Abstract

The hypersensitive reaction of White Burley tobacco to tobacco necrosis virus (TNV) was characterized by the development of non-self-limiting necrotic local lesions, the acquisition of a systemic resistance against infection and the formation of pathogenesis-related (PR) proteins. The progressive radial spread of the lesions and the high amount of TNV antigen in the outer halo of the lesions indicated that mechanisms restricting TNV spread and multiplication were not operating. Prior TNV inoculation followed by challenge inoculation with the same virus showed that a systemic acquired resistance was induced against the establishment of challenge-infection sites (partial resistance), but that where lesions became established, they developed normally. Since resistance against virus multiplication or cell-to-cell spread was not induced, it is suggested that different mechanisms may control the different types of resistance. In halo lesions but not in control tissues, four PR proteins of host origin appeared and accumulated during lesion growth. These proteins had electrophoretic mobilities identical to those of the PR proteins induced by tobacco mosaic virus in Xanthi-nc tobacco. The White Burley PR proteins also appeared in leaves inoculated with tomato bushy stunt virus (giving self-limiting lesions) or tobacco rattle virus (giving necrotic lesions followed by systemic invasion of plant tissues), and were also found in tissues in which resistance against challenge infection was induced. These results do not support the hypothesis that PR proteins interfere with TNV multiplication or cell-to-cell spread and thus have a defensive role.

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