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Induced Interference by Synthetic Polyanions with the Infection of Tobacco Mosaic Virus. Adina Stein, Virus Laboratory, Agricultural Research Organization, The Volcani Center, Bet Dagan, Israel; G. Loebenstein, Virus Laboratory, Agricultural Research Organization, The Volcani Center, Bet Dagan, Israel. Phytopathology 62:1461-1466. Accepted for publication 25 May 1972. DOI: 10.1094/Phyto-62-1461.

Polycarboxylates, with maleic or acrylic acids as the anionic component of the polymer, were evaluated as to their effect on infection and lesion development of tobacco mosaic virus (TMV). Two effects were observed: inhibition and induced interference. The polyanions tested did not inactivate TMV in vitro, but inhibited infection when present during inoculation. Inhibition ranged between 0 and 75%, depending on the concentration of the polyanion, but no effect on lesion size was observed. Ethylene-maleic anhydride (EMA) 31 was least inhibitory. When copolymers with a maleic acid component were injected intercellularly into leaves of Nicotiana tabacum ‘Samsun NN’, N. glutinosa, or Phaseolus vulgaris ‘Scotia’, they induced resistance which developed gradually after application. In the resistant tissue, both lesion number and size decreased significantly. The EMA polymers in particular were potent inducers of interference, irrespective of their molecular weights. Polymers with an acrylic or methacrylic acid component did not induce interference. The esterified vinyl methyl ether-maleic acid, in which the carboxylate groups of maleic acid were partially blocked, was also ineffective as an inducer of interference. Best distinction between inhibition and induced interference was obtained with EMA 31, at a concentration of 0.5 mg/ml, which did not inhibit infection when present during inoculation. Interference, in respect when present during inoculation. Interference, in respect to lesion number, became apparent 24 hr after injection, reaching 75-80% between the 3rd and 15th days. Lesion diameter decreased 50-60%. The development of interference was sensitive to actinomycin D, when applied close in time to the injection of EMA 31. It is suggested that for the development of the polyanion- induced interference, the transcription mechanism of the cell has to operate, and that the respective polyanions activate that part of the genome responsible for localization.