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Stemphylium leaf spot of spinach, caused by Stemphylium beticola and S. vesicarium , is a disease of economic importance in fresh market, processing, and seed production. There have been increasing reports of difficulty managing the disease in the southern United States using fungicides in Fungicide Resistance Action Committee (FRAC) group 11. Isolates of S. beticola and S. vesicarium obtained from spinach leaves and seed from 2001 to 2020 were screened for resistance to azoxystrobin and pyraclostrobin in vitro, in vivo, and using PCR assays to detect mutations in cytochrome b associated with resistance in other fungi (F129L, G137R, and G143A). EC 50 values for mycelial growth and conidial germination of S. vesicarium isolates in vitro were significantly less (mean of 0.35 μg/ml) than that of S. vesicarium (mean of 14.17 μg/ml) with both fungicides. All isolates were slightly more sensitive to pyraclostrobin than azoxystrobin in both assays. In vivo assays of plants inoculated with the isolates of S. vesicarium demonstrated poor efficacy of fungicides with each of the two active ingredients. Only the G143A mutation was detected in all spinach isolates of S. vesicarium , including an isolate of S. vesicarium collected in 2003 and 82.9% of isolates from spinach seed lots harvested from crops grown in or after 2017 in Europe, New Zealand, and the United States. The FRAC 11 mutations were not detected in any isolates of S. beticola . The in vitro, in vivo, and DNA mutation assays suggest FRAC group 11 fungicide resistance is widespread in spinach isolates of S. vesicarium but not S. beticola., Competing Interests: The author(s) declare no conflict of interest.

Fusarium wilt of spinach, caused by Fusarium oxysporum f. sp. spinaciae , is an important disease during warm conditions in production regions with acid soils, yet little is known about what confers pathogenicity to spinach in F. oxysporum f. sp. spinaciae genetically. To identify candidate fungal genes that contribute to spinach Fusarium wilt, each of 69 geographically diverse F. oxysporum isolates was tested for pathogenicity on each of three spinach inbreds. Thirty-nine isolates identified as F. oxysporum f. sp. spinaciae caused quantitative differences in disease severity among the inbreds that revealed two distinct pathogenicity groups of F. oxysporum f. sp. spinaciae . Putative effector gene profiles, predicted from whole-genome sequences generated for nine F. oxysporum f. sp. spinaciae isolates and five nonpathogenic, spinach-associated F. oxysporum (NPS) isolates, distinguished the F. oxysporum f. sp. spinaciae isolates from the NPS isolates, and separated the F. oxysporum f. sp. spinaciae isolates into two groups. Five of the putative effector genes appeared to be unique to F. oxysporum f. sp. spinaciae , as they were not found in 222 other publicly available genome assemblies of F. oxysporum , implicating potential involvement of these genes in pathogenicity to spinach. In addition, two combinations of the 14 known Secreted in Xylem ( SIX ) genes that have been affiliated with host pathogenicity in other formae speciales of F. oxysporum were identified in genome assemblies of the nine F. oxysporum f. sp. spinaciae isolates, either SIX8 and SIX9 or SIX4 , SIX8 , and SIX14 . Characterization of these putative effector genes should aid in understanding mechanisms of pathogenicity in F. oxysporum f. sp. spinaciae , developing molecular tools for rapid detection and quantification of F. oxysporum f. sp. spinaciae , and breeding for resistance to Fusarium wilt in spinach.[Formula: see text] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY 4.0 International license.

The article highlights the Iris yellow spot virus as a threat to onion bulb and seed production. It discusses the history of Iris yellow spot virus in the United States and around the world, the epidemiology of the virus and the onion thrips vector, management of Iris yellow spot and thrips, and outlook and future directions of the virus.

Carrot (Daucus carota subsp, sativus) seed crops in Oregon and Washington were surveyed in 2001–02 and 2002–03 for development of Xanthomonas campestris pv. carotae, causal agent of bacterial blight. For each state and season, 20 plants were sampled from each of 7 to 12 direct-seeded crops twice in the fall or winter and three times from spring to summer; and from each of 2 m 4 steckling (root-to-seed) crops three times from spring to summer. X. campestris pv. carotae was detected in 1 of 15 and 6 of 32 stock seed lots planted in the fall in Oregon and Washington, respectively, and in 2 of 6 steckling shipments planted in each state in the spring. The pathogen was detected at 10² to 108 CFU/g foliage in 1 of 22 and 10 of 14 direct-seeded crops within 2 months of planting in 2001 and 2002, respectively. The prevalence of X. campestris pv. carotae then increased through the season in most seed crops, although bacterial blight symptoms were not observed until April in Oregon and July in Washington in both seasons. In August 2002 and 2003, X. campestris pv. carotae was detected in all 10 and 13 crops surveyed in Oregon, respectively; and in 11 of 12 and 7 of 10 crops in Washington, respectively. The pathogen was typically less prevalent in steckling versus direct-seeded crops. X. campestris pv. carotae was detected in 20 of 22 and 19 of 23 harvested seed lots in Oregon and Washington, respectively, at populations ranging from 1.3 ⊗ 10¹ to 1.4 ⊗ 108 CFU/g seed. Airborne X. campestris pv. carotae, detected ≥1,600 m downwind of crops being threshed in Oregon in September of 2003 and 2004, may provide a source of inoculum for newly planted seed crops between overlapping biennial seasons for carrot seed production. Despite the prevalence of this pathogen in the Pacific Northwest, carrot seed lots free of X. campestris pv. carotae were detected, demonstrating the ability to produce clean seed in this region by adhering to recommended practices for management of bacterial blight. [ABSTRACT FROM AUTHOR]

