Beginning in the early 1980s, there were reports of white oak (Quercus alba L.) leaves losing interveinal tissues throughout the Midwest [Green, 1985; Haugen et al., 2000; Leatherberry et al., 2004; Wisconsin Department of Agriculture, Trade and Consumer Protection (WDATCP), 2003]. The first flush of affected white oak leaves in the spring may lose most interveinal tissues, resulting in only the main veins and some residual interveinal tissues (leaf tatters). Leaf tatters can affect a substantial portion of a white oak tree's canopy reducing its overall health, making it susceptible to other stresses and reducing its aesthetic value. The second flush of leaves in late spring is normal but leaf tatters can reoccur over multiple seasons on white oak of all ages. The vegetation surrounding injured white oak trees remains unaffected (J.E. Appleby, personal observation). Our previous study (Samtani et al., 2008) found that white oak seedlings developed leaf tatters after treatment with acetochlor + atrazine or s-metolachlor at the leaf unfolding stage. This article investigates more chloroacetanilide herbicides; determines if atrazine contributes to leaf tatters injury; and compares white and northern red oak injury (Quercus rubra L.).
Acetochlor, s-metolachlor, and dimethenamid-P are commonly used chloroacetanilide herbicides on corn. During 2005, acetochlor, dimethenamid-P, and s-metolachlor were applied to 23%, 4%, and 23%, respectively, of the 76 million acres of planted corn in the 19 program states (U.S. Department of Agriculture, 2006). Compared with data from a 1995 survey, chloroacetanilide use in corn has remained about the same. In 1995, acetochlor, dimethenamid-P, and s-metolachlor applications were applied on 18%, 3%, and 29%, respectively, of the 64 million acres of planted corn in 17 states included in the survey (U.S. Department of Agriculture, 1996). Corn acreage treated with alachlor decreased from 8% in 1995 to 1% in 2005. Lack of surveys on the leaf tatters, the growth-stage specificity of the injury on oaks, and the timing of chloroacetanilide applications hinders determining any correlation between leaf tatter injury and acres treated with chloroacetanilides.
In susceptible plants, chloroacetanilides inhibit β-ketoacyl-CoA synthase that adds two carbon units from malonyl–coenzyme A (CoA) to a C18 fatty acid (Lassner et al., 1996; Millar and Kunst, 1997). Inhibition of β-ketoacyl-CoA synthase depletes very-long chain fatty acids (VLCFA) in susceptible plants. The major site of VLCFA synthesis is in the epidermal cells where they are used for production of waxes that cover the aerial surfaces of plants (Millar and Kunst, 1997; Post-Beittenmiller, 1996). In oaks, wax deposition occurs during leaf expansion (Neinhuis and Barthlott, 1998; Osborn and Taylor, 1990), which is consistent with our previous finding that white oak at the leaf unfolding stage is injured by chloroacetanilides.
Within Illinois in 2006, 87% of the corn acreage was treated with atrazine and it is common to use premixes of atrazine with chloroacetanilides for a broader range of weed control (Taylor-Lovell and Wax, 2001; U.S. Department of Agriculture, 2006). In tolerant plants, both atrazine and chloroacetanilide herbicides are rapidly detoxified by conjugation with glutathione (Marrs, 1996; Shukla and Devine, 2006). In susceptible plants, atrazine may interact with chloroacetanilide herbicides to increase leaf tatter injury. Atrazine also inhibits electron flow through Photosystem II, reducing subsequent carbon assimilation into sugars (Trebst, 2006). The reduction in primary carbon assimilation could reduce fatty acid synthesis, compounding chloroacetanilide inhibition of VLCFA synthesis. Atrazine has a synergistic interaction with some herbicides such as mesotrione and alachlor, increasing weed injury and control (Akobundu et al., 1975; Bollman et al., 2006).
In the midwestern United States, the relatively flat topography and intermingling of agricultural fields, natural areas, and residential development contribute to herbicide drift injury. Off-target herbicide movement is between 1% and 10% of field use rates (Al-Khatib and Peterson, 1999; Al-Khatib et al., 2003). Herbicide drift modifies plant morphology and development, potentially altering species composition and diversity (Boutin, 1999; Freemark and Boutin,1995). White oak and northern red oak are native to eastern North America from Nova Scotia to Minnesota, Kansas, and Georgia. Northern red oak is a fast-growing tree, withstands air pollution, and is considered one of the best oaks for city plantings (Dirr, 1990). Although the range of the two species overlap, reports of leaf tatter injury are more common on white than northern red oak. We hypothesized that red oaks are less susceptible to chloroacetanilides than white oak. We also hypothesized that the degree of leaf tatter injury varies among chloroacetanilides. The objectives were to determine if: 1) white and red oak differ in susceptibility to chloroacetanilide herbicides; 2) the amount of injury varies among acetochlor, s-metolachlor, and dimethenamid-P; and 3) atrazine applied with chloroacetanilides increases leaf tatters.
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