Genetic Factors Influencing Adverse Effects of Mesotrione and Nicosulfuron on Sweet Corn Yield

Abstract

Sensitivity to certain P450‐metabolized herbicides in corn (Zea mays L.) is largely conditioned by a single cytochrome P450 (CYP) gene. Little to no research has been done to evaluate the effect of CYP genotype on sweet corn yield. Yield of 23 sweet corn hybrids of known CYP genotype was evaluated in 2007, 2008, and 2009 following postemergence applications of mesotrione, an hydroxyphenylpyruvate dioxygenase (HPPD) inhibitor, or nicosulfuron, an acetolactate synthase (ALS) inhibitor, at two growth stages. Mesotrione and nicosulfuron were evaluated in separate experiments. Treatments included herbicide application during the V3 to V5 or V5 to V7 growth stages and a nontreated control. Crop injury, measured 7 d after treatment (DAT), ranged from 0 to 87% for mesotrione and 0 to 54% for nicosulfuron among CYP genotypes. Injury from both mesotrione and nicosulfuron was most severe following application during V3 to V5 growth stages on hybrids with mutant (i.e., nonfunctional) cyp alleles. Only hybrids homozygous for mutant cyp alleles (i.e., cypcyp) suffered yield losses from mesotrione, ranging from 9 to 40%. These hybrids were not evaluated for nicosulfuron because applications of ALS‐inhibiting herbicides kill cypcyp hybrids. Nicosulfuron reduced the yield of CYPcyp hybrids only; whereas mesotrione did not. Yield losses from nicosulfuron ranged from 9 to 35% among CYPcyp hybrids and were associated with moderate to severe loss of kernel rows (i.e., ear pinching). Yield of CYPCYP hybrids was not affected by mesotrione or nicosulfuron.