Enzymatically isolated mesophyll cells of soybean [Glycine max (L.) Merr. ‘Kino’] and cotton (Gossypium hirsutum L. ‘Stoneville 1613 glandless’) were used to study the effects of three surfactants, I = ‘Sterox SK’ (polyoxyethylene thioether), II = ‘Renex 36’ (polyoxyethylene-6-tridecylether), and III = ‘WSCP’ [polyoxyethylene (dimethylimino) ethylene (dimethylimino) ethylene dichloride] alone or in combination with two herbicides, D-497 (1,1-dimethyl-4,6-diisopropyl-5-indanylethyl ketone) and oryzalin (3,5-dinitro-N4,N4-dipropylsulfanilamide) on cell permeability, photosynthetic 14CO2 fixation and cellular ultrastructure. Greatest amount of efflux of 14C-labeled material from soybean cells was caused by III, whereas other surfactants or herbicides produced only slightly higher effluxes than the controls. Mixtures of oryzalin-I or -II were the only combinations that enhanced efflux in soybean cells above that of cells treated with the surfactant or herbicide alone. However, on cotton cells all surfactants and oryzalin caused considerable leakage but no synergistic effects. Sugars were the predominant compounds leaked from the treated and control cells. Disorganization of all cellular membranes was caused by III whereas I and II disrupted only the chloroplast grana-intergrana thylakoids, causing abnormal grana. Herbicidal damage to the cell ultrastructure was minimal. Cells treated with combinations of surfactants and herbicides produced only those ultrastructural symptoms that the individual chemicals caused when applied alone. Photosynthetic CO2 fixation was inhibited in both cotton and soybean cells treated with surfactants and (or) herbicides. Interference with membrane integrity, either directly by interaction with membranes or indirectly by interference with cellular energy generating systems that maintain membrane integrity is the postulated mode of action of these surfactants and herbicides.

A weevil, (Rhinocyllus conicus Froelich) was introduced into Missouri in 1975 to aid in reducing populations of musk thistle, (Carduus nutans L.). The weevil was recovered in 1976 from as far as 3.2 km from the release site and 4.8 km in 1977. Infestation levels of flower heads at the release site ranged from 46 to 90%. Native parasites (Bracon mellitor Say) and [Aliolus curculionis (Fitch)] were reared from weevil larvae.

Western ironweed (Vernonia baldwinii Torr.) and gray goldenrod (Solidago nemoralis Ait.) were mowed at various frequencies during two growing seasons in two experiments for each species. The initial mowings were made in late May or early June when rapid growth was taking place, presumably at the expense of carbohydrate reserves and also on June 15 and July 1. Subsequent mowings were made whenever the weed regrowth had reached 15 to 20 cm. The greatest reduction of western ironweed occurred with multiple mowing when the initial mowing was made on May 20. The degree of control was less in the second experiment than in the first. Multiple mowing was highly effective for reducing the stands of gray goldenrod; but in one of the two experiments, single mowings per season were almost as effective as multiple mowings.

The degree and longevity of quackgrass [Agropyron repens (L.) Beauv.] control provided by autumn applications of pronamide [3,5-dichloro(N-1,1-dimethyl-2-propynyl)benzamide] was influenced greatly by alfalfa (Medicago sativa L.) stand density, as well as by rate of application and soil type. When applications were made to a field with a sparse alfalfa stand (10 to 20 crowns/m2), quackgrass yields were reduced the year following pronamide application, but quackgrass reinfested the plots the second year after treatment. Quackgrass yields one and two seasons following autumn treatment with 2.2 kg/ha pronamide were 1480 and 3890 kg/ha compared to 4480 and 4870 kg/ha for control plots. Annual applications of pronamide were necessary to maintain quackgrass control in the sparse alfalfa stand. Pronamide application to a vigorous, dense alfalfa stand (40 to 50 crowns/m2) provided quackgrass control which persisted into the second year after treatment. Quackgrass control ratings one and two seasons after application of 1.1 kg/ha pronamide were 100 and 90%. Pronamide treatments reduced first cutting quackgrass yields, and increased first cutting alfalfa yields. Treatment of the sparse alfalfa stand with 2.2 kg/ha pronamide resulted in first cutting alfalfa and quackgrass yields of 2420 and 990 kg/ha compared to 1430 and 3940 kg/ha for controls. Treatment of a dense alfalfa stand with 1.1 kg/ha pronamide resulted in first cutting alfalfa and quackgrass yields of 3850 and 300 kg/ha compared to 1710 and 1660 kg/ha for controls. Total herbage yields from all cuttings were either slightly decreased when fields with sparse alfalfa stands were treated or remained constant or slightly increased when more dense alfalfa stands were treated. Pronamide applied with potash as the carrier was as effective as when applied in water. Pronamide treatment resulted in increased crude protein concentration in first cutting herbage at all locations in all years. Crude protein concentration in first cutting control herbage ranged from 13.3 to 16.1%. Crude protein concentration in first cutting herbage from plots treated with 1.1 kg/ha pronamide ranged from 17.7 to 20.6%, depending on year and location. In vitro digestible dry matter (IVDDM) concentrations were increased by most rates of pronamide in first, second, and third cutting herbage. IVDDM for first cutting control herbage was 51.4% compared to 61.3% for herbage treated with 2.2 kg/ha pronamide. Acid detergent fiber concentration in first cutting herbage was not affected by pronamide.

Fluridone {1-methyl-3-phenyl-5-[3-(trifluromethyl)phenyl]-4(1H)-pyridinone} and norflurazon [4-chloro-5-(methylamino)-2-(α,α,α-trifluoro-m-tolyl)-3(2H)-pyridazinone] inhibited carotenoid synthesis in wheat (Triticum aestivum L. ‘Maricopa’) seedlings and caused the accumulation of colorless carotenoid precursors, phytoene, and phytofluene. These data suggested that dehydrogenation reactions following phytoene formation were inhibited by the herbicides. Chlorophyll accumulated in the treated seedlings grown under 10 lux of light but was destroyed in seedlings illuminated with 16 klux of light. Seedlings illuminated with 16 klux of light lacked chloroplast ribosomes and normal ultrastructure whereas dark grown seedlings contained pastid ribosomes and had normal etioplast ultrastructure. The disruption of the chloroplasts and loss of chlorophyll was due to the absence of carotenoids in the treated plants, which would normally act to protect the chloroplasts from photodestruction.