Abstract
Tobacco mosaic virus mutant Ni 2519 has a selected temperature-sensitive defect in the spreading of local lesions, and additional reported defects in virus assembly and in host range. Here we show that the temperature-sensitive local lesion-spreading defect (which maps in the assembly origin within the gene encoding protein p30) is probably independent of mutations in the pseudoassembly origin or of host range defects resulting from other mutations in the coat protein. One new host range mutant has been isolated.
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