR among the examined Ads, BAd3 the second longest, and EDS-76 had the shortest ITR. A TAAT sequence located between the 10th and 13th nt counted from the ends was conserved in all Ads examined so far. To determine phylogenetic relationships among human and animal Ads, sequences of their ITRs were compared, and a phylogenetic tree was constructed by using the maximum-likelihood method. It is the method involving statistical analysis of computing the probability of a particular set of sequences on a given tree and maximizing this probability over all evolutionary trees [Felsenstein, J. Mol. Evol. 17 (1981) 368-376]. From these analyses, it was found that members belonging to the same human Ad subgenus are related closely to each other, whereas representatives of different human subgenera are distributed rather divergently among animal Ads.

Adenoviridae↗

PubMed1984

Characterization of the guinea pig cytomegalovirus genome by molecular cloning and physical mapping.

Fragments of guinea pig cytomegalovirus (GPCMV) DNA produced by HindIII or EcoRI restriction endonuclease digestion were cloned into vectors pBR322 and pACYC184, and recombinant fragments representing ca. 97% of the genome were constructed. Hybridization of 32P-labeled cloned and gel-purified HindIII, EcoRI, and XbaI fragments to Southern blots of HindIII-, EcoRI-, and XbaI-cleaved GPCMV DNA verified the viral origin of cloned fragments and allowed construction of HindIII, EcoRI, and XbaI restriction maps. On the basis of the cloning and mapping experiments, the size of GPCMV DNA was calculated to include 239 kilobase pairs, corresponding to a molecular weight of 158 X 10(6). No cross-hybridization between any internal fragments was seen. We conclude that the GPCMV genome consists of a long unique sequence with terminal repeat sequences but without internal repeat regions. In addition, GPCMV DNA molecules exist in two forms. In the predominant form, the molecules demonstrate sequence homology between the terminal fragments; in the minor population, one terminal fragment is smaller by 0.7 X 10(6) daltons and is not homologous with the fragment at the other end of the physical map. The structural organization of GPCMV DNA is unique for a herpesvirus DNA, similar in its simplicity to the structure reported for murine cytomegalovirus DNA and quite dissimilar from that of human cytomegalovirus DNA.

Animals↗