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At least 343 records · Page 19Linked to original sources
PubMed1991

Two regions of the mouse mammary tumor virus long terminal repeat regulate the activity of its promoter in mammary cell lines.

In vivo expression of the mouse mammary tumor virus (MMTV) is restricted to a few organs, with the highest rate of transcription found in the mammary gland. Using a series of mammary and nonmammary murine cell lines, we have identified two regulatory elements, located upstream of the hormone responsive element, that specifically regulate the MMTV promoter. The first element displays an enhancerlike activity and is coincident with the binding of a nuclear factor (designated MP4; position -1078 to -1052 in the long terminal repeat) whose presence is apparently restricted to mammary cell lines. The second regulatory region mediates a repressive activity and is mapped to the long terminal repeat segment from -415 to -483. This repression is specific for a particular subtype of mammary cells (RAC cells) able to grow under two differentiation states (A. Sonnenberg, H. Daams, J. Calafat, and J. Hilgers, Cancer Res. 46:5913-5922, 1986). The MMTV promoter in mammary cell lines thus appears to be modulated by two cis-acting elements that are likely to be involved in tissue-specific expression in vivo.

Animals↗
PubMed1991

Unregulated expression of the erythropoietin receptor gene caused by insertion of spleen focus-forming virus long terminal repeat in a murine erythroleukemia cell line.

A murine erythroleukemia (MEL) cell line, F5-5, expressed 10,000 binding sites for erythropoietin (EPO) per cell, 10-fold more than was expressed by other murine erythroleukemia cell lines and normal erythroid progenitors. Northern (RNA) and Southern blot analyses revealed overexpression of mRNA for the EPO receptor (EPOR) and rearrangement of one of the EPOR gene alleles in F5-5 cells, respectively. Molecular cloning of F5-5-derived cDNA encoding EPOR revealed that the 5' noncoding region of the EPOR cDNA corresponds to the 3' long terminal repeat sequence of the polycythemic strain of Friend spleen focus-forming virus (F-SFFVP). The aberrant EPOR transcripts containing the 3' long terminal repeat sequence were mainly expressed in F5-5 cells. The same integration upstream of the EPOR gene was also observed in other subclones and the parent cell line. It is possible that overexpression of EPOR by viral promoter insertion will confer growth advantage to an F-SFFVP-infected erythroid progenitor cell, leading to positive clonal selection through further leukemogenic steps.

Amino Acid Sequence↗
PubMed1988

The site-specific ribosomal DNA insertion element R1Bm belongs to a class of non-long-terminal-repeat retrotransposons.

Two types of insertion elements, R1 and R2 (previously called type I and type II), are known to interrupt the 28S ribosomal genes of several insect species. In the silkmoth, Bombyx mori, each element occupies approximately 10% of the estimated 240 ribosomal DNA units, while at most only a few copies are located outside the ribosomal DNA units. We present here the complete nucleotide sequence of an R1 insertion from B. mori (R1Bm). This 5.1-kilobase element contains two overlapping open reading frames (ORFs) which together occupy 88% of its length. ORF1 is 461 amino acids in length and exhibits characteristics of retroviral gag genes. ORF2 is 1,051 amino acids in length and contains homology to reverse transcriptase-like enzymes. The analysis of 3' and 5' ends of independent isolates from the ribosomal locus supports the suggestion that R1 is still functioning as a transposable element. The precise location of the element within the genome implies that its transposition must occur with remarkable insertion sequence specificity. Comparison of the deduced amino acid sequences from six retrotransposons, R1 and R2 of B. mori, I factor and F element of Drosophila melanogaster, L1 of Mus domesticus, and Ingi of Trypanosoma brucei, reveals a relatively high level of sequence homology in the reverse transcriptase region. Like R1, these elements lack long terminal repeats. We have therefore named this class of related elements the non-long-terminal-repeat (non-LTR) retrotransposons.

