Inactivation of a host resistance mechanism as an explanation for heat activation of TMV-infected bean leaves

In response to heat treatment, both U1 and U2 infected Pinto bean primary leaves produced more and also larger lesions, the size of which was a function of heat dose ( Yarwood, 1958; Rappaport and Wu, 1963). The kinetics of lesion size enlargement resembles that of protein denaturation or killing of...

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Veröffentlicht in:Virology (New York, N.Y.) N.Y.), 1969-04, Vol.37 (4), p.658-666
Hauptverfasser: Wu, J.H., Blakely, L.M., Dimitman, J.E.
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Sprache:eng
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Zusammenfassung:In response to heat treatment, both U1 and U2 infected Pinto bean primary leaves produced more and also larger lesions, the size of which was a function of heat dose ( Yarwood, 1958; Rappaport and Wu, 1963). The kinetics of lesion size enlargement resembles that of protein denaturation or killing of plant tissues by heat. Using a fluorescence microscope and aniline blue staining, the deposition of callose material on cell walls was studied in relation to the development of necrotic local lesions. Those lesions which ceased to enlarge were surrounded by cell walls which showed intense callose fluorescence. There seemed to be a positive correlation between the ultimate size of viral lesions and the rate of callose deposition on the walls of adjacent nonnecrotic cells. Postinoculation heat treatment delayed the hypersensitive necrotic death of infected cells and decreased the rate and amount of callose deposition. It is inferred that the combination of these two effects of heat results in larger lesions. The increase in number of lesions is interpreted as the result of an increase in size of many micro-lesions not visible to the naked eye without heat treatment. In this view, the virus-replicating system and the movement of established virus are more resistant to heat inactivation than the host hypersensitive reaction. An important concomitant of the hypersensitive reaction, as the evidence presented indicates, is the deposition of callose on the walls of uninfected cells surrounding the necrotic cells. The callose deposition is believed to be a factor in sealing off the infected cells, thus preventing the spread of virus.
ISSN:0042-6822
1096-0341
DOI:10.1016/0042-6822(69)90284-0