|Nordby, Jonathan - UNIV OF ILLINOIS|
|Pataky, Jerald - UNIV OF ILLINOIS|
|Riechers, Dean - UNIV OF ILLINOIS|
Submitted to: Weed Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: January 28, 2008
Publication Date: May 16, 2008
Citation: Nordby, J.N., Williams, M., Pataky, J.K., Riechers, D.E. 2008. A common genetic basis in sweet corn inbred C1 for cross sensitivity to multiple cytochrome P450-metabolized herbicides. Weed Science. 56:376-382. Interpretive Summary: Weed management in sweet corn relies heavily on older herbicide chemistries with less than favorable environmental profiles. More recently developed herbicides with better environmental profiles are slow to be registered for use in sweet corn because, in part, some hybrids are susceptible to herbicide-induced injury. Study was undertaken to determine if there were associations between sensitivity of sweet corn to nicosulfuron, mesotrione, dicamba + diflufenzopyr, carfentrazone, foramsulfuron, nicosulfuron, bromoxynil, and bentazon. Responses of hybrids, inbreds, and S2:4 families to these herbicides lead us to believe the same recessive gene conditions sensitivity the herbicides, although additional genes may affect tolerance to bromoxynil and bentazon. Significance of this research is that a single gene appears to contribute to sensitivity to five different herbicide modes of action. This research provides additional evidence that a single recessive gene conditions sensitivity to herbicides with unique modes of action in corn, leading to a novel hypothesis for eliminating herbicide-sensitive hybrids in breeding programs. Given the ubiquitous production of corn in the U.S., advancement in this field has broad, large-scale impact.
Technical Abstract: Nicosulfuron, mesotrione, dicamba + diflufenzopyr, and carfentrazone are postemergence herbicides from different chemical families with different modes of action. An association between the sensitivity of sweet corn to these herbicides was observed when 143 S2 families (S3 plants) of a cross between Cr1 (sensitive inbred) x Cr2 (tolerant inbred) were evaluated in greenhouse trials. The ratio of tolerant: segregating: sensitive families was not significantly different from a 3:2:3 ratio, which would be expected if a single gene conditioned the response to the herbicides. In field studies, responses of 60 selected S2:4 families also were associated for these herbicides, as well as foramsulfuron and primisulfuron. When compared with primisulfuron and nicosulfuron, the inclusion of a safener in the commercial formulation of foramsulfuron did not confer tolerance in the sensitive inbred Cr1, suggesting that the sensitivity to sulfonylureas cannot be overcome with a safener. Responses to bromoxynil and bentazon in field trials were similar to the aforementioned herbicides tested, but some differences were noted. For example, families that were tolerant to nicosulfuron, mesotrione, dicamba + diflufenzopyr, carfentrazone, foramsulfuron, and primisulfuron were tolerant to bentazon; whereas families that were sensitive or segregated for responses to the herbicides had varied responses to bentazon. Our data indicate that a single gene is associated with the tolerance to these herbicides in sweet corn, although an additional gene(s) may affect tolerance to bromoxynil and bentazon. Further research is needed to determine if the gene that affects herbicide sensitivity in Cr1 occurs in other sweet corn and field corn inbreds that have been reported as sensitive to the herbicides evaluated in this study.