Poliovirus-Induced Rna Polymerase and the Effects of Virus-Specific Inhibitors on Its Production

Baltimore, David; Eggers, Hans J.; Franklin, Richard M.; Tamm, Igor

doi:10.1073/pnas.49.6.843

Cited by 192 publications

(77 citation statements)

References 24 publications

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“…It can therefore be distinguished sharply from DNA-primed RNA polymerases occurring in bacteria (Krakow & Ochoa, 1963;Nakamoto, Fox & Weiss, 1964;Stevens & Henry, 1964), and in the chromatin fraction from plant and animal sources (Huang & Bonner, 1962;Ro & Busch, 1964;Eason & Smellie, 1965). It has some features in common with the RNA-primed RNA polymerases found on viral infection of bacteria (Haruna, Nozu, Ohtaka & Spiegelman, 1963;Weissman, Borst, Burdon, Billeter & Ochoa, 1964) or animal cells Baltimore, Eggers, Franklin & Tamm, 1963;Eason & Smellie, 1965). In contrast with the last-named enzymes, however, the microsomal system shows no stimulation of the incorporation of any one labelled ribonucleotide by the presence of the three complementary ribonucleotides.…”

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confidence: 94%

The synthesis of polyribonucleotides by cytoplasmic enzymes

Wykes¹,

Smellie²

1966

Biochemical Journal

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[3H]CTP and analysis by sucrosedensity-gradient centrifugation showed no labelling of the ribosomal RNA. Radioactive material appeared between the 4s region and the meniscus of the sucrose gradient. In agreement with this observation, determinations of the chain length of the product showed that only short sequences of polynucleotides were synthesized. It is concluded that only homopolyribonucleotide synthesis is catalysed by the microsomal fractions and that there is little or no synthesis of RNA-like heteropolymers.

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confidence: 94%

The synthesis of polyribonucleotides by cytoplasmic enzymes

Wykes¹,

Smellie²

1966

Biochemical Journal

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“…In some cases this was found in cytoplasmic fractions but no results were reported for the discarded nuclear fractions Baltimore, Eggers, Franklin & Tamm, 1963). Cline, Eason & Smellie (1963) showed an increase in RNA-dependent polymerase activity in both nuclear and cytoplasmic fractions of cells after infection by EMC virus.…”

Section: Discussionmentioning

confidence: 98%

Sites of Synthesis of Encephalomyocarditis Virus Components in Infected L-Cells

Bellett

Harris

Sanders

1965

Journal of General Microbiology

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SUMMARYL-cells were fractionated at various times after infection with EMC virus and assayed for haemagglutinin, virus and phenol-extractable infective RNA. A second fraction of infective RNA was obtained by sodium dodecyl sulphate (SDS) extraction of the samples after phenol extraction. The infectivity of SDS-extracted RNA increased earlier than that of phenol-extracted RNA, but the maximum titre was less than 10 yo of the maximum titre extracted by phenol. The early rise in SDS-extracted RNA was largely confined to the nuclear fraction, and the infectivity of phenol-extracted RNA appeared to increase in the nuclear fraction before the cytoplasmic fraction. There was a simultaneous increase in the titres of both fractions of RNA, haemagglutinin and virus in the cytoplasmic fraction from 3 to 5 hr after infection, and the maximum titres of infective RNA were found in the cytoplasm 4-54hr after infection. It was concluded that synthesis of viral RNA begins near the nuclear membrane and then spreads outwards through the cytoplasm, but that there is no conclusive evidence as to whether this process begins in the nuclei or the perinuclear cytoplasm.

