Isoxadifen safening mechanism in sweet corn genotypes with differential response to P450-metabolized herbicides.

Three sweet corn genotypes, two inbred lines (IBER001 and IBER002) and their hybrid (ER00X), differ in their phenotypic responses to several P450-metabolized herbicides, used in sweet corn, namely, foramsulfuron, iodosulfuron, rimsulfuron and tembotrione. Foramsulfuron is a sulfonylurea herbicide commonly formulated with the safener isoxadifen that is used for selective post-emergence weed control in corn. Our goal was to elucidate the mechanism of these genotypes' responses to foramsulfuron and safener isoxadifen and examine the heritability of those responses. IBER001 was sensitive to foramsulfuron+isoxadifen, with an ED of 3.6gaiha, while IBER002 and ER00X were tolerant with ED values of 808 and 700gaiha, respectively. ALS enzyme extracted from each of the different genotypes was equally sensitive to foramsulfuron. Pre-treatment with malathion, a known cytochrome P450 inhibitor, increased foramsulfuron injury in IBER002 and ER00X, but had no effect on those lines when isoxadifen was applied with the herbicide. Foramsulfuron-treated IBER001 was severely injured regardless of the presence of malathion and/or isoxadifen. Pre-treatment with malathion similarly increased the phytotoxicity of iodosulfuron+safener (mefenpyr) and rimsulfuron to the tolerant genotypes, but did not increase the level of injury caused by the tembotrione+isoxadifen treatment. Segregation of F2 and backcross progenies according to their responses to foramsulfuron+isoxadifen revealed a pattern of inheritance typical of a trait controlled by a single gene inheritance, with a recessive allele conferring sensitivity. Our results support the hypothesis that foramsulfuron selectivity is associated with P450 metabolism and that isoxadifen positively affects P450 activity. The sensitive genotype that does not respond to isoxadifen is presumably homozygous for a deficient or non-functioning P450 gene.