Synthesis of tobacco mosaic virus in intact tobacco leaves systemically inoculated by differential temperature treatment

Dawson, William O.; Schlegel, David E.; Lung, M. C. Y.

doi:10.1016/0042-6822(75)90061-6

Cited by 60 publications

(31 citation statements)

References 10 publications

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“…We hope that by manipulating the growth conditions of the plant (e.g., by differential temperature treatment; ref. 29) we can obtain sufficient synchrony for a more detailed analysis of the molecular events governing these responses.…”

Section: Discussionmentioning

confidence: 99%

Induction of HSP70 and polyubiquitin expression associated with plant virus replication

Aranda

Escaler

Wang

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

136

107

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By examining the front of virus invasion in immature pea embryos infected with pea seed-borne mosaic virus (PSbMV), the selective control of different host genes has been observed. From our observations, the early responses to PSbMV replication can be grouped into three classes, inhibited host gene expression, induced host gene expression, and no effect on a normal host function. The expression of two heat-inducible genes encoding HSP70 and polyubiquitin was induced coordinately with the onset of virus replication and the down-regulation of two other genes encoding lipoxygenase and heat shock cognate protein. The down-regulation was part of a general suppression of host gene expression that may be achieved through the degradation of host transcripts. We discuss the possibilities of whether the induction of HSP70 and polyubiquitin genes represents a requirement for the respective protein products by the virus or is merely a consequence of the depletion of other host transcripts. The former is feasible, as the induction of both genes does result in increased HSP70 and ubiquitin accumulation. This also indicates that, in contrast to some animal virus infections, there is not a general inhibition of translation of host mRNAs following PSbMV infection. This selective control of host gene expression was observed in all cell types of the embryo and identifies mechanisms of cellular disruption that could act as triggers for symptom expression.For maximum efficiency, a virus must balance the exploitation of host cellular processes against consequential cellular damage. How this is achieved is not well understood. However, examples from a wide range of animal viruses (reviewed in ref. 1) and our earlier work with the plant virus pea seed-borne mosaic virus (PSbMV; ref.2) suggest that a major component in the control exerted by the virus is the shutoff of transcription and͞or translation of host mRNAs. Because the virus must use the host machinery for polynucleotide and protein synthesis, either the control must be highly selective or virus replication must depend on long-lived host mRNAs and͞or proteins. A similar argument may also apply to the use of host processes for the correct folding and turnover of viral proteins.The host shutoff phenomenon has been studied in most detail for poliovirus in which viral proteins interfere with DNA polymerase I, II, and III transcription (3-5) and translation (6, 7) and for herpes simplex virus 1 in which host translation is inhibited and there is a rapid degradation of capped mRNAs by a viral protein with riboexonuclease activity (8). For PSbMV replicating in pea embryonic tissues, there is a transient host shutoff associated with a loss of host gene transcripts associated with diverse areas of metabolism (2).In common with all viruses, PSbMV replication is associated with the translation of viral RNA and the multifarious activities of virus-encoded proteins. Hence, the basic translational machinery and processes required to assist in the correct folding and turnover of prote...

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Section: Discussionmentioning

confidence: 99%

Induction of HSP70 and polyubiquitin expression associated with plant virus replication

Aranda

Escaler

Wang

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

136

107

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“…The duration of the experiment was 96 h. Appreciable virus accumulated in cells infected only during the first 80 h because there is a 16-hour period after infection of a cell before appreciable virus accumulates [7,8]. Thus, the time-course of AMD inhibition was com pared to the spread of the infection during the first 80 h (solid line in fig.…”

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confidence: 99%

Time-Course of Actinomycin D Inhibition of Tobacco Mosaic Virus Multiplication Relative to the Rate of Spread of the Infection

Dawson

1978

Intervirology

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The time-course of inhibition of tobacco mosaic virus synthesis in mechanically inoculated leaves by actinomycin D was not correlated with cell-to-cell spread of the infection, as previously shown to be the case with 2-thiouracil and guanidine inhibition. The amount of inhibition by actinomyci¤ D declined after inoculation much more rapidly than the infection spread. An actinomycin-D-sensitive step or its product occurred in cells before they became infected.

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“…It was demon strated previously that moving TMV-infected tissue to 40° immediately ter- minated SS TMV RNA synthesis with a less rapid decline in RI and RF syn thesis [2], To determine whether the different functions of TMV RNA replicase cease at 40° due to an active enzyme that cannot function at that temperature or whether some function is destroyed by the 40° incubation, the ability of infected tissue to produce TMV RNA upon return to 25° was examined. Leaves 'systemically inoculated' with TMV at 3° were incubated at 25° for 24 h, a time at which the infection reaches the rapid, linear phase of TMV replication [3]. The leaves were then shifted to 40° for different time intervals after which they were either incubated with 32P for 2 h at 40° or shifted to 25° and immediately labeled at that temperature.…”

Section: Resultsmentioning

confidence: 99%

“…Young leaves of tobacco plants (Nicotiana tabacum L.var.Xanthi) were 'systemically inoculated' at 3° with TMV, strain U l, using the differential temperature inoculation pro cedure [3]. Virus replication was initiated by moving the plants into a plant growth chamber at 25°.…”

Section: Methodsmentioning

confidence: 99%

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Recovery of Tobacco Mosaic Virus RNA Replication after Incubation at 40°

Dawson¹

1978

Intervirology

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Incubation of tobacco mosaic virus (TMV)-infected tissue at 40° for 12 h destroyed the capacity for TMV RNA replication. Upon shift of the tissue from 40 to 25°, synthesis of TMV RNA did not resume. Incubation at 40° for 1 h did not destroy the TMV RNA replicase, because viral RNA synthesis resumed upon return to 25°. However, upon further incubation at 25°, the synthesis rate of TMV RNA gradually declined. Upon still further incubation at 25° (16–20 h), the synthesis of TMV RNA in tissue incubated at 40° for either 1 or 12 h recovered. This recovery was inhibited by cycloheximide but not by 2-thiouracil.

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Synthesis of tobacco mosaic virus in intact tobacco leaves systemically inoculated by differential temperature treatment

Cited by 60 publications

References 10 publications

Induction of HSP70 and polyubiquitin expression associated with plant virus replication

Induction of HSP70 and polyubiquitin expression associated with plant virus replication

Time-Course of Actinomycin D Inhibition of Tobacco Mosaic Virus Multiplication Relative to the Rate of Spread of the Infection

Recovery of Tobacco Mosaic Virus RNA Replication after Incubation at 40°

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Synthesis of tobacco mosaic virus in intact tobacco leaves systemically inoculated by differential temperature treatment

Cited by 60 publications

References 10 publications

Induction of HSP70 and polyubiquitin expression associated with plant virus replication

Induction of HSP70 and polyubiquitin expression associated with plant virus replication

Time-Course of Actinomycin D Inhibition of Tobacco Mosaic Virus Multiplication Relative to the Rate of Spread of the Infection

Recovery of Tobacco Mosaic Virus RNA Replication after Incubation at 40&deg;

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Recovery of Tobacco Mosaic Virus RNA Replication after Incubation at 40°