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ARS Home » Midwest Area » Urbana, Illinois » Global Change and Photosynthesis Research » Research » Publications at this Location » Publication #373446

Research Project: Understanding and Responding to Multiple-Herbicide Resistance in Weeds

Location: Global Change and Photosynthesis Research

Title: Expression and comparison of sweet corn CYP81A9s in relation to nicosulfuron sensitivity

item CHOE, EUNSOO - Former ARS Employee
item Williams, Martin

Submitted to: Pest Management Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/4/2020
Publication Date: 5/2/2020
Citation: Choe, E., Williams II, M.M. 2020. Expression and comparison of sweet corn CYP81A9s in relation to nicosulfuron sensitivity. Pest Management Science.

Interpretive Summary: From the mid-1980s to early 2010s, herbicide sensitivity among certain hybrids and inbreds plagued the sweet corn industry. The problem was largely solved when a team of ARS and University of Illinois scientists developed the understanding of the genetic and biochemical basis of herbicide sensitivity in sweet corn. While a specific gene (Nsf1) was identified as the critical factor responsible for multiple herbicide tolerance (including nicosulfuron) in both field corn and sweet corn, the functional connection of Nsf1 to herbicide tolerance had not been fully established. Using nicosulfuron, this research provides evidence that plant response to herbicide varies depending on nsf1 alleles due to cytochrome P450 sequence variation. While previous research largely solved the problem of herbicide sensitivity in sweet corn, the impact of this work is that it provides a deeper understanding of herbicide action within the plant that has broad application to all types of maize and perhaps other plants.

Technical Abstract: BACKGROUND: Nicosulfuron, a sulfonylurea herbicide widely used for grass weed control in corn production, injures some sweet corn hybrids and inbreds. A specific cytochrome P450 (P450), CYP81A9, is suggested to be responsible for sensitivity to nicosulfuron and other P450-metabolized herbicides. Corn CYP81A9 enzymes were expressed in E. coli and investigated to find the factor(s) associated with their function and variation in metabolizing nicosulfuron. RESULT: Recombinant expressed CYP81A9s from tolerant sweet corn inbreds produced an active form of P450, while CYP81A9 from a sensitive inbred produced an inactive form. Nicosulfuron bound to tolerant CYP81A9s, and produced reverse-type I ligand, while sensitive CYP81A9 showed no interaction with nicosulfuron. Investigation of 106 sweet corn inbreds showed variation in nicosulfuron injury. A survey of sweet corn CYP81A9 sequences showed mutations in codons for amino acids at 269, 284, 375, and 477 occurred in sweet corn inbreds with complete loss of P450 function (with mean injury > 91%) and amino acid changes at 208 and 472 occurred in inbreds with moderate and complete loss of P450 function (with mean injury > 14%). CONCLUSION: Our results support that CYP81A9 enzyme is responsible for metabolizing nicosulfuron in sweet corn, and different types of amino acid changes in CYP81A9 sequence are associated with variation in nicosulfuron injury. Therefore, a careful selection of the tolerant allele will be critical for improving tolerance to nicosulfuron and several other P450-metabolized herbicides.