A chloride-deficient leaf spot syndrome of wheat

A leaf spot complex that results in tissue necrosis and whose origin is unknown frequently damages selected winter wheat (Triticum aestivum L.) cultivars in Montana and neighboring regions. This study was undertaken to determine leaf spot origin (physiologic or pathogenic), cultivar susceptibility, and response to Cl nutrition. Winter wheat studies at seven sites (1993-1995) compared cultivars (Redwin, Tiber, CDC Kestrel, Manning, Stephens, Sierra, and Promontory), propiconazole (1-[[2-(2,4-dichlorophenyl)-4-propyl-1,3-dioxolan-2-yl]methyl]-1H-1,2,4-triazole) fungicide treatments, and multiple Cl fertilizer rates (0-90 kg ha(-1)). Chlorotic or necrotic lesions developed at all sites, but not all cultivars were affected similarly. CDC Kestrel was the most susceptible cultivar. Flag leaf spot severity (portion of tissue area affected) was as great as 40% in this cultivar. Redwin, Sierra, and Promontory were the next most susceptible cultivars, followed by Stephens and Manning. Tiber, a variant line row selection of Redwin, was leaf spot tolerant. Multiple propiconazole applications had no effect on leaf spot severity, and infectious organism(s) could not be isolated from symptomatic tissue. Thus, leaf spot origin was probably physiologic and not infectious. Chloride fertilization (11-22 kg ha (-1)) greatly suppressed or eliminated leaf spotting, and increased yield in one or more cultivars at six of seven sites (up to 998 kg ha(-1)). Physiologic leaf spot occurrence and severity in affected cultivars was linked to inadequate CI nutrition, and a possible osmotic imbalance in leaf mesophyll cells. Damage was usually minor when whole-plant CI at head emergence was greater than or equal to 1.0 g kg(-1). Leaf spot damage increased exponentially as plant Cl dropped below this concentration. The name Cl-deficient leaf spot syndrome is proposed to describe this phenomenon in wheat.