Seed transmission of Pantoea stewartii was evaluated by assays of more than 76,000 plants in greenhouse and field grow-out trials. Fourteen P. stewartii-infected seed lots were obtained from two dent corn inbreds and two sweet corn cultivars that were inoculated with either a rifampicin and nalidixic acid-resistant strain (rif-9A) or a wild-type strain (SS104) of P. stewartii. Four additional seed lots were collected from naturally infected inbreds. Percentages of infected kernels ranged from 0.8 to 72%, as determined by agar plating or by individual-kernel enzyme-linked immunosorbent assay (ELISA). Plants grown from this seed were assayed by a stem-printing technique that consisted of cutting and pressing a cross-section of each stem onto agar media. Prints were examined for development of P. stewartii colonies after 24 and 48 h. The transmission rate from seed produced on the inoculated plants was 0.066% (28 of 42,206 plants), based on all seedlings assayed. Transmission was estimated to be 0.14% from infected kernels. The transmission rate from seed produced on naturally infected plants was 0.0029% (1 of 34,924 plants), based on all seedlings, and 0.022% from infected kernels. Seed transmission occurred significantly less often (P = 0.034) from seed produced on naturally infected plants than from seed produced on inoculated plants, probably due to greater kernel damage caused by ear shank inoculation. The rarity of seed transmission of P. stewartii from heavily infected seed lots that would ordinarily be rejected due to poor germination suggests that the likelihood of seed transmission from good quality commercial seed corn is virtually nonexistent.

Between 2002 and 2015, a comprehensive survey of sunflower fields across seven Midwestern U.S. states was conducted 12 times and continues to be conducted every other year. The surveyors collected data on yield, agronomic management factors, disease, insect, weed, and bird damage. All surveyors were volunteers and came from universities (extension and research staff), USDA-ARS, and seed and chemical companies. In the 12 years the survey was conducted, data from 2,267 fields were collected. The results are presented annually at the National Sunflower Association Research Forum and are used to set sunflower research priorities. While 10 diseases are surveyed annually, we focus this article on the importance, findings, implications, and impacts of the five most important: downy mildew, Phomopsis stem canker, rust, Rhizopus head rot, and Sclerotinia head rot. This survey is unique among field crops in both scope and scale, and this manuscript discusses salient and clandestine benefits of intense and long-term disease surveys.

The relationship between the amount of foliar disease on maize plants and seed contamination by the causal bacterium, Pantoea stewartii, was studied by comparing disease severity on adult plants with results from laboratory seed tests. Seventy-seven naturally infected maize lines (25 in 1990 and 52 in 1992) were selected and assigned to one of six disease severity classes based on the percentage of ear leaf tissue killed by Stewart's wilt: trace to 2%, 6 to 14%, 25 to 34%, 35 to 49%, 50 to 74%, and 75 to 100%. Ears were harvested from 10 to 20 plants representative of the disease class for each maize line, and seeds were tested by enzyme-linked immunosorbent assay (ELISA) of bulk-seed samples. Seed infection percentages were estimated from the bulk-test results by using statistical equations for group testing. The accuracy of the bulk-seed method for estimating seed infection was validated by comparison with 300-kernel single-seed tests. Infected seed was detected only from seed of plants with ≥25% disease severity; however, 45 of 63 such seed lots had no infection. Three seed lots had >5% infected seeds, all from plants with >50% disease severity. The results suggest a possible threshold level between 15 and 25% disease severity for Stewart's wilt on leaves before bacteria are detected in seed. This study describes a relatively simple method for estimating the incidence of infected seeds in a seed lot and contributes additional evidence to indicate that the chance of spreading P. stewartii from U.S.-produced maize seeds is low.

Basal stalk rot (BSR), caused by Sclerotinia sclerotiorum, is a devastating disease in sunflower worldwide. The progress of breeding for Sclerotinia BSR resistance has been hampered due to the lack of effective sources of resistance for cultivated sunflower. Our objective was to transfer BSR resistance from wild annual Helianthus species into cultivated sunflower and identify the introgressed alien segments associated with BSR resistance using a genotyping-by-sequencing (GBS) approach. The initial crosses were made between the nuclear male sterile HA 89 with the BSR resistant plants selected from wild Helianthus argophyllus and H. petiolaris populations in 2009. The selected resistant F1 plants were backcrossed to HA 458 and HA 89, respectively. Early generation evaluations of BSR resistance were conducted in the greenhouse, while the BC2F3 and subsequent generations were evaluated in the inoculated field nurseries. Eight introgression lines; six from H. argophyllus (H.arg 1 to H.arg 6), and two from H. petiolaris (H.pet 1 and H.pet 2), were selected. These lines consistently showed high levels of BSR resistance across seven environments from 2012 to 2015 in North Dakota and Minnesota, USA. The mean BSR disease incidence (DI) for H.arg 1 to H.arg 6, H.pet 1, and H.pet 2 was 3.0, 3.2, 0.8, 7.2, 7.7, 1.9, 2.5, and 4.4%, compared to a mean DI of 36.1% for Cargill 270 (susceptible hybrid), 31.0% for HA 89 (recurrent parent), 19.5% for HA 441 (resistant inbred), and 11.6% for Croplan 305 (resistant hybrid). Genotyping of the highly BSR resistant introgression lines using GBS revealed the presence of the H. argophyllus segments in linkage groups (LGs) 3, 8, 9, 10, and 11 of the sunflower genome, and the H. petiolaris segments only in LG8. The shared polymorphic SNP loci in the introgression lines were detected in LGs 8, 9, 10, and 11, indicating the common introgression regions potentially associated with BSR resistance. Additionally, a downy mildew resistance gene, Pl17, derived from one of the parents, HA 458, was integrated into five introgression lines. Germplasms combining resistance to Sclerotinia BSR and downy mildew represent a valuable genetic source for sunflower breeding to combat these two destructive diseases.

Stewart’s wilt of corn caused by the bacterium Pantoea stewartii subsp. stewartii is a seed-borne disease of major phytosanitary importance. Many countries have imposed restrictions on corn seed imports from regions where the disease occurs to prevent the potential introduction of the pathogen. Current laboratory testing methods (enzyme-linked immunosorbent assay [ELISA] and polymerase chain reaction [PCR]) cannot readily distinguish P. stewartii subsp. stewartii from the closely related subspecies Pantoea stewartii subsp. indologenes. However, P. stewartii subsp. indologenes, a nonpathogen on corn, is occasionally found on corn seed as part of the resident bacterial population and can yield false positive test results. A real-time PCR targeting the cpsAB intergenic sequence was developed to specifically detect P. stewartii subsp. stewartii from corn seeds and distinguish it from P. stewartii subsp. indologenes. The assay successfully detected P. stewartii subsp. stewartii from corn seed, and P. stewartii subsp. indologenes-contaminated seed lots, which previously yielded false positives by ELISA and published PCR methods, were negative. The absence of P. stewartii subsp. stewartii and the presence of P. stewartii subsp. indologenes in this seed were confirmed by size differentiation of the cpsAB amplicons in a conventional PCR. By distinguishing the two subspecies, the assays described would avoid false positive results and help prevent unnecessary restrictions on international movement of corn seed.