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  • 1
    Online Resource
    Online Resource
    The soluble glycoprotein of vesicular stomatitis virus is formed during or shortly after the translation process
    American Society for Microbiology ; 1986
    In:  Journal of Virology Vol. 57, No. 3 ( 1986-03), p. 968-975
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 57, No. 3 ( 1986-03), p. 968-975
    Abstract: Gs protein is a shorter, soluble form of the viral G protein of vesicular stomatitis virus (VSV) lacking the membrane-anchoring domain. Production of Gs protein appears to be a general property of VSV because infection of BHK-21 cells by five different isolates of the VSV serotype Indiana led in all cases to the synthesis of Gs protein. Moreover, it is formed in a variety of eucaryotic cell lines after VSV infection. In pulse-chase experiments, we observed a time-dependent change in the ratio of G to Gs protein released into the growth medium, suggesting that Gs is formed intracellularly rather than on the cell surface. Further experiments revealed that Gs protein can be synthesized in vitro in the reticulocyte lysate system after addition of a viral mRNA fraction and in a coupled transcription-translation system with VSV core particles. In the presence of microsomal membranes both G and Gs protein were glycosylated in the reticulocyte lysate, confirming that the authentic Gs protein is synthesized in vitro. The addition of various protease inhibitors to the cell-free system and variation of the incubation conditions did not alter the ratio of G to Gs formation. Taken together, these experiments suggest strongly that Gs protein is not a product of a membrane-associated proteolytic activity but is formed during or shortly after the translation process. Our attempts to detect a specific, shorter mRNA coding for the Gs protein by molecular hybridization procedures did not reveal the existence of such a mRNA species.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/jvi.57.3.968-975.1986
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1986
    detail.hit.zdb_id: 1495529-5
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  • 2
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    DNA methylation represses the murine alpha 1(I) collagen promoter by an indirect mechanism.
    Informa UK Limited ; 1994
    In:  Molecular and Cellular Biology Vol. 14, No. 9 ( 1994-09), p. 5950-5960
    Details
    In: Molecular and Cellular Biology, Informa UK Limited, Vol. 14, No. 9 ( 1994-09), p. 5950-5960
    Abstract: Several lines of evidence indicate that DNA methylation plays a role in the transcriptional regulation of the murine alpha 1(I) collagen gene. To study the molecular mechanisms involved, a reporter gene construct containing the alpha 1(I) promoter and part of the first exon linked to the luciferase gene (Col3luc) was methylated in vitro and transfected into murine fibroblasts and embryonal carcinoma cells. Methylation resulted in repression of the alpha 1(I) promoter in both cell types, although it was less pronounced in embryonal carcinoma cells than in fibroblasts. The extent of repression depended on the density of methylation. DNase footprint and mobility shift assays indicated that the trans-acting factors binding to the alpha 1(I) promoter and first exon are ubiquitous factors and that their DNA binding is not inhibited by methylation. Transfection of Col3luc into Drosophila SL2 cells together with expression vectors for the transcription factors Sp1 and NF-1 showed that DNA methylation also inhibits the alpha 1(I) promoter in nonvertebrate cells, although to a much lesser extent than in murine cells. However, Sp1 and NF-1 transactivated the unmethylated and methylated reporter gene in SL2 cells equally well, confirming that these factors can bind and transactivate methylated DNA and indicating that DNA methylation represses the alpha 1(I) promoter by an indirect mechanism. This was further confirmed by cotransfection experiments with unspecific methylated competitor DNA which partially restored the activity of the methylated alpha 1(I) promoter. Our results suggest that DNA methylation can inhibit promoter activity by an indirect mechanism independent of methyl-C-binding proteins and that in vertebrate cells, chromatin structure and methyl-C-binding proteins cooperatively mediate the transcriptional inhibitory effect of DNA methylation.
    Type of Medium: Online Resource
    ISSN: 0270-7306 , 1098-5549
    URL: Article
    DOI: 10.1128/MCB.14.9.5950
    RVK:
    WA 15000
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 1994
    detail.hit.zdb_id: 1474919-1
    SSG: 12
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  • 3
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    Retrovirus integration and chromatin structure: Moloney murine leukemia proviral integration sites map near DNase I-hypersensitive sites
    American Society for Microbiology ; 1987
    In:  Journal of Virology Vol. 61, No. 2 ( 1987-02), p. 336-343
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 61, No. 2 ( 1987-02), p. 336-343
    Abstract: The chromatin conformation of mouse genome regions containing Moloney murine leukemia proviral intergration sites in two Mov mouse strains and randomly selected integration sites in virus-infected mouse 3T3 fibroblasts was analyzed. All integrations have occurred into chromosomal regions containing several DNase-hypersensitive sites, and invariably the proviral integration sites map within a few hundred base pairs of a DNase-hypersensitive site. The probability that this close association between proviral integration sites and DNase-hypersensitive sites was due to chance was calculated to be extremely low (2 X 10(-4]. Because the proviral integrations analyzed were not selected for an altered phenotype, our results suggest that DNase-hypersensitive regions are preferred targets for retrovirus integration.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/jvi.61.2.336-343.1987
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1987
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  • 4
    Online Resource
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    Coupled in vitro transcription and translation of vesicular stomatitis virus messenger RNA.
