Analysis of recombinant DNA clones of the endogenous BALB/c murine leukemia virus WN1802N: variation in long terminal repeat length

Boone, Lawrence R.; Myer, F. E.; Yang, Da; Kiggans, James O.; Koh, C. K.; Tennant, Raymond W.; Yang, Wei‐Pang

doi:10.1128/jvi.45.1.484-488.1983

Cited by 14 publications

(10 citation statements)

References 30 publications

(27 reference statements)

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“…This finding is consistent with studies of endogenous LTR sequences in other strains of mice (Boone et al, 1983;Khan and Martin, 1983), in avian cells (Hughes et al, 1981), and in feline cells (Casey et al, 1981). Since enhancer regions are present in the U3 regions this may have implications with respect to the control of transcription by these endogenous elements during normal development and carcinogenesis.…”

Section: Studies Related To Long Terminal Repeat Sequencessupporting

confidence: 89%

Multistage carcinogenesis involves multiple genes and multiple mechanisms

et al. 1984

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Section: Studies Related To Long Terminal Repeat Sequencessupporting

confidence: 89%

Multistage carcinogenesis involves multiple genes and multiple mechanisms

et al. 1984

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“…Thus, our results of CAT gene expression with the two ecotropic LTRs are consistent with the idea that these protein-binding motifs serve as positive enhancer elements in the transcriptional mechanism (2,11,25,26,35,38). Indeed, highly infectious ecotropic MuLVs selected by serial cell or animal passages generally show duplicated enhancer sequences (4,11,15,22,37,56,62,63), A J. VIROL. Inhibitory effect of 5' sequences of two MuLV-related proviral LTRs on CAT expression activity of the LTR of ecotropic MuLV pWN41 proviral clone.…”

Section: Discussionsupporting

confidence: 89%

“…The eight clones derived from RFM/ Un mouse chromosomal DNA (4,33,46,47) were of three classes: the 700-bp LTR (polytropic) class represented by pRFM6 and pRFM16; the 750-bp LTR (modified polytropic) class represented by pRFM1, pRFM3, pRFM9, and pRFM17; and the solitary LTR of presumed xenotropic MuLV origin represented by pRFM7 and pRFM8. The three clones of BALB/c mouse origin were pAL10 of the 700-bp LTR class (51), pWN41 of the N-ecotropic WN1802N MuLV and pWNB5 of the B-ecotropic WN1802B MuLV (4). The characteristic structural features of these LTRs, as well as the restriction sites used for molecular construction, are depicted in Fig.…”

Section: Corresponding Nucleotide Sites Sequence Duplications (mentioning

confidence: 99%

Negative regulatory element associated with potentially functional promoter and enhancer elements in the long terminal repeats of endogenous murine leukemia virus-related proviral sequences

Ch’ang

Yang

Myer

et al. 1989

J Virol

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Three series of recombinant DNA clones were constructed, with the bacterial chloramphenicol acetyltransferase (CAT) gene as a quantitative indicator, to examine the activities of promoter and enhancer sequence elements in the 5' long terminal repeat (LTR) of murine leukemia virus (MuLV)-related proviral sequences isolated from the mouse genome. Transient CAT expression was determined in mouse NIH 3T3, human HT1080, and mink CCL64 cultured cells transfected with the LTR-CAT constructs. The 700-base-pair (bp) LTRs of three polytropic MuLV-related proviral clones and the 750-bp LTRs of four modified polytropic proviral clones, in complete structures either with or without the adjacent downstream sequences, all showed very little or negligible activities for CAT expression, while ecotropic MuLV LTRs were highly active. The MuLV-related LTRs were divided into three portions and examined separately. The 3' portion of the MuLV-related LTRs that contains the CCAAC and TATAA boxes was found to be a functional promoter, being about one-half to one-third as active as the corresponding portion of ecotropic MuLV LTRs. A MboI-Bg/II fragment, representing the distinct 190- to 200-bp inserted segment in the middle, was found to be a potential enhancer, especially when examined in combination with the simian virus 40 promoter in CCL64 cells. A PstI-MboI fragment of the 5' portion, which contains the protein-binding motifs of the enhancer segment as well as the upstream LTR sequences, showed moderate enhancer activities in CCL6 cells but was virtually inactive in NIH 3T3 cells and HT1080 cells; addition of this fragment to the ecotropic LTR-CAT constructs depressed CAT expression. Further analyses using chimeric LTR constructs located the presence of a strong negative regulatory element within the region containing the 5' portion of the enhancer and the immediate upstream sequences in the MuLV-related LTRs.

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“…Restriction enzyme analysis of the replicating form of the endogenous BALB/c MLV WN1802N has also revealed LTRs with variable size and shown that the size variations occurred in a region of the LTR that corresponds with the position of the enhancers in MoMLV (7). The restriction pattern suggests that duplication of an enhancer is involved, but the altered LTRs were not sequenced to verify this hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Replication of Mus dunni Endogenous Retrovirus Depends on Promoter Activation Followed by Enhancer Multimerization

Wolgamot

Miller

1999

J Virol

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Mus dunni endogenous virus (MDEV) is an apparently intact retrovirus that normally lies transcriptionally silent in cultured M. dunni cells, but the provirus can be activated by treatment of the cells with hydrocortisone or 5-iodo-2′-deoxyuridine. Sequence analysis of a molecular clone of the replicating virus revealed a simple retrovirus with a chimeric VL30/GALV-like structure. Interestingly, in the region of the long terminal repeat (LTR) that typically contains the retroviral transcription enhancers, we found over six 80-bp repeats with only a single mismatch, indicating that acquisition of the repeats was a recent event. Here we provide evidence for the following model of MDEV activation and replication. The MDEV provirus in M. dunnicells has a chimeric structure similar to that of the molecular clone but has only 1.15 copies of the 80-bp repeat sequence found in the molecular clone. Activating chemicals directly stimulate transcription from the LTR, allowing a low level of virus replication. Copying errors made during reverse transcription allow multimerization of the 80-bp enhancer region, resulting in viruses with higher transcriptional rates and improved fitness, but increased enhancer copy number is likely balanced by the natural instability of retroviral repeats and constraints imposed by virion packaging limits. The resultant population of replicating MDEV is widely heterogeneous, having from 2.15 to 13.15 enhancer repeats in the LTR. These results reveal a novel mechanism for regulation of transcription and replication of an endogenous retrovirus, in terms of both activation of the virus by the steroid hydrocortisone and the large number and variation in enhancer repeats observed.

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Analysis of recombinant DNA clones of the endogenous BALB/c murine leukemia virus WN1802N: variation in long terminal repeat length

Cited by 14 publications

References 30 publications

Multistage carcinogenesis involves multiple genes and multiple mechanisms

Multistage carcinogenesis involves multiple genes and multiple mechanisms

Negative regulatory element associated with potentially functional promoter and enhancer elements in the long terminal repeats of endogenous murine leukemia virus-related proviral sequences

Replication of Mus dunni Endogenous Retrovirus Depends on Promoter Activation Followed by Enhancer Multimerization

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