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Grain Yield, Kernel Weight, and Disease Responses of Winter Wheat Cultivars to Chloride Fertilization

Montana State Univ., Southern Agric. Res. Ctr., Huntley, MT 59037,
Montana State Univ., Eastern Agric. Res. Ctr., Sidney, MT 59270,
Montana State Univ., Northern Agric. Res. Ctr., Havre, MT 59501,

^* Corresponding author.

Wheat yields in the Great Plains are frequently improved by potash (0-0-60 N-P-K) application on soils with seemingly abundant supplies of available K. The CI component in this fertilizer may cause many of the observed yield responses. Field research was undertaken to determine the effects of CI on grain yield, plant CI, kernel weight and growth rate, and foliar disease and/or disease-like symptoms of winter wheat cultivars. Two sites with five CI levels (0, 22, 45, 90, and 135 kg ha^–l) and two cultivars (Redwin, Cree) were used in 1988. Seven sites with two CI levels (0 and 45 kg ha^–1) and six cultivars (Redwin, Cree, Weston, Manning, QT542, Neeley) were used from 1991 to 1992. Chloride increased yield by an average of 267 kg ha^–1 (7%) at seven responsive sites. Size of yield response to CI was generally not affected by cultivar selection, but differed greatly with location. Whole-plant CI analyses were useful in discriminating between yield responsive ( 3.0 g kg^–1) and nonresponsive (>3.0 g kg^–1) sites to CI fertilization. Improved CI nutrition enhanced plant development, increase immature kernel weights, and accelerated kernel growth during the grain-fill period. Fertilizer CI increased mature kernel weights, up to 17%, at eight sites. Kernel weight was the most important yield component affected by CI. Physiological leaf spot in Redwin and Manning, flag leaf senescence in Weston and QT542, powdery mildew (Erysiphe graminis DC. f. sp. tritici Em. Marchal), and leaf rust (Puccinia recondita Roberge ex Desmaz. f. sp. tritici) were suppressed by fertilizer CI. These phenomena may explain in part the yield responses to CI; however, yield response to CI occurred even without foliar disease and disease-like suppression.

Received for publication August 12, 1993.

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