    Proceedings of the National Academy of Sciences ; 1975
    In:  Proceedings of the National Academy of Sciences Vol. 72, No. 7 ( 1975-07), p. 2545-2549
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 72, No. 7 ( 1975-07), p. 2545-2549
    Abstract: The virion transcriptase (nucleosidetriphosphate: RNA nucleotidyltransferase, EC 2.7.7.6) of vesicular stomatitis virus was fully active when ribonucleoprotein cores from purified virions were added to cell-free protein synthesizing systems of eukaryotic origin. Synthesis of mRNA was linear for at least 3 hr and the newly synthesized viral mRNA was efficiently utilized for the synthesis of viral proteins N (nucleoprotein), NS, and M (matrix); small amounts of a putative G (glycoprotein protein precursor and several unidentified polypeptides were regularly synthesized. The ratio of the various newly synthesized viral proteins was identical after different periods of coupled mRNA and protein synthesis. Identical proteins were obtained when the cell-free protein synthesizing systems were programmed with purified VSV mRNA synthesized in vitro. No detectable L protein was synthesized, even though transcripts complementary to the complete viral genome were detectable in the mRNA preparation by hybridization.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.72.7.2545
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 1975
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 5
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    Retrovirus-induced interference with collagen I gene expression in Mov13 fibroblasts is maintained in the absence of DNA methylation.
    Informa UK Limited ; 1991
    In:  Molecular and Cellular Biology Vol. 11, No. 1 ( 1991-01), p. 47-54
    Details
    In: Molecular and Cellular Biology, Informa UK Limited, Vol. 11, No. 1 ( 1991-01), p. 47-54
    Abstract: We have studied the role of DNA methylation in repression of the murine alpha 1 type I collagen (COL1A1) gene in Mov13 fibroblasts. In Mov13 mice, a retroviral provirus has inserted into the first intron of the COL1A1 gene and blocks its expression at the level of transcriptional initiation. We found that regulatory sequences in the COL1A1 promoter region that are involved in the tissue-specific regulation of the gene are unmethylated in collagen-expressing wild-type fibroblasts and methylated in Mov13 fibroblasts, confirming and extending earlier observations. To directly assess the role of DNA methylation in the repression of COL1A1 gene transcription, we treated Mov13 fibroblasts with the demethylating agent 5-azacytidine. This treatment resulted in a demethylation of the COL1A1 regulatory sequences but failed to activate transcription of the COL1A1 gene. Moreover, the 5-azacytidine treatment induced a transcription-competent chromatin structure in the retroviral sequences but not in the COL1A1 promoter. In DNA transfection and microinjection experiments, we found that the provirus interfered with transcriptional activity of the COL1A1 promoter in Mov13 fibroblasts but not in Xenopus laevis oocytes. In contrast, the wild-type COL1A1 promoter was transcriptionally active in Mov13 fibroblasts. These experiments showed that the COL1A1 promoter is potentially transcriptionally active in the presence of proviral sequences and that Mov13 fibroblasts contain the trans-acting factors required for efficient COL1A1 gene expression. Our results indicate that the provirus insertion in Mov13 can inactivate COL1A1 gene expression at several levels. It prevents the developmentally regulated establishment of a transcription-competent methylation pattern and chromatin structure of the COL1A1 domain and, in the absence of DNA methylation, appears to suppress the COL1A1 promoter in a cell-specific manner, presumably by assuming a dominant chromatin structure that may be incompatible with transcriptional activity of flanking cellular sequences.
