First Report of a Disease of Peony Caused by Alfalfa mosaic virus

During the summers of 2001 and 2002, Japanese peony (Paeonia albiflora Pall., synonym P. lactiflora, family Paeoniaceae) plants, cultivated in the Botanical Garden of the University of Parma (Emilia Romagna Region of northern Italy), were found affected by a disease with virus-like symptoms. The oldest leaves showed yellow, mosaic, oak-like arabesques and line-patterns; the remaining leaves and pink flowers were symptomless. A disease of peony, known as peony ring spot disease, has been reported worldwide (Europe, United States, Japan, and New Zeland) for several years and is associated with strains of Tobacco rattle virus (TRV) (1). Electron microscopic observations of peony leaf sap (leaf dip preparations stained with uranyl acetate and phospotungstic acid) did not show the presence of any rod-shaped virus particles, including TRV. Mechanical inoculations of sap from symptomatic leaves caused symptoms typical of Alfalfa mosaic virus (AMV) on Chenopodium amaranticolor Coste & Reyn. (local chlorotic and necrotic lesions and systemic periveinal line-patterns), Ocimum basilicum L. (yellow mosaic), Vigna unguiculata (L.) Walp. (red, local necrotic lesions), and Nicotiana tabacum cv. Samsun (white, necrotic lesions, systemic leaf malformation, and mosaic), and N. glutinosa L. (systemic leaf variegation). Symptomatic leaves of peony and infected herbaceous plants were analyzed for virus presence by protein A sandwich enzyme-linked immunosorbent assay (PAS-ELISA). The polyclonal antisera tested were those to AMV (PVAS 92, American Type Culture Collection, Manassas, VA), AMV-Vinca minor L. (DiSTA collection, Italy), and the nepoviruses Strawberry latent ringspot virus, Tomato ringspot virus, and Cherry leaf roll virus. PAS-ELISA revealed only the presence of AMV. Immunoelectron microscopy and gold-labeled decoration confirmed the identity of the virus. In 2001, five symptomless peony plants (provided by a commercial grower and previously analyzed for AMV and TRV presence) were grafted with shoots from peony showing yellow mosaic on the leaves and maintained in a greenhouse under aphid-proof cage. During the summer of 2002, one of the grafted plants showed a mild mosaic on the leaves; PAS-ELISA revealed this peony was infected by AMV. To our knowledge, this is the first report of AMV in peony. Reference: (1) Chang et al. Ann. Phytopathol. Soc. Jpn. 42:325, 1976.

The Expression Level of the 3a Movement Protein Determines Differences in Severity of Symptoms Between Two Strains of Tomato Aspermy Cucumovirus

Two strains of tomato aspermy cucumovirus, 1-TAV and V-TAV, differ in the severity of the symptoms induced in Nicotiana tabacum: 1-TAV induces a severe chlorotic mottle that appears 5 days post inoculation (d.p.i.) in the second systemic leaf, while V-TAV-infected plants show a mild chlorotic mottle, unevenly distributed in the leaf lamina, that appears 7 d.p.i. in the third or fourth systemic leaf. The manipulation of full-length cDNA clones giving infectious transcripts of V-TAV RNAs 1, 2, and 3 and 1-TAV RNA 3 revealed that the slow, mild phenotype of V-TAV maps to the movement protein (MP) gene. By site-directed mutagenesis it was further shown that this phenotype co-segregates with a single nucleotide substitution that introduces an in-frame UAA stop codon at the fourth position of the MP open reading frame of V-TAV. The presence of this stop codon results in a diminished expression of the MP in both tobacco protoplasts and leaves. Analyses of the progress of infection and of the time course of MP and coat protein accumulation show that the low level of MP in V-TAV-infected leaves limits the rate of cell-to-cell movement and leads to the mild phenotype. Data from the infectivity of RNA 3 transcripts with or without this stop codon, plus data from in vitro translation of virion or transcript RNA 3, suggest that the small amount of MP observed in V-TAV-infected leaves is expressed from a minor RNA 3 subpopulation lacking the stop codon.

Peronospora farinosa f. sp. betae. [Descriptions of Fungi and Bacteria].

A description is provided for Peronospora farinosa f. sp. betae. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: Beta spp., including the cultivated varieties of B. vulgaris subsp. vulgaris, e.g. chard, fodder beet, mangold, red beet, spinach beet and sugar beet. DISEASE: Downy mildew of beet. Typical infection is systemic and the young leaves at the centre of the rosette are attacked. Infected leaves are at first pale green; they fail to expand fully, their colour changes to yellowish green, and they become swollen, brittle and are usually incurred. Conidia are formed in great profusion, first on the under surface of infected leaves but spreading to the upper surface in wet weather. After sporulation the leaves die prematurely. Some leaves are only partly infected; the tip remains healthy and the division between diseased and healthy tissue is sharply defined. Under humid conditions, early in the season, the fungus may cause a non-systemic leaf-spot on young plants. All aerial parts of the seed plant in its second year may become infected. GEOGRAPHICAL DISTRIBUTION: Africa (Kenya, Morocco); Asia (Israel, USSR); Australasia (Australia, N.S.W., Victoria. New Zealand); Europe (widespread); North America (Canada, U.S.A.); South America (Argentina). Note that CMI Map No. 28, ed. 3, 1969, shows records of P. farinosa on Beta, Spinacia and Chenopodium spp. TRANSMISSION: The disease can be transmitted by oospores, perennial mycelium or by continual reinfection from living plants. Oospores, on debris in the ground, are a potential source of inoculum but have only been reported of economic importance on seed crops in France. Seed crops and groundkeepers can provide a source of living inoculum overwinter and this is the most common and economically important source of the fungus (Byford & Hull, 1967). Seed may be contaminated by oospores and mycelium and there is evidence that oospores on imported seed were responsible for the introduction of the disease into Australia (15, 193).