Submitted to: Journal of the American Society for Horticultural Science
Publication Type: Peer reviewed journal
Publication Acceptance Date: 1/16/2009
Publication Date: 6/1/2009
Citation: Pataky, J.K., Williams, M.M. II, Reichers, D.E., Meyer, M.D. 2009. A Common Genetic Basis for Cross-Sensitivity to Mesotrione and Nicosulfuron in Sweet Corn Hybrid Cultivars and Inbreds Grown Throughout North America. Journal of the American Society for Horticultural Science. 134:252-260. Interpretive Summary: In previous research we found that sweet corn inbred line Cr1 was sensitive to a number of herbicides from five different herbicide classes. Furthermore, a single mutant P450 gene appeared to condition sensitivity in Cr1 to these herbicides. We wanted to know how prevelant this mutant gene was in other sweet corn and field corn germplasm with known sensitive responses to one or more herbicides. To test this hypothesis, a number of test crosses were made with candidate sweet corn hybrids, sweet corn inbreds, and field corn inbreds, and evaluated for their response to nicosulfuron and mesotrione. Based on our results, a common genetic basis for sensitivity to nicosulfuron and mesotrione is prevalent in commercially-adapted sweet corn. Forty-five of the 54 sweet corn hybrids and 29 of 40 sweet corn inbreds evaluated in our study appear to be either homozygous or heterozygous for an allele that is the same as or very closely linked to the allele in Cr1 that condition sensitivity. Remaining hybrids and inbreds appear homozygous tolerant. Widespread prevalence of this mutant gene is evidenced by allelism in hybrids and inbreds from 12 different seed and food processing companies and include sugary, sugary enhancer and shrunken-2 endosperm types. The impact of this research is we found a common genetic basis for herbicide sensitivity for hybrids grown commercially for processing and fresh consumption in nearly every market in North America and in many regions throughout the world. This research provides additional information that plant breeders and herbicide manufacturers can use to reduce the risk of herbicide injury in sweet corn, and possibly field corn.
Technical Abstract: In previous research, the sweet corn inbred line Cr1 was observed to be sensitive to multiple postemergence herbicides, including four acetolactate synthase (ALS)-inhibiting herbicides, three 4-hydroxyphenylpyruvate dioxygenase (HPPD)-inhibiting herbicides, a growth regulator herbicide combination, a protoporphyrinogen oxidase (PPO)-inhibiting herbicide, and a photosystem II (PSII)-inhibiting herbicide. The inbred Cr1 appears to contain a single gene or a group of very closely-linked genes that regulates multiple cytochrome P450 enzymes or a major cytochrome P450 enzyme. The objective of this study was to determine if the genetic basis of cross-sensitivity to nicosulfuron and mesotrione in Cr1 is prevalent among commercially-adapted, herbicide-sensitive sweet corn inbreds and hybrids and selected field corn inbreds. Fifty-four sweet corn hybrids, 40 sweet corn inbreds, and 27 field corn inbreds were evaluