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Sweet potato feathery mottle virus (SPFMV, genus Potyvirus, family Potyviridae), Sweet potato chlorotic stunt virus (SPCSV, genus Crinivirus, family Closteroviridae) and sweet potato virus G (SPVG) were detected in naturally infected sweet potato plants grown in the Delta region in Egypt. Before this study, SPVG was reported only from China. Two isolates of SPFMV and one isolate of SPVG were characterized for the 3'-proximal genomic sequences. Phylogenetic analyses indicated that the SPFMV isolates belong to the "russet crack" strain group (RC). Serological tests using monoclonal antibodies, and phylogenetic analysis of a partial sequence of the Hsp70 gene, indicated that the Egyptian SPCSV belongs to the so-called non-East African strain group of SPCSV.

ABSTRACT Isolates of Sweetpotato feathery mottle virus (SPFMV, genus Potyvirus, family Potyviridae) were obtained in several districts of Uganda from sweetpotato plants infected with the sweetpotato virus disease (SPVD), the most important disease of this crop in Africa. A monoclonal antibody (MAb 7H8) raised against the coat proteins (CP) of a mixture of the SPFMV strain C (United States) and the isolate SPV-I (West Africa) distinguished Ugandan SPFMV isolates into those detectable and not detectable by the MAb. These two serotypes differed in prevalence in different districts of Uganda and in two common sweetpotato cultivars. Both serotypes could be transmitted simultaneously by single aphids. The serotypes differed in their ability to systemically coinfect sweetpotatoes that were infected with Sweetpotato chlorotic stunt virus (SPCSV, genus Crinivirus), the virus required to induce SPVD in SPFMV-infected plants. One sweetpotato breeding line, resistant to SPFMV from the New World, was infected by graft-inoculation with all SPFMV isolates from Uganda. Another SPFMV-resistant sweetpotato line became infected with SPFMV and developed SPVD only following coinoculation with SPCSV.

Resistance to Potato virus Y (PVY) has been obtained in our previous studies through expression of the PVY P1 gene in sense or antisense orientation in potato cv. Pito. In the present study, the mechanism and strain specificity of the resistance were analyzed. Several features including low steady-state P1 mRNA expression in the resistant P1 plants indicated that resistance was based on post-transcriptional gene silencing (PTGS). Resistance was specific to PVY(O) isolates, the PVY strain group from which the P1 transgene was derived. However, according to group analyses, there was no distinguishing characteristic between the PVY(O) and PVY(N) strains P1 gene sequences. Therefore, the ability of the PVY(N) strains to overcome resistance could not be explained solely based on their P1 gene sequences. Infection with PVY(N) of the PVY(O)-resistant transgenic lines led to a recovery of expression of the P1 transgene. These data suggested that factors other than sequence homology are required in determination of the resistance specificity.

When infecting alone, Sweet potato feathery mottle virus (SPFMV, genus Potyvirus) and Sweet potato chlorotic stunt virus (SPCSV, genus Crinivirus) cause no or only mild symptoms (slight stunting and purpling), respectively, in the sweet potato (Ipomoea batatas L. ). In the SPFMV-resistant cv. Tanzania, SPFMV is also present at extremely low titers, though plants are systemically infected. However, infection with both viruses results in the development of sweet potato virus disease (SPVD) characterized by severe symptoms in leaves and stunting of the plants. Data from this study showed that SPCSV remains confined to phloem and at a similar or slightly lower titer in the SPVD-affected plants, whereas the amounts of SPFMV RNA and CP antigen increase 600-fold. SPFMV was not confined to phloem, and the movement from the inoculated leaf to the upper leaves occurred at a similar rate, regardless of whether or not the plants were infected with SPCSV. Hence, resistance to SPFMV in cv. Tanzania was not based on restricted virus movement, neither did SPCSV significantly enhance the phloem loading or unloading of SPFMV. It is also noteworthy that SPVD is an unusual synergistic interaction in that the potyvirus component is not the cause of synergism but is the beneficiary. It is hypothesized that SPCSV is able to enhance the multiplication of SPFMV in tissues other than where it occurs itself, perhaps by interfering with systemic phloem-dependent signaling required in a resistance mechanism directed against SPFMV., (Copyright 2000 Academic Press.)

ABSTRACT The sequences of the 16S rRNA genes (nucleotides 29 to 1,521) from various Streptomyces strains pathogenic to potato were compared. These included 10 pathogenic Streptomyces strains isolated from potato scab lesions in Finland, the type strains of S. aureofaciens NRRL 2209(T) and S. lydicus ATCC 25470(T), 'S. griseus subsp. scabies' ATCC 10246, and two S. griseus strains that were originally deposited to the collection as pathogens. The nucleotide sequence (>94.5% sequence identity [SI]) and length (1,469 to 1,481 nucleotides) of the analyzed region varied. Phylogenetic analysis of 16S rRNA genes placed Finnish strains into three species, supported by previously characterized morphological and physiological traits. Six Finnish strains, including two strains that deviated from the others in one trait (no spiral sporophores or D-xylose utilization), had identical 16S rRNA genes and were identified as S. scabies (99.9% SI to S. scabies ATCC 49173). Three Finnish strains were identified as S. turgidiscabies, a species previously described only in Japan (99.9% SI to S. turgidiscabies ATCC 700248). Finnish strain 317 and S. aureofaciens NRRL 2209 (99.8% SI) were placed in a distinct phylogenetic cluster together with Kitosatospora spp., which suggests that S. aureofaciens may belong to the recently revived genus Kitosatospora. In pathogenicity tests, S. scabies caused characteristic symptoms of common scab, S. turgidiscabies caused mainly pitted scab, and S. aureofaciens caused netted scab and necrotic lesions on stolons of potato cultivars Bintje and Matilda in the greenhouse. The nec1 gene and the intergenic region between nec1 and the 5' transposase pseudogene ORFtnp were successfully amplified by polymerase chain reaction from S. scabies ATCC 49173 and the pathogenic Finnish strains of S. scabies, but not from a nonpathogenic strain of S. scabies, three pathogenic and two nonpathogenic strains of S. turgidiscabies, and S. aureofaciens.