Several downy mildew resistance genes in Arabidopsis require signaling via a homologue of yeast SGT1

A fast neutron mutant in Arabidopsis (Columbia) was identified that exhibits enhanced downy mildew (edm1) susceptibility to several Peronospora parasitica isolates, including the RPP7-diagnostic isolate Hiks1. The mutation was mapped to chr.4 and physically characterised as a 35kb deletion spanning seven genes. One of these genes restored wild-type resistance to all of the P. parasitica isolates. This gene (AtSGT1b) encodes a predicted protein that is orthologous to yeast SGT1, originally described as a key regulatory protein in centromere function and ubiquitin-mediated proteolysis. AtSGT1b contains three tatratrico-peptide repeats at the N terminus followed by a bipartite “CS” (CHORD containing Sgt) domain and an SGT specific (SGTS) domain at the carboxyl terminus. Altered expression of this gene is being investigated in Arabidopsis and Brassica olarecea to determine its potential use for crop improvement.

First Report of Downy Mildew Caused by Peronospora parasitica on Iberis sempervirens in Italy

Iberis sempervirens (evergreen candytuft) is a garden species belonging to the Brassicaceae family. During June 2004, a damaging foliar disease was observed in several commercial farms near Albenga (northern Italy) on I. sempervirens plants grown outdoors in containers. More than 30% of the plants were affected. Symptoms appeared on both sides of leaves, buds, flowers, and fruits. Initially, leaves were slightly chlorotic, but within 5 to 7 days a characteristic whitish furry growth developed on the lower and upper leaf surfaces. The efflorescence was particularly evident on the lower surfaces of leaves and consisted of sporangiophores and sporangia. The appearance and severity of the disease increased because of overhead sprinkler irrigation. Microscopic observations revealed dichotomously branched sporangiophores with slender curved tips. Sporangiophores with a length of 115 to 410 μm (average 295 μm) ended with sterigmata bearing single sporangia. Sporangia were ovoid and measured 18 to 28 × 25 to 45 μm (average 22 × 35 μm). The pathogen was identified as Peronospora parasitica on the basis of its morphological characteristics (3). Pathogenicity was confirmed by inoculating leaves of 10 45-day-old healthy plants grown in 14-cm-diameter pots with a sporangial suspension (1 × 103 conidia/ml). Ten noninoculated plants served as controls. Plants were maintained outdoors at 50% light intensity with temperatures ranging between 16 and 25°C (average 18°C) and 85 to 100% relative humidity. The pathogenicity test was carried out twice. After 18 days, typical symptoms of downy mildew developed on the inoculated plants and P. parasitica was observed on the leaves. Noninoculated plants did not show symptoms. To our knowledge, this is the first report of P. parasitica on evergreen candytuft in Italy. P. parasitica was previously reported on I. sempervirens in the United Kingdom (1) and on I. amara in California (2). Voucher specimens are available at the AGROINNOVA Collection, University of Torino, Italy. References: (1) S. Francis and G. Waterhouse. Trans. Br. Mycol. Soc. 91:1, 1988. (2) P. R. Muller et al. Index of Plant Diseases in the United States. USDA Handbook No. 165, 1960. (3) D. M. Spencer. The Downy Mildews. Academic Press, New York, 1981.

First Report of Downy Mildew of Arugula Caused by Peronospora parasitica in Argentina

Acreage of arugula (Eruca sativa), a crucifer used as a component of green salad mixes, has increased recently in Argentina. During 2004, a foliar disease affected commercial crops in Pilar (northeast of Buenos Aires Province). Arugula plants were affected from the seedling stage to harvest. Severely diseased plants were unmarketable and not harvested. Sunken, round, necrotic lesions (1 to 4 mm in diameter) were observed on the cotyledons. Diseased leaves had irregular, necrotic lesions (2 to 3 mm in diameter) that sometimes became confluent, forming a linear pattern. Necrotic tan patches developed on older leaves. Lesions on the abaxial surface appeared depressed and a gray mold, a typical sign of a downy mildew, was visible. Sporangiophores had dichotomous branches ending in slender curved tips. Sporangia were ovoid with a mean length of 20 μm (17.8 to 22.1 μm) and a mean width of 16 μm (14 to 18.2 μm). Pathogenicity tests were conducted by placing excised diseased leaves onto healthy 30-day-old arugula plants (1). Inoculated plants were placed in plastic bags, previously sprayed with water, for 48 h and maintained in the greenhouse thereafter. Downy mildew symptoms and signs that were similar to those observed in the fields developed 10 days after inoculation. The pathogen was identified as Peronospora parasitica (2). To our knowledge, this is the first report of P. parasitica on arugula in Argentina. References: (1) S. T. Koike. Plant Dis. 82:1063, 1998. (2) W. D. Yerkes and C. G. Shaw. Phytopathology 49:499, 1959.

Arabidopsis ssi2-Conferred Susceptibility to Botrytis cinerea Is Dependent on EDS5 and PAD4

Loss of a stearoyl-ACP desaturase activity in the Arabidopsis thaliana ssi2 mutant confers susceptibility to the necrotroph, Botrytis cinerea. In contrast, the ssi2 mutant exhibits enhanced resistance to Pseudomonas syringae, Peronospora parasitica, and Cucumber mosaic virus. The altered basal resistance to these pathogens in the ssi2 mutant plant is accompanied by the constitutive accumulation of elevated salicylic acid (SA) level and expression of the pathogenesis-related 1 (PR1) gene, the inability of jasmonic acid (JA) to activate expression of the defensin gene, PDF1.2, and the spontaneous death of cells. Here, we show that presence of the eds5 and pad4 mutant alleles compromises the ssi2-conferred resistance to Pseudomonas syringae pv. maculicola. In contrast, resistance to B. cinerea was restored in the ssi2 eds5 and ssi2 pad4 double-mutant plants. However, resistance to B. cinerea was not accompanied by the restoration of JA responsiveness in the ssi2 eds5 and ssi2 pad4 plants. The ssi2 eds5 and ssi2 pad4 plants retain the ssi2-conferred spontaneous cell death phenotype, suggesting that cell death is not a major factor that predisposes the ssi2 mutant to infection by B. cinerea. Furthermore, the high SA content of the ssi2 pad4 plant, combined with our previous observation that the SA-deficient ssi2 nahG plant succumbs to infection by B. cinerea, suggests that elevated SA level does not have a causal role in the ssi2-conferred susceptibility to B. cinerea. Our results suggest that interaction between an SSI2-dependent factor or factors and an EDS5- and PAD4- dependent mechanism or mechanisms modulates defense to B. cinerea.