Studies on the Formation of Diffusion Barriers in Hypersensitive Hosts of Tobacco Mosaic Virus and the Role of Necrotization in the Formation of Diffusion Barriers as well as in the Localization of Virus Infections<sup>1</sup>)

Schuster, G.; Flemming, M.

doi:10.1111/j.1439-0434.1976.tb01740.x

Cited by 14 publications

(4 citation statements)

References 12 publications

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“…The blocking of the plasmodesmata by callose deposition or paramural body formation has been suggested as a factor contributing to viral localization in necrotic lesions4, 14,18,20). In our experiments callose accumulation was not observed in TMV-localized areas in cucumber cotyledons, as found by Cohen and Loebenstein2).…”

Section: Discussionsupporting

confidence: 82%

Inhibition of Cell-to-Cell Movement of Viruses or Substances in Tobacco Mosaic Virus Localized Sites of Cucumber Cotyledons.

Uekusa

Teraoka

Hosokawa

et al. 1993

Jpn. J. Phytopathol.

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Cucumber cotyledons, in which tobacco mosaic virus (TMV) had been localized without causing necrotic lesions, were challenge-inoculated with cucumber green mottle mosaic virus (CGMMV) or cucumber mosaic virus (CMV) on the opposite side of the TMV-inoculated leaf surface. Under fluorescent antibody staining of the leaf section, the challenge viruses were not observed within the TMV-infected areas while the other area was fully infected. Radioisotope-labelled substances (amino acids, uridine or glucose) incorporated to cotyledons through hypocotyls did not distribute to these TMV-localized areas. Cell-to-cell movement of microinjected fluorescent tracer was strongly inhibited in TMV-infected area as compared with uninfected area. Transport of photosynthetic prod ucts out of TMV-infected areas was also inhibited, while the cells in these areas retained the same CO2-assimilatory activity (measured by 14C-CO2) as uninfected areas. These results suggest that some mechanisms inhibiting cell-to-cell movement of virus and sub stances are induced in TMV-infected area, and which may be involved in localization of TMV in cucumber cotyledons.

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Section: Discussionsupporting

confidence: 82%

Inhibition of Cell-to-Cell Movement of Viruses or Substances in Tobacco Mosaic Virus Localized Sites of Cucumber Cotyledons.

Uekusa

Teraoka

Hosokawa

et al. 1993

Jpn. J. Phytopathol.

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“…They also could not detect the presence of callose in inoculated leaves before the occurrence of necrotic lesions. Callose deposition was also observed in living cells of leaf tissues around TMV local necrotic lesions, indicating that it formed a physical barrier to virus movement (Beffa et al 1996;Krasavina et al 2002;Schuster and Flemming 1976;Shimomura 1979;Shimomura and Dijkstra 1975;Stobbs et al 1977;Wu and Dimitman 1970). Similarly, callose deposition was also detected around local lesions in potato plants infected with Potato virus Y (PVY) (Hinrichs-Berger et al 1999), in Sorghum bicolor infected with Maize dwarf mosaic virus (Choi 1999), and in Gomphrena globosa infected with Potato virus X (PVX) (Allison and Shalla 1974;Pennazio et al 1981).…”

Section: Discussionmentioning

confidence: 76%

Callose deposition at plasmodesmata is a critical factor in restricting the cell-to-cell movement of Soybean mosaic virus

Zhao

Liu

et al. 2011

Plant Cell Rep

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Callose is a β-l,3-glucan with diverse roles in the viral pathogenesis of plants. It is widely believed that the deposition of callose and hypersensitive reaction (HR) are critical defence responses of host plants against viral infection. However, the sequence of these two events and their resistance mechanisms are unclear. By exploiting a point inoculation approach combined with aniline blue staining, immuno-electron microscopy and external sphincters staining with tannic acid, we systematically investigated the possible roles of callose deposition during viral infection in soybean. In the incompatible combination, callose deposition at the plasmodesmata (PD) was clearly visible at the sites of inoculation but viral RNA of coat protein (CP-RNA) was not detected by RT-PCR in the leaf above the inoculated one (the upper leaf). In the compatible combination, however, callose deposition at PD was not detected at the site of infection but the viral CP-RNA was detected by RT-PCR in the upper leaf. We also found that in the incompatible combination the fluorescence due to callose formation at the inoculation point disappeared following the injection of 2-deoxy-D-glucose (DDG, an inhibitor of callose synthesis). At same time, in the incompatible combination, necrosis was observed and the viral CP-RNA was detected by RT-PCR in the upper leaf and HR characteristics were evident at the inoculation sites. These results show that, during the defensive response of soybean to viral infection, callose deposition at PD is mainly responsible for restricting the movement of the virus between cells and it occurs prior to the HR response.

