Abstract

Infection of Nicotiana tabacum var. “Samsun” and “Samsun NN” with tobacco mosaic virus “Wageningen” U 1 (TMV W U 1) at 30 °C leads to systemic mosaic symptoms in both varieties. Electrophoretic patterns of soluble leaf proteins in polyacrylamide gels showed identical changes for both varieties and were the same as those in the combination TMV W U 1-Samsun at 20 °C and similar to those in the combination TMV W U 1-Samsun EN, in which identical symptoms are induced. Four new protein components (I to IV) accumulating at 20 °C in Samsun NN plants showing local lesions did not increase in amount after transfer of these plants to 30 °C; bands I, II and IV were considerably reduced, whereas band III appeared unaffected. When Samsun plants were infected with the Holmes' ribgrass strain of TMV (TMV HR) at 20 °C, both free TMV HR coat protein and relatively small amounts of the new components I to IV were apparent, proving that these components cannot be products of the N gene. The formation of small local lesions on the variety Samsun EN upon infection with TMV HR resulted in induction of the new components I to IV in apparently trace amounts, whereas quantitative changes seemed to be extremely limited. Inoculation of Samsun NN plants with TMV HR led to symptoms under greenhouse conditions only. In this combination, systemic acquired resistance was expressed when traces of protein components I to IV were present. In general, the changes in soluble proteins were connected with the type of symptoms—either mosaic or localized necrosis—produced, rather than the genetic make-up of the host plant variety.

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