Inheritance of Cross-Sensitivity in Sweet Corn to Herbicides Applied Postemergence
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J. AMER. SOC. HORT. SCI. 131(6):744–751. 2006. Inheritance of Cross-sensitivity in Sweet Corn to Herbicides Applied Postemergence Jerald K. Pataky1 and Jonathan N. Nordby Department of Crop Sciences, University of Illinois, Urbana, IL 61801 Martin M. Williams II United States Department of Agriculture–Agricultural Research Service, Invasive Weed Management Research, University of Illinois, Urbana, IL 61801 Dean E. Riechers Department of Crop Sciences, University of Illinois, Urbana, IL 61801 ADDITIONAL INDEX WORDS. bentazon, carfentrazone, dicamba + difl ufenzopyr, foramsulfuron, mesotrione, nicosulfuron, primisulfuron, rimsulfuron, cytochrome P450, herbicide selectivity, herbicide tolerance, Zea mays ABSTRACT. Some sweet corn (Zea mays L.) hybrids and inbreds can be severely injured by applications of postemergence herbicides. An association was observed between the responses of sweet corn hybrids and inbreds to nicosulfuron and mesotrione, and F2 families derived from a cross of a sensitive (Cr1) and a tolerant (Cr2) sweet corn inbred segregated for response to these two herbicides. These observations prompted us to examine the inheritance of sensitivity in sweet corn to multiple postemergence herbicide treatments with different modes of action and to determine if there was a common genetic basis for cross-sensitivity to these herbicides. The sensitive and tolerant inbreds, progeny in the F1, F2, BC1, and BC2 generations, and BC1S1, BC2S1, F2:3 (S1:2) and F3:4 (S2:3) families were screened for responses to eight herbicide treatments. Based on segregation of tolerant and sensitive progeny and segregation of family responses, our data indicate that a single recessive gene in Cr1 conditioned sensitivity to four acetolactate synthase (ALS)-inhibiting herbicides (foramsulfuron, nicosulfuron, primisulfuron, and rimsulfuron), a 4-hydroxyphenylpyruvate dioxygenase (HPPD)-inhibiting herbicide (mesotrione), a growth regulator herbicide combination (dicamba + difl ufenzopyr), and a protoporphyrinogen oxidase (PPO)-inhibiting herbicide (carfentrazone). Based on highly signifi cant positive correlations of phenotypic responses among BC1S1, BC2S1, F2:3, and F3:4 families, the same gene (or closely linked genes) appeared to condition responses to each of these herbicide treatments. The dominant allele also conditions tolerance to bentazon [a photosystem II (PSII)-inhibiting herbicide] although another gene(s) also appeared to affect bentazon tolerance. The potential for crop injury limits the use of postemergence were more likely to be sensitive to mesotrione than nicosulfu- herbicides in sweet corn. Under certain environmental conditions, ron-tolerant hybrids and vice versa. This association was more some hybrids and inbreds can be severely injured by postemer- evident among inbreds and F2 families derived from a cross of gence applications of several herbicides, including nicosulfuron a sensitive inbred, Cr1, and a tolerant inbred, Cr2. A similar but (Burton et al., 1994; Grey et al., 2000; Monks et al., 1992; Morton less explicit association also was observed among responses of and Harvey, 1992; O’Sullivan and Bouw, 1998; O’Sullivan et inbreds and F2 families to dicamba + difl ufenzopyr and carfentra- al., 1995, 2000; Robinson et al., 1993, 1994; Stall and Bewick, zone (M.M. Williams, J.K. Pataky, J.N. Nordby, D.E. Riechers, 1992; Williams et al., 2005), mesotrione (Masiunas et al., 2004; C.L. Sprague, and J.B. Masiunas, unpublished). Segregation of O’Sullivan et al., 2002; Williams et al., 2005), bentazon (Diebold F2 families for response to nicosulfuron and mesotrione fi t a 1:2:1 et al., 2004), primisulfuron (Burton et al., 1994; Grey et al., 2000; pattern that would be expected if sensitivity was conditioned by a Monks et al., 1992; O’Sullivan and Sikkema, 2002), rimsulfu- single recessive gene. The strong association between responses ron (O’Sullivan and Bouw, 1998; O’Sullivan et al., 1995), and of inbreds and F2 families to nicosulfuron and mesotrione, and foramsulfuron (Diebold et al., 2003). Consequently, evaluations possibly to dicamba + difl ufenzopyr and carfentrazone, suggested of new sweet corn hybrids and inbreds for sensitivity to herbicides that the same gene may condition response to multiple herbicide and evaluations of new herbicides for potential injury on widely treatments. However, sample size of F3 plants in F2 families was used sweet corn germplasm have become routine. small. Additional experiments with larger sample sizes were During a recent screening program, an association was observed deemed necessary to confi rm these preliminary observations between the responses of sweet corn hybrids to nicosulfuron and (Williams et al., 2005). mesotrione (Williams et al., 2005). Nicosulfuron-sensitive hybrids Differences in rates of metabolic inactivation are the primary basis for differential sensitivity in corn and other plants to sulfonyl- urea herbicides such as nicosulfuron (Barrett, 1995; Burton et al., Received for publication 13 Mar. 2006. Accepted for publication 17 June 2006. The authors greatly appreciate the cooperation of Crookham Company, Caldwell, 1994; Fonné-Pfi ster et al., 1990; Green, 1998; Green and Ulrich, Idaho. A portion of this research was supported by funding from the Midwest 1993; Harms et al., 1990; Hinz and Owen, 1996). Nicosulfuron Food Processors Association. Mention of a trademark, proprietary product, or is hydroxylated by cytochrome P450 enzymes in corn as a Phase vendor does not constitute a guarantee or warranty of the product by the U.S. I detoxifi cation reaction (Kreuz et al., 1996). Cytochrome P450 Dept. of Agriculture and does not imply its approval to the exclusion of other products or vendors that also may be suitable. activity in corn also metabolizes herbicides in at least fi ve other 1Corresponding author; e-mail: [email protected] chemical families; however, the number of P450s involved and regulation of their levels of activity are not clearly understood 744 J. AMER. SOC. HORT. SCI. 131(6):744–751. 2006. J 00828 744 11/16/06 12:29:22 PM (Barrett, 1995, 2000; Boldt et al., 1992). Corn has many cytochrome A better understanding of the phenotypic and genetic rela- P450 genes (Frey et al., 1995). Interestingly, a few or possibly even tionships between responses of sweet corn to various herbicides one P450 in corn are primarily responsible for herbicide metabolism will help sweet corn breeders identify and eliminate sensitive (Barrett, 1995; Barrett et al., 1994). A fi eld corn inbred, GA209, germplasm in breeding programs and will allow herbicide originally identifi ed as bentazon-sensitive, was more sensitive to manufacturers to construct pesticide labels that adequately ad- imazethapyr, nicosulfuron, primisulfuron, and chlortoluron and dress the risks of using herbicides on sweet corn. The objectives slightly more sensitive to dicamba than B73, a bentazon-tolerant of this study were to examine the inheritance of sensitivity in inbred (Barrett et al., 1997). Within a 24-h period after excised sweet corn to eight postemergence herbicide treatments (ben- shoots of GA209 and B73 were treated with radiolabeled bentazon, tazon, carfentrazone, dicamba + difl ufenzopyr, foramsulfuron, imazethapyr, and nicosulfuron, 75% or more of the amount of mesotrione, nicosulfuron, primisulfuron, and rimsulfuron) having each herbicide absorbed was metabolized by B73 but <25% was fi ve different modes of action (PSII-inhibiting, PPO-inhibiting, metabolized by GA209 (Barrett et al., 1997). growth regulator, ALS-inhibiting, and HPPD-inhibiting), and to The genetic basis for herbicide sensitivity in corn has been determine if there is a common genetic basis resulting in cross- examined for several herbicides. Based on responses of progeny sensitivity to these herbicides. from crosses of a bentazon-sensitive fi eld corn inbred, GA209, and bentazon-tolerant corn lines, Fleming et al. (1988) proposed Materials and Methods that tolerance to bentazon was conditioned by a single gene des- ignated as Ben. Subsequently, Bradshaw et al. (1994) reported PLANT MATERIAL. Sweet corn inbreds Cr1 and Cr2 (Crookham that sensitivity of GA209 to bentazon was controlled by a single Co., Caldwell, Idaho) were identifi ed as sensitive and tolerant, recessive gene or possibly by two recessive genes designated as respectively, to nicosulfuron and mesotrione in previous trials ben1 and ben2. Co-dominance was proposed for sensitivity to (Williams et al., 2005). The F1, F2, BC1, and BC2 generations chlorsulfuron based on intermediate responses of crosses of toler- were produced by crossing Cr1 and Cr2 and self-pollinating or ant (T) and sensitive (S) corn lines compared to tolerant responses backcrossing. These generations were evaluated for responses to of T x T crosses and sensitive responses of S x S crosses (Landi four or eight different herbicide treatments in greenhouse or fi eld et al., 1989). Tolerance to primisulfuron was conditioned by a trials, respectively. Reciprocal F1 and backcross generations were single dominant gene when a tolerant fi eld corn inbred, 4C0, was included in each trial. BC1S1, BC2S1, and F3 (S2 plants) generations crossed with a sensitive inbred, 4N5 (Harms et al., 1990). Green were produced by self-pollinating BC1, BC2, and F2 plants ear- and Ulrich (1993) reported that sensitivity of fi eld corn and sweet to-row for an additional generation. These generations also were corn to three sulfonylurea herbicides (nicosulfuron, primisulfuron, evaluated in fi eld trials for responses to fi ve herbicide treatments.