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“…Therefore, the explanation based on "turning off and on of resistance genes" (LOEBENSTEIN 1972) in UV irradiated leaves is not suitable in this TMV-Pinto bean system, since UV accelerated large lesion formation in darkness can be counteracted by sugar supply, and it is not known that UV damaged DNA could be repaired by sugars. However, the thickening of cell walls in the cells adjacent to necrotic cells might be explained by activation of callose synthetase, by which cells add callose to pre-existing cell wall (SCHUSTER and FLEMMING 1976, SHIMOMURA and DIJKSTRA 1976, ALLISON and SHALLA 1974, HIRUKI and Tu 1972, Wu et al 1969). In enzyme activation as well as in callose synthesis, which may be related to increased activity of Golgi apparatus for glycoprotein synthesis (KIMMINS and BROW 1973), energy supply may be critical.…”

Section: Discussionmentioning

confidence: 99%

Increased Resistance to the Spread of Tobacco Mosaic Virus in Pinto Bean Leaves Caused by Sugar and Light

Dimitman

1984

Journal of Phytopathology

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Ultraviolet light (UV) irradiation increased expansion of TMV lesions in detached Pinto bean primary leaves incubated in darkness. However, if after UV‐irradiation the leaves were incubated in the light, no increase in lesion expansion occurred. The light effect was considered not to be due to photorepair of UV damaged DNA, since non‐photorepairing treatments such as incubation in red light, or delayed exposure to white light after UV irradiation also prevented increase in lesion expansion. The effect of visible light in preventing TMV‐lesion enlargement was shown to be related to photosynthetic energy supply to the host cell defense mechanism since incubation of infected leaves in the presence of the photosynthesis inhibitor 3‐(3,4‐dichlorophenyl)‐l,l‐dimethyl urea (DCMU) in light caused large lesions whether leaves were irradiated by UV or not. Supplying 0.1 M sucrose in the dark also inhibited lesion enlargement in UV‐irradiated or nonirradiated leaves. Dinitrophenol (DNP) negated the sucrose effect in the dark. However, in light incubation, DNP did not induce large lesions indicating that DNP did not interfere with energy supply in the light. It is concluded that the Pinto bean leaf cells can use energy derived both from mitochondria and chloroplasts for building the resistance mechanism to virus spread. In this case, cellular resistance to virus spread seems to be correlated with callose deposition on the walls of noninfected cells adjacent to the necrotic cells. Energy supply in various forms will assist host cells in building the resistance mechanism as well as retarding senescence. Detachment, prolonged dark incubation, or exogenous supply of DNP led to accelerated senescence which in turn led to secondary enlargement of lesions. The cause of such secondary enlargement may be explained by starvation of cells and disappearance of callose.

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Studies on the Formation of Diffusion Barriers in Hypersensitive Hosts of Tobacco Mosaic Virus and the Role of Necrotization in the Formation of Diffusion Barriers as well as in the Localization of Virus Infections¹)

Cited by 14 publications

References 12 publications

Inhibition of Cell-to-Cell Movement of Viruses or Substances in Tobacco Mosaic Virus Localized Sites of Cucumber Cotyledons.

Inhibition of Cell-to-Cell Movement of Viruses or Substances in Tobacco Mosaic Virus Localized Sites of Cucumber Cotyledons.

Callose deposition at plasmodesmata is a critical factor in restricting the cell-to-cell movement of Soybean mosaic virus

Increased Resistance to the Spread of Tobacco Mosaic Virus in Pinto Bean Leaves Caused by Sugar and Light

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Studies on the Formation of Diffusion Barriers in Hypersensitive Hosts of Tobacco Mosaic Virus and the Role of Necrotization in the Formation of Diffusion Barriers as well as in the Localization of Virus Infections1)

Cited by 14 publications

References 12 publications

Inhibition of Cell-to-Cell Movement of Viruses or Substances in Tobacco Mosaic Virus Localized Sites of Cucumber Cotyledons.

Inhibition of Cell-to-Cell Movement of Viruses or Substances in Tobacco Mosaic Virus Localized Sites of Cucumber Cotyledons.

Callose deposition at plasmodesmata is a critical factor in restricting the cell-to-cell movement of Soybean mosaic virus

Increased Resistance to the Spread of Tobacco Mosaic Virus in Pinto Bean Leaves Caused by Sugar and Light

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Studies on the Formation of Diffusion Barriers in Hypersensitive Hosts of Tobacco Mosaic Virus and the Role of Necrotization in the Formation of Diffusion Barriers as well as in the Localization of Virus Infections¹)