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“…Under these conditions non-reproducing ME virus determines the membrane changes at the cell surface (Zeichhardt et al, 1982). (ii) In a mixed infection in the presence of guanidine, poliovirus reproduction is inhibited (Baltimore et al, 1963); however, reproduction of ME virus is advanced (Diefenthal et al, 1973;Zeichhardt et al, 1981). The reproduction of ME virus is accelerated by 1 h in a simultaneous mixed infection and by as much as 3 h when the cells are preinfected with poliovirus for at least 2 h. Under these conditions poliovirus is not rescued by superinfecting ME virus, i.e.…”

Section: Discussionmentioning

confidence: 99%

A Poliovirus-induced Cytoplasmic Membrane Complex is Exploited by the RNA Polymerase of Superinfecting Mouse Elberfeld (ME) Virus

Zeichhardt

Habermehl

Wetz

1983

Journal of General Virology

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SUMMARYThe preexistence of a cytoplasmic membrane complex in HEp-2 cells, induced by poliovirus when inhibited in its reproduction by guanidine, was a prerequisite for accelerated reproduction of superinfec, ting Mouse Elberfeld (ME) virus. Guanidineinhibited poliovirus induced a membrane complex of 470S that was successively modified into a faster sedimenting membrane complex (up to 700S) by superinfecting ME virus and exploited for ME virus reproduction. The modified membrane complex was the site for ME virus-specific RNA polymerization characterized by the existence of in vivo and in vitro activity of ME virus RNA polymerase associated with the modified membrane complex. Proof of membrane-bound RNA polymerase and newly synthesized ME virus RNA including replicative intermediate led to the conclusion that superinfecting ME virus exploits the 'poliovirus/guanidine'-induced complex as the site of action of its replication complex.Mixed infections with the two picornaviruses, poliovirus and Mouse Elberfeld (ME) virus, revealed that virus-specific membrane alterations of the infected cells may occur independently of virus reproduction. (i) In cells simultaneously infected with both viruses, ME virus reproduction is inhibited by interfering poliovirus. Under these conditions non-reproducing ME virus determines the membrane changes at the cell surface (Zeichhardt et al., 1982). (ii) In a mixed infection in the presence of guanidine, poliovirus reproduction is inhibited (Baltimore et al., 1963); however, reproduction of ME virus is advanced (Diefenthal et al., 1973;Zeichhardt et al., 1981). The reproduction of ME virus is accelerated by 1 h in a simultaneous mixed infection and by as much as 3 h when the cells are preinfected with poliovirus for at least 2 h. Under these conditions poliovirus is not rescued by superinfecting ME virus, i.e. complementation does not take place between ME and poliovirus reproduction. As we were able to show recently (Zeichhardt et al., 1981), poliovirus inhibited by guanidine, nevertheless, induces a cytoplasmic membrane complex of 470S (Fig. 1). In a superinfection with ME virus this complex is successively modified into an ME virus-specific membrane complex of 700S depending on the length of superinfection. In cells preinfected with poliovirus for 4 h the complex sediments at 700S after a 6 h superinfection with ME virus (Fig. 1), whereas in a single infection with ME virus the 700S complex is formed not earlier than 8 h post-infection. From this it has been concluded that ME virus is reproduced with a shortened latent period by exploiting the 'poliovirus/guanidine'-induced and preexisting membrane complex for its own reproduction. The present communication shows that the modified complex serves as a site for ME virusspecific RNA synthesis.Growth of HEp-2 cells in monolayer cultures, propagation of poliovirus type 1 (strain Mahoney) and ME virus (laboratory strain), double infection experiments with both viruses and separation of cytoplasmic membrane complexes were performed as descri...

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Poliovirus-Induced Rna Polymerase and the Effects of Virus-Specific Inhibitors on Its Production

Cited by 192 publications

References 24 publications

The synthesis of polyribonucleotides by cytoplasmic enzymes

The synthesis of polyribonucleotides by cytoplasmic enzymes

Sites of Synthesis of Encephalomyocarditis Virus Components in Infected L-Cells

A Poliovirus-induced Cytoplasmic Membrane Complex is Exploited by the RNA Polymerase of Superinfecting Mouse Elberfeld (ME) Virus

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