    Type of Medium: Online Resource
    ISSN: 0270-7306 , 1098-5549
    URL: Article
    DOI: 10.1128/MCB.11.1.47
    RVK:
    WA 15000
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 1991
    detail.hit.zdb_id: 1474919-1
    SSG: 12
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  • 6
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    Factors involved in the generation and replication of rhabdovirus defective T particles
    American Society for Microbiology ; 1976
    In:  Journal of Virology Vol. 17, No. 3 ( 1976-03), p. 805-815
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 17, No. 3 ( 1976-03), p. 805-815
    Abstract: Previous indications that cloned B virions might be genetically predisposed to generate a particular defective T particle are shown to be inaccurate. T particle generation was found to be a much more random process than was previously believed. We show that the previously observed generation of particular sizes of T particles by B virion pools is due to the random generation of T particles during preparation of first-passage pools of cloned B virions, and these breed true during the additional passages needed to produce visible quantities of T particles. It is also shown that different host cell lines selectively amplify different T particles, suggesting a strong role of host cell factors in T particle replication. Surprisingly, our line of HeLa cells did not generate or replicate detectable T particles of vesicular stomatitis virus (VSV) Indiana after either serial undiluted passage or direct addition of T particles, even though the added T particles strongly interfered with B virion replication. In contrast to VSV, rabies virus generates large amounts of T particles during the first passage of cloned B virions, and every rabies-infected baby hamster kidney-21 cell culture evolves into a persistent carrier state. We find that T particle RNA is biologically inactive although T particle nucleocapsid ribonucleoprotein replicates and interferes in cells coinfected with B virions. Efforts to study the mechanism of T particle generation by in vitro attempts to generate T particles or modify their size (using sheared ribonucleoprotein or chemical or UV mutagenesis) were unsuccessful. The kinetics of UV and nitrous acid inactivation of T particles indicate a smaller target size relative to B virions, even after correcting for lengths of RNA molecules. The intercalating dye proflavine does not photosensitize VSV B virions or T particles when present during replication, indicating that there is little or no RNA base pairing in the helical nucleocapsids of either.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/jvi.17.3.805-815.1976
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1976
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  • 7
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    Transcriptionally active genome regions are preferred targets for retrovirus integration
    American Society for Microbiology ; 1990
    In:  Journal of Virology Vol. 64, No. 2 ( 1990-02), p. 907-912
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 64, No. 2 ( 1990-02), p. 907-912
    Abstract: We have analyzed the transcriptional activity of cellular target sequences for Moloney murine leukemia virus integration in mouse fibroblasts. At least five of the nine random, unselected integration target sequences studied showed direct evidence for transcriptional activity by hybridization to nuclear run-on transcripts prepared from uninfected cells. At least four of the sequences contained multiple recognition sites for several restriction enzymes that cut preferentially in CpG-rich islands, indicating integration into 5' or 3' ends or flanking regions of genes. Assuming that only a minor fraction (less than 20%) of the genome is transcribed in mammalian cells, we calculated the probability that this association of retroviral integration sites with transcribed sequences is due to chance to be very low (1.6 x 10(-2]. Thus, our results strongly suggest that transcriptionally active genome regions are preferred targets for retrovirus integration.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/jvi.64.2.907-912.1990
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1990
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  • 8
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    Retrovirus-induced insertional mutagenesis: mechanism of collagen mutation in Mov13 mice.
    Informa UK Limited ; 1991
    In:  Molecular and Cellular Biology Vol. 11, No. 10 ( 1991-10), p. 5154-5163
    Details
    In: Molecular and Cellular Biology, Informa UK Limited, Vol. 11, No. 10 ( 1991-10), p. 5154-5163
    Abstract: The Mov13 mouse strain carries a mutation in the alpha 1(I) procollagen gene which is due to the insertion of a Moloney murine leukemia provirus into the first intron. This insertion results in the de novo methylation of the provirus and flanking DNA, the alteration of chromatin structure, and the transcriptional inactivity of the collagen promoter. To address the mechanism of mutagenesis, we reintroduced a cloned and therefore demethylated version of the Mov13 mutant allele into mouse fibroblasts. The transfected gene was not transcribed, indicating that the transcriptional defect was not due to the hypermethylation. Rather, this result strongly suggests that the mutation is due to the displacement or disruption of cis-acting regulatory DNA sequences within the first intron. We also constructed a Mov13 variant allele containing a single long terminal repeat instead of the whole provirus. This construct also failed to express mRNA, indicating that the Mov13 mutation does not revert by provirus excision as has been observed for other retrovirus-induced mutations.
    Type of Medium: Online Resource
    ISSN: 0270-7306 , 1098-5549
    URL: Article
    DOI: 10.1128/MCB.11.10.5154
    RVK:
    WA 15000
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 1991
    detail.hit.zdb_id: 1474919-1
    SSG: 12
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  • 9
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    Online Resource
    Regulatory elements in the 5'-flanking region and the first intron contribute to transcriptional control of the mouse alpha 1 type I collagen gene.
    Informa UK Limited ; 1989
    In:  Molecular and Cellular Biology Vol. 9, No. 5 ( 1989-05), p. 2224-2227
    Details
    In: Molecular and Cellular Biology, Informa UK Limited, Vol. 9, No. 5 ( 1989-05), p. 2224-2227
    Abstract: We have identified two blocks of regulatory sequences located in the 5'-flanking region and the first intron of the mouse alpha 1 type I collagen (COL1A1) gene. Both blocks were found to contain positive as well as negative regulatory elements. Sequences located within 222 base pairs upstream of the transcription start site showed a strong stimulatory effect on the COL1A1 promoter and were sufficient for tissue-specific regulation of the COL1A1 gene. The combined upstream and intron regulatory sequences showed a marked inhibition of COL1A1 promoter activity in fibroblasts. This finding suggests that additional, more remote regulatory sequences may be required for establishing the high level of activity of the endogenous COL1A1 gene in fibroblastoid cells.
    Type of Medium: Online Resource
    ISSN: 0270-7306 , 1098-5549
    URL: Article
    DOI: 10.1128/MCB.9.5.2224
    RVK:
    WA 15000
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 1989
    detail.hit.zdb_id: 1474919-1
    SSG: 12
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