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Etiology of Sweet Potato Russet Crack Disease. R. N. Campbell, Professor of Plant Pathology, Department of Plant Pathology, University of California, Davis 95616; D. H. Hall(2), and Nancy M. Mielinis(3). (2)(3)Extension Plant Pathologist, and Staff Research Associate II, Department of Plant Pathology, University of California, Davis 95616. Phytopathology 64:210-218. Accepted for publication 21 August 1973. DOI: 10.1094/Phyto-64-210.

Sweet potato russet crack is characterized by necrotic lesions on fine roots of the cultivar ‘Jersey’ grown in pasteurized soil in the glasshouse. These lesions appeared 4 wk after graft inoculation of virus-free stock plants, or 6.5 wk after vine cuttings were rooted. As fleshy roots enlarged, they also showed necrotic lesions. The causal agent was confirmed to be graft-transmissible from sweet potato to sweet potato or to Ipomoea setosa, thence to sweet potato. Additionally, I. nil and I. tricolor were shown to be hosts and the causal agent was sap-transmissible from sweet potato to I. nil and from I. nil to I. nil. The causal agent was transmitted in a stylet-borne manner by Myzus persicae, and was associated with a flexuous, rod-shaped virus particle. The sweet potato feathery mottle virus (FMV), as redefined from previous literature, also occurred in the russet crack-affected plants and it was sometimes isolated from russet crack by sap transmission and once by aphid transmission. It was not possible to isolate a distinct russet crack causal agent free from FMV. The only difference between FMV and the russet crack culture was the necrotic root reaction of ‘Jersey’ sweet potato inoculated with the russet crack culture. In cross-protection trials, sweet potatoes infected by FMV were protected from russet crack symptom expression. It is hypothesized that russet crack is caused by a strain of FMV; i.e., RC-FMV.