There are no previous reports of Verticillium wilt in fresh and processing spinach (Spinacia oleracea) crops in the United States. In 2002, a hybrid spinach seed crop in the Pacific Northwest developed late-season wilt symptoms. Assays of the harvested seed and stock seed of the male and female parents revealed 59.5, 44.0, and 1.5%, respectively, were infected with Verticillum dahliae. Assays of 13 stock or commercial seed lots grown in 2002 and 62 commercial lots harvested in 2003 in Denmark, Holland, New Zealand, and the United States revealed the prevalence of Verticillium spp. in commercial spinach seed. Sixty-eight lots (89%) were infected with Verticillium spp. at incidences ranging from 0.3 to 84.8%. Five spinach seed isolates of V dahliae were pathogenic on each of three spinach cultivars by root-dip inoculation. V dahliae was detected on 26.4% of the seed from 7 of 11 inoculated plants but on none of the seed from 6 control plants, demonstrating systemic movement of V dahliae. Seed-to-seed transmission was also demonstrated by planting naturally infected seed lots. This is the first report of Verticillium wilt of spinach in the primary region of spinach seed production in the United States. [ABSTRACT FROM AUTHOR]

Of 12 onion seed lots harvested in the semi-arid Columbia Basin of Washington in 1999 or 2000, 8 were infected and 10 infested with Botrytis aclada at incidences of 1 to 10% and 2 to 26%, respectively. Twenty to forty plants were sampled from each of nine direct-seeded, biennial seed crops in April, June, and July 2001 and assayed for Botrytis spp. Six direct-seeded crops were sampled in October and November 2001 and April, June, and July 2002. One bulb-to-seed crop was sampled in April, June, and July 2002. The incidence of B. aclada increased through each season, reaching 100% in most fields by July. Infections were primarily asymptomatic, with no apparent relationship between plant infection and infection of harvested seed. B, cinerea, B. squamosa, and B. porri were detected in 16, 4, and 4% of the fields, respectively, at lower incidences than B. aclada. Harvested seed from 15 of the fields were infected with B. aclada at <1 to 28%. B, cinerea, B. porri, and B. squamosa were detected in three, three, and none of the harvested lots, respectively. [ABSTRACT FROM AUTHOR]

The landscape of scientific publishing is experiencing a transformative shift toward open access, a paradigm that mandates the availability of research outputs such as data, code, materials, and publications. Open access provides increased reproducibility and allows for reuse of these resources. This article provides guidance for best publishing practices of scientific research, data, and associated resources, including code, in The American Phytopathological Society journals. Key areas such as diagnostic assays, experimental design, data sharing, and code deposition are explored in detail. This guidance aligns with that observed by other leading journals. We hope the information assembled in this paper will raise awareness of best practices and enable greater appraisal of the true effects of biological phenomena in plant pathology. [ABSTRACT FROM AUTHOR]

Stunting caused by Rhizoctonia spp. is economically important in irrigated onion bulb crops in the semiarid Columbia Basin of Oregon and Washington, where cereal winter cover crops commonly are planted the previous fall to prevent wind erosion of soil. The cover crop is killed with herbicide application just before or shortly after onion seeding, so that the dead rows of cereal plants provide a physical barrier tall enough to protect onion seedlings against wind and sand blasting but not tall enough to shade onion seedlings. However, the cover crop also serves as a green bridge for Rhizoctonia spp. on cereal roots to colonize the onion roots, potentially resulting in severe stunting of onion seedlings. To determine the effect of timing of application of the herbicide glyphosate to reduce this green bridge effect and, subsequently, onion stunting, three herbicide application intervals preceding onion planting were evaluated in a grower's onion field in each of 2012 and 2014 in the Columbia Basin. The wheat cover crop was killed with a glyphosate application 27, 17, and 3 days before onion seeding in 2012 and 19, 10, and 3 days before seeding in 2014. As the interval between herbicide application and onion planting increased from 3 days to 19 and 27 days, the number of patches of stunted onion plants decreased by >55%, total area of stunted patches decreased by 54 to 63%, and patch severity index decreased by 59 to 65%. Similarly, the Rhizoctonia solani AG 8 DNA concentration in soil sampled from the dead cover crop rows declined as the interval between glyphosate application and onion seeding increased in the 2012 trial but not in the 2014 trial. R. solani AG 3 and AG 8 DNA concentrations in soil sampled from the cover crop rows were significantly positively correlated with the number of patches of stunted onion plants (r = 0.490 and 0.607 at P = 0.039 and 0.008, respectively), total area of stunted patches (r = 0.496 and 0.659 at P = 0.035 and 0.003, respectively), and patch severity index (r = 0.492 and 0.635 at P = 0.038 and 0.005, respectively) in the 2012 trial; however, these variables were only correlated significantly with R. solani AG 3 DNA concentration in the 2014 trial. Increasing the interval between herbicide application to the cover crop and onion planting provides a practical management tool for stunting in onion bulb crops. [ABSTRACT FROM AUTHOR]