Ergot (caused by Claviceps africana Frederickson, Mantle & de Milliano) of sorghum [Sorghum bicolor (L.) Moench] recently has become a global disease problem and is a major threat to hybrid seed production. Host‐plant resistance is one option for control; however, the genetic and physiological bases for ergot resistance are poorly understood. The objective of this study was to evaluate resistance to C. africana in 18 genetically diverse sorghum lines, including cultivated landraces and wild accessions, as well as in potential alternate hosts, including grassy weeds and range grasses commonly found in sorghum‐producing areas in the central Great Plains of the USA. These entries were evaluated for ergot resistance in the greenhouse following spray inoculation with conidial suspensions during flowering. The results of this analysis indicated that only Sorghum ssp. were susceptible to ergot; however, within the sorghum germplasm pool, several wild accessions were identified with resistance to ergot. Two of these resistant entries, IS14131 and IS14257, were characterized further in male‐sterile (A3 cytoplasm) genetic backgrounds to evaluate the physiological basis for their resistance. Parent lines, male‐sterile hybrids, and susceptible checks were evaluated for ergot resistance following spray inoculation with ergot in experiments in a winter nursery at Guayanilla, Puerto Rico, and in a greenhouse at Manhattan, KS, during the winter and spring of 2000. The expression of ergot resistance in IS14131 and IS14257 and in corresponding male‐sterile hybrids suggests that these sorghums may harbor genes for resistance to ergot.

Given the close relationship and similar geographic origin of these species, the possibility of host-plant resis-

No abstract

Field trials were conducted in Lubbock, TX in 2010 and 2011 to evaluate tank-mix combinations of glyphosate and glufosinate in GlyTol®LibertyLink®cotton for control of Palmer amaranth. Herbicide treatments included glyphosate and glufosinate applied at various tank-mix rate combinations (1X:1X, 1X:0.75X, 1X:0.5X, 1X:0.25X and 1X:0X of glyphosate plus glufosinate), proportional tank-mix rate combinations (1X:0X, 0.75X:0.25X, 0.5X:0.5X, 0.25X:0.75X, and 0X:1X of glyphosate plus glufosinate, where X is 0.84 kg ae ha−1of glyphosate or 0.58 kg ai ha−1of glufosinate ammonium), and in sequential (1X followed by 1X) applications of both herbicides in an overall weed management system. Greenhouse studies were conducted to quantify antagonistic or synergistic effects. Treatments included a nontreated control; glyphosate at 0.84, 0.63, 0.42, and 0.21 kg ha−1; glufosinate at 0.58, 0.44, 0.29, and 0.15 kg ha−1; and all tank-mix combinations of each herbicide rate. Dry weights were converted to percent growth values for each rate of the two herbicides alone, and these values were used to calculate expected responses of tank-mix combinations with the use of Colby's method. Expected values were compared to observed percent growth values using an augmented mixed-model method. Results of field studies indicated that tank mixes of glyphosate and glufosinate were less effective at controlling Palmer amaranth than glyphosate applied alone. The addition of any rate of glufosinate to a 1X rate of glyphosate reduced Palmer amaranth control compared to glyphosate alone. Greenhouse studies confirmed antagonism seen in the field. These results indicate that sequential applications of these two herbicides are a better option for Palmer amaranth weed management.

During the 2009 to 2010 growing season, symptoms of an unknown leaf spot were observed on spinach (Spinacia oleracea L.) in production fields in southwest Texas. Approximately 500 ha were affected, especially cvs. Rakaia and Viceroy. Disease incidence was 30 and 2% for Rakaia and Viceroy, respectively. Diseased plants exhibited small (1 to 3 mm in diameter), tan, necrotic lesions with a circular to oval shape and were void of any signs of a pathogen. Symptomatic leaves were surface sterilized in 1.5% NaOCl for 1 min, rinsed with sterile water, and air dried. Leaf sections (~1 cm2) were cut and placed on acidified potato dextrose agar (APDA), or APDA supplemented with streptomycin (SAPDA). Fungal mycelia growing from the edges of infected leaf sections were transferred to PDA and incubated at 25°C with a 12-h/12-h light/dark cycle. After 14 days of incubation, dark brown mycelia giving rise to unbranched conidiophores bearing brown, deeply septate, ovoid conidia were observed. Conidia measured 16.8 to 27.3 × 13.1 to 19.6 μm. On the basis of these morphological characteristics, the fungus was identified as Stemphylium botryosum (3). Cultures were transferred to clarified V8 juice agar to obtain inoculum for pathogenicity tests. Eight-week-old plants (n = 20) of spinach cvs. Hybrid 310, Wintergreen, Ashley, and Rakaia were sprayed until runoff with a suspension containing 0.001% Tween 80 and 1 × 104 conidia/ml. Noninoculated plants served as a control treatment. Plants were placed in a growth chamber and incubated in the dark at 25°C and 95% relative humidity. Following 36 h of incubation, plants were transferred to a plastic enclosure and maintained at 23 ± 4°C. After 7 to 10 days, tan, oval-shaped lesions were observed on all inoculated spinach plants. All control plants, with the exception of Rakaia, failed to develop symptoms. Isolates of S. botryosum were recovered on SAPDA from symptomatic leaves, confirming Koch's postulates. Previous reports have shown that S. botryosum can be transmitted from infected seed (1), thus, additional plants of each cultivar (n = 36) were grown in the greenhouse to determine the potential for seedborne contamination. After 8 weeks, leaf spot symptoms identical to those observed on the original plants developed on 75% of the Rakaia plants, while symptom development on the other cultivars was negligible. Isolates of S. botryosum were only recovered from symptomatic Rakaia leaves. Similar field observations were made during the 2001 to 2002 growing season; however, attempts to isolate S. botryosum in that season were unsuccessful. Recent outbreaks of Stemphylium leaf spot have been reported in Arizona (4), California (3), Delaware and Maryland (2), and Washington (1). To our knowledge, this is the first report of S. botryosum on spinach in Texas. While the origin of inoculum causing the disease in Texas is unknown, S. botryosum may have been seedborne (2). The implementation within the past few years of very high density plantings of spinach (1.9 to 3.7 million seeds/ha) may lead to an increase in incidence and severity of this disease in Texas. References: (1) L. J. du Toit and M. L. Derie. Plant Dis. 85:920, 2001. (2) K. L. Everts and D. K. Armentrout. Plant Dis. 85:1209, 2001. (3) S. T. Koike et al. Plant Dis. 85:126, 2001. (4) S. T. Koike et al. Plant Dis. 89:1359, 2005.