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VIEW ARTICLE   |    DOI: 10.1094/MPMI-6-045


Impeded Phloem-Dependent Accumulation of the Masked Strain of Tobacco Mosaic Virus. Richard S. Nelson. Plant Biology Division, Samuel Roberts Noble Foundation, Ardmore, OK 73402, U.S.A. Guoxuan Li(1), Richard A. J. Hodgson(2), Roger N. Beachy(2), and Michael H. Shintaku(1). (1)Plant Biology Division, Samuel Roberts Noble Foundation, Ardmore, OK 73402, U.S.A., and (2)Department of Biology, Washington University, St. Louis, MO 63130, U.S.A. MPMI 6:45-54. Accepted 22 October 1992. Copyright 1993 The American Phytopathological Society.


The Holmes’ masked (M) strain of tobacco mosaic virus produces mild (attenuated) symptoms compared with those of the U1 strain. We compared the accumulation of M strain viral protein and RNA with that of the severe U1 strain in protoplasts and leaf tissue from Nicotiana tabacum ‘Xanthi nn.’ In protoplasts or inoculated leaves, the accumulation of coat protein, movement protein, 126-and 183-kDa proteins, and all species of viral RNA were similar for the M and U1 strains. In addition, the specific infectivity of extracts from M-inoculated tissue was similar to that of extracts from U1-inoculated tissue. However, in tissue infected as a result of phloem transport, accumulation of M strain coat protein and viral RNA was transiently less than that observed for the U1 strain. Results from tissue print and temperature shift experiments indicated that the lower level of M strain accumulation was apparent in the petioles of inoculated leaves from 2.5 to 4 days postinoculation and in the shoot apex at least through 11 days postinoculation. We conclude that, in comparison with the U1 strain, the M strain is capable of normal rates of replication and cell-to-cell movement in inoculated leaves, but accumulation (i.e., replication or movement) over long distances (i.e., by phloem movement) is inhibited. This inhibition is observed in both developed tissue (petioles of inoculated leaves) and in developing tissue (tissue near the shoot apex).

Additional Keywords: attenuated viruses, pathogenicity, symptom determinants.