Seedling Growth lnhibitors

The seedling growth inhibitors include the dinitroanilines, acetanilides, and thiocarbamates. All of these herbicides must be used preplant incorporated or preemergence to the weeds to be effective. In some uses, the herbicides are applied after crop emergence but before weed emergence.

Seedling growth inhibitors interfere with new plant growth, thereby reducing the ability of seedlings to develop normally in the soil. Plants can take up these herbicides after germinating, until the seedling emerges from the soil. Therefore, these herbicides are only effective on seedling annual or perennial weeds. Plants that have emerged from the soil uninjured are likely to remain unaffected.

Seedling growth inhibitors are active at two main sites, the developing shoot and the root. Much more is known about the action of seedling root inhibiting herbicides than seedling shoot inhibitor herbicides. The root inhibitors stop plant cells from dividing, which inhibits shoot elongation and lateral root formation. Uptake is through developing roots and shoots. Because herbicide movement within the plant is limited, herbicide injury is confined primarily to plant roots and shoots. Shoot inhibiting herbicides are taken up by developing roots and shoots and can move via the xylem to areas of new growth. Present evidence suggests that these herbicides can affect multiple sites within a plant, primarily interfering with lipid and protein synthesis.

A. Root Inhibitors

1. Dinitroanilines

a. Use: Ethalfluralin (Sonalan) for soybean, sunflower and dry bean.
Pendimethalin (Prowl) for corn (preemergence only) soybean, dry bean, and sunflower.
Trifluralin (Treflan) for soybean, dry bean, sunflower, alfalfa, small grain, Canola (rapeseed), mustard and pea.

b. Injury Symptoms: Dinitroaniline residual in soil may cause sugarbeet to be severely stunted with small leaves that are more erect than normal (Photo 22). The roots of damaged sugarbeet seedlings may turn brown and die starting at the point where the root joins the hypocotyl, about 1 to 1.5 inches below the soil surface (Photo 23). Plants with dead roots may die or they may survive by producing secondary roots from the hypocotyl (Photo 24). Identical symptoms on roots of seedling sugarbeet also can be caused by imidazolinone, sulfonylurea or sulfona-mide herbicides and by Aphanomyces, a fungal disease. Affected plants will be smaller than unaf-fected plants. Plant regrowth by secondary root production would be prevented by drought in the surface 2 inches of soil and injured plants would die. Imidazolinone, sulfonylurea and sulfonamide herbicides also can cause similar seedling root death.

c. Site of Action. Tubulin protein involved in cell division.

B. Shoot Inhibitors

1. Acetanilides

a. Use: Alachlor (Lasso) for corn, dry bean, sorghum, sunflower and soybean.
Acetochlor (Harness Plus, Surpass) for corn.
Metolachlor (Dual) for corn, dry bean, sorghum, potato and soybean.
Propachlor (Ramrod) for corn, flax, and sorghum.
Dimethenamid (Frontier) for corn.

b. Injury Symptoms: Acetanilides cause no distinctive symptoms on sugarbeet. Some plants may die before emergence. Emerged but injured plants are normal in appearance but stunted.

c. Site of Action: Specific site(s) unknown, believed to have multiple sites of action.

2. Thiocarbamates

a. Use. EPTC (Eptam) for alfalfa, potato, dry bean, flax, safflower, sugarbeet and sunflower.
EPTC plus safener (Eradlcane) for corn.
Butylate plus safener (Susan+) for corn.
Triallate (Far-Go) for wheat barley, lentils and pea.
Cycloate (Ro-Neet) for sugarbeet.

b. Injury Symptoms: Thiocarbamates reduce the formation of epicuticular wax on leaves, which can cause leaves to stick together rather than unfold normally (Photo 25). Affected plants may be stunted, leaves may be shortened and thickened, or true leaf development may be inhibited (Photo 26). Some severely stunted plants may die while others will start producing new leaves and will produce a nearly normal-sized root at harvest. Severely stunted plants may grow very little for two or more weeks after emergence and then make a complete or nearly complete recovery.

c. Site of Action: Specific site(s) unknown, believed to have multiple sites of action.