Amino Acid Sequence↗
PubMed1994

Endogenous nonecotropic proviruses mapped with oligonucleotide probes from the long terminal repeat region.

We characterized endogenous proviruses in C57BL/6J, DBA/2J, and C3H/HeJ mouse strains with oligonucleotide probes derived from long terminal repeat (LTR) sequences of three classes of nonecotropic murine leukemia virus. The segregation of proviral-host DNA junction fragments was followed in BXH and BXD recombinant inbred (RI) strain sets, and most fragments mapped readily to defined chromosomal regions. Most of the LTR fragments appear to correspond to proviruses mapped previously with oligonucleotide env region probes of the same viral class. At least 22 elements represent new proviral loci, no more than half of which may be solo LTRs, and an additional six may correspond to proviruses identified previously with less specific hybridization probes. Together with proviruses identified previously with env probes, the LTR probe-reactive elements represent the majority of endogenous murine leukemia proviruses in the mouse genome.

Animals↗
PubMed1985

Comparison of the transcriptional properties of the Friend and Moloney retrovirus long terminal repeats: importance of tandem duplications and of the core enhancer sequence.

The effects of sequence differences within the long terminal repeats (LTRs) of various murine retroviruses on transcription are examined by linking genetically engineered recombinant LTRs to the protein coding region of the herpes simplex virus thymidine kinase (TK) gene and assaying TK expression in tissue culture fibroblasts. The Goldberg/Hogness box region and the enhancer region are examined independently. We find that the Friend and Moloney Goldberg/Hogness boxes (TATAAAA and AATAAAA, respectively) give similar results in this assay, whereas differences between the sequences in the enhancer region have a marked effect. Tandem duplications increase the transcription level of the LTR. A single nucleotide transition in the core enhancer sequence has as large an effect on transcription as the presence of a tandem duplication: thymidine in the fifth position of the core enhancer (TCTGTGGTAAG) leads to a much higher transcriptional activity than cytidine. The LTRs have been implicated by others in the oncogenic potential of murine retroviruses, which is perhaps dependent on the transcriptional properties endowed in part by the core enhancer and tandem duplications.

Base Sequence↗
PubMed1990

Transcriptional activation from the long-terminal repeat of human immunodeficiency virus in vitro.

The mechanism of trans-acting regulation of transcription from the long terminal repeat (LTR) of human immunodeficiency virus (HIV) has been investigated. The roles of the cis-acting elements within HIV LTR, as well as the trans-acting factors present in HIV-infected cells, have been evaluated by an in vitro transcription system. Our observations indicate that both the sequence downstream from the CAP site of HIV LTR (located at nucleotide positions +1 to +56; called the TAR element) and the GC boxes (-77 to -45) are required for full transcriptional stimulation and that both the virus-encoded tat protein and one or more cellular factors might be involved. These results demonstrate the presence of a combinatorial regulation of HIV transcription by multiple factors, which may confer the provirus with greater flexibility in regulated viral gene expression.

Binding, Competitive↗
PubMed1991

Activation of feline immunodeficiency virus long terminal repeat by feline herpesvirus type 1.

By transfection of a recombinant plasmid containing the feline immunodeficiency virus (FIV) long terminal repeat (LTR) linked to the chloramphenicol acetyltransferase (CAT) gene followed by infection of feline herpesvirus type 1 (FHV-1) into Crandell feline kidney cells and Felis catus whole fetus 4 cells, enhancement of CAT activity was demonstrated. Furthermore, individual feline T-lymphocytes were productively co-infected with both FIV and FHV-1 in vitro as determined by two-color immunofluorescence and electron microscopy analyses. These results revealed the transactivation of the FIV LTR by FHV-1 and the dual infection of T-lymphocytes with both viruses. The possibility that FHV-1 might be a cofactor which plays a role in the pathogenesis of FIV infection is discussed.

Animals↗
PubMed1984

Trans-acting transcriptional activation of the long terminal repeat of human T lymphotropic viruses in infected cells.

The transcription initiation signals for retroviruses lie within the long terminal repeat (LTR) sequences that flank the integrated provirus. Two subtypes of human T lymphotropic virus (HTLV) are associated with different disease phenotypes. In this article it is shown that marked differences exist in the ability of LTR sequences of these subtypes to function as transcriptional elements in differentiated cell types. It is also shown that trans-acting regulatory factors present in HTLV-infected cells stimulate gene expression directed by these LTR sequences in a type-specific manner. These results have implications for understanding the diverse biological effects of HTLV infection.

Cell Transformation, Neoplastic↗
PubMed2006

TORC1 and TORC2 coactivators are required for tax activation of the human T-cell leukemia virus type 1 long terminal repeats.

Human T-cell leukemia virus type 1 (HTLV-1) Tax protein activates viral transcription from the long terminal repeats (LTR). Mechanisms through which Tax activates LTR have been established, but coactivators of this process remain to be identified and characterized. Here we show that all three members of the TORC family of transcriptional regulators are coactivators of Tax for LTR-driven expression. TORC coactivation requires CREB, but not ATF4 or other bZIP factors. Tax physically interacts with TORC1, TORC2, and TORC3 (TORC1/2/3), and the depletion of TORC1/2/3 inhibited Tax activity. TORC coactivation can be further enhanced by transcriptional coactivator p300. In addition, coactivators in the p300 family are required for full activity of Tax independently of TORC1/2/3. Thus, both TORC and p300 families of coactivators are essential for optimal activation of HTLV-1 transcription by Tax.

Activating Transcription Factor 4↗
PubMed1984

Generation of AKR mink cell focus-forming viruses: a conserved single-copy xenotrope-like provirus provides recombinant long terminal repeat sequences.

AKV and AKR mink cell focus-forming virus-specific probes from the envelope and long terminal repeat (LTR) regions were prepared for study of the structure of recombinant proviruses in tumor tissues of AKR mice. The results showed that (i) all somatically acquired proviruses possessed, besides a recombinant gp70 gene, an altered U3 LTR; (ii) in a substantial portion of the somatically acquired AKR mink cell focus-forming proviruses, the LTR comprised sequences derived from the same xenotropic-like provirus; (iii) this U3 LTR donating parental provirus (Xeno-dL) was present only once per genome equivalent in several mouse strains; (iv) in the strains containing the Xeno-dL provirus, the provirus was present in the same chromosomal site; (v) restriction analysis of the Xeno-dL revealed that the mink cell focus-forming gp70 sequences were derived from a parental provirus, different from Xeno-dL. Therefore, at least two non-ecotropic parents participate in the generation of leukemogenic AKR mink cell focus-forming viruses: a xenotropic-like virus, Xeno-dL, donating U3 LTR sequences, and another xenotropic-like virus or viruses providing gp70 sequences.

AKR murine leukemia virus↗
PubMed1986

Activation of enhancer sequences in type II human T-cell leukemia virus and bovine leukemia virus long terminal repeats by virus-associated trans-acting regulatory factors.

The ability of the sequences present in the long terminal repeats (LTRs) of human T-cell leukemia viruses type I and II (HTLV-I and HTLV-II) and of bovine leukemia virus to function as enhancer elements was investigated. Recombinant plasmids that contained the HTLV-I, HTLV-II, and bovine leukemia virus LTRs at a distance from a simian virus 40 promoter element located 5' to the bacterial gene encoding chloramphenicol acetyltransferase (EC 2.3.1.28) were constructed. We report that all three LTR sequences contain enhancer elements capable of increasing the level of gene expression directed from a distal heterologous promoter. The enhancer present in the HTLV-I LTR was active in uninfected cells of lymphoid and nonlymphoid origin. In contrast, the enhancer activity of the HTLV-II and bovine leukemia virus LTR sequences was evident only in virus-infected cells. This activity is likely due to virus-associated trans-acting transcriptional factors previously shown to be present in HTLV- and bovine leukemia virus-infected cells. The implication of these observations for virus replication and transforming activity are discussed.

Acetyltransferases↗
PubMed1989

Characterization of enhancer elements and their mutations in the long terminal repeat of feline endogenous RD-114 proviruses.

To locate the enhancer regions of the feline endogenous RD-114 long terminal repeat (LTR), we examined expression of the chloramphenicol acetyltransferase gene driven by various segments of the U3 region from two different proviral loci (CRL3 and CR1). Transient expression assays demonstrated that the primary signal sequence for transcription enhancement was located within the 63-base-pair (bp) element of the CRL3 DNA occurring between positions -184 and -121 from the CAP site (+1), whereas the similar region of CR1 was almost inactive. This element from both CRL3 and CR1 contained a single 30-bp sequence (direct repeat [DR]-B2) found in duplicate tandem copies in the LTR of the infectious RD-114 provirus. Two 9-bp inverted repeats marked the DR-B unit of the active element, and a prominent base deletion in one of these repeats in CR1 DNA appeared to be related to loss of enhancer activity. Another segment of CRL3 (-296 to -184), also displaying enhancer function, contained tandem repeated sequences (DR-A1 and DR-A2). The Dr-A2 unit, which lacked the 5' 20-bp sequence of the 47-pb DR-A1, could not function as an enhancer by itself, but it contributed to enhancer effects in cooperation with either the DR-A1 or DR-B2 region. The CR1 LTR contained a single DR-A1 sequence with extensive mutations, and the region (-313 to -181) containing this DR-A1 unit was nonfunctional, similar to the DR-B2 region of CR1. Site-directed mutagenesis analysis of another enhancer element, an octamer motif occurring between CAAT and TATA boxes of all RD-114 LTRs sequenced, revealed that this element was necessary for full enhancer function of the U3 region but with a variable effect, depending on the cell types in which chloramphenicol acetyltransferase expression was determined.

Animals↗
PubMed1992

Interactions of HTF4 with E-box motifs in the long terminal repeat of human immunodeficiency virus type 1.

We have identified three consensus E-box motifs in the long terminal repeat of human immunodeficiency virus type 1. One of these E boxes interacts selectively with representative members of the class A group of basic helix-loop-helix proteins, including HTF4, E47, and their heterodimers. Our analyses implicate the helix-loop-helix proteins in regulation of human immunodeficiency virus type 1 gene expression.

Basic Helix-Loop-Helix Proteins↗
PubMed1994

Negative regulation of the 5' long terminal repeat (LTR) by the 3' LTR in the murine proviral genome.

To assess the influence of the 3' long terminal repeat (LTR) on the promoter/enhancer activity of the 5' LTR, a set of isogenic retroviral vectors differing only in the U3 region of the 3' LTR was constructed. These U3 elements were derived from viruses with different tissue tropism. The 5' LTR originated from Moloney murine leukemia virus and directed the transcription of a reporter gene (chloramphenicol acetyltransferase [CAT] gene), giving rise to plasmids of the general configuration LTR-CAT-LTR'. Following transfection of these chimeric constructs into various cell types, the CAT activity in a given cell line was inversely related to the activity of the downstream U3 region when used in a single-LTR construct in that cell type, indicating negative regulation of the 5' LTR by the chimeric 3' LTR'. Our data indicate that a highly active 3' LTR interferes with gene expression from the 5' LTR. Potential mechanisms for this down-regulation are discussed.

Animals↗
PubMed1985

Nucleotide sequence analysis and enhancer function of long terminal repeats associated with an endogenous African green monkey retroviral DNA.

The nucleotide sequence and enhancer activity of the long terminal repeats (LTRs) associated with a cloned endogenous African green monkey (AGM) retroviral DNA designated as lambda-AGM-1 was studied. A unique feature of the endogenous AGM proviral LTRs was the presence of multiple copies of two types of directly repeating units in the U3 region: 16 8-base-pair (bp) repeats were present in the 5' LTR and 12 were present in the 3' LTR which were bound by a 6-bp perfect direct repeat; tandem duplication of a 32-bp sequence resulted in 3.5 copies in the 5' LTR and 2.5 copies in the 3' LTR. Nucleotide sequence homology was seen between the 8-bp direct repeats located in the AGM proviral LTRs and a 10-bp repeat unit of the deca-satellite present in AGM cellular DNA. The 32-bp repeats of the AGM proviral LTRs contained sequences which were related to the SV40 21-bp repeats and to the "core" of the SV40 72-bp enhancer element. Furthermore, the AGM provirus was distinct from known infectious retroviruses due to the presence of a primer-binding sequence complementary to the 3' terminus of mammalian tRNAGly. Functional analysis of the 3' LTR present in lambda-AGM-1 DNA by chloramphenicol acetyltransferase assay demonstrated enhancer activity associated with the 32-bp direct repeats. Sequences outside the 32-bp unit were necessary for full activator function, suggesting the presence of multiple enhancer domains in the AGM provirus.

Acetyltransferases↗
PubMed1996

[Effect of specific nucleotide sequences on the transcription activity of long terminal repeats of avian retroviruses].

Influence of specific nucleotide sequences on the constitutive transcriptional activity of the Rous sarcoma long terminal repeats (LTR) was studied. The possible function of different elements of the transcriptional control region of the avian retroviral LTR was discussed on the basis of a comparative analysis of the effect of specific nucleotide insertions on LTR activity in vivo and in vitro.

Avian Sarcoma Viruses↗
PubMed1985

Excision of copia element in a revertant of the white-apricot mutation of Drosophila melanogaster leaves behind one long-terminal repeat.

The spontaneous mutation white-apricot (wa) in Drosophila melanogaster has a considerably lighter eye colour than the wild-type, and is caused by the insertion of a copia transposable element into a small intron of the white gene. We have analyzed an X-ray induced wa revertant (waR59K1), whose eye pigmentation is incompletely restored, by in situ hybridization, Southern blotting and sequencing analysis. At the site where copia had originally inserted, we found one long terminal repeat of copia, flanked by a 5 bp duplication with the same polarity as the direction of transcription of the white locus. These results suggest that the wa reversion is due to homologous recombination between the two long terminal repeats of copia.

Animals↗
PubMed1990

The malignant histiocytosis sarcoma virus, a recombinant of Harvey murine sarcoma virus and Friend mink cell focus-forming virus, has acquired myeloid transformation specificity by alterations in the long terminal repeat.

The malignant histiocytosis sarcoma virus (MHSV), in contrast to other viruses with the ras oncogene, induces acute histiocytosis in newborn and adult mice. Molecular structure and function studies were initiated to determine the basis of its unique macrophage-transforming potential. Characterization of the genomic structure showed that the virus evolved by recombination of the Harvey murine sarcoma virus (Ha-MuSV) and a virus of the Friend-mink cell focus-forming virus family. Structural analysis of MHSV showed two regions of the genome that are basically different from the Ha-MuSV: (i) the ras gene, which is altered by a point mutation in codon 181 leading to a Cys----Ser substitution of the p21 protein, and (ii) the U3 region of the long terminal repeat, which is largely derived from F-MCFV and contains a deletion of one direct repeat as well as a duplication of an altered enhancer-like region. Biological studies of Ha-MuSV, MHSV, and recombinants between the two viruses show that the U3 region of the MHSV long terminal repeat is essential for the malignancy and specificity of the disease. A contributing role of the ras point mutation in determining macrophage specificity, however, cannot be excluded.

Amino Acid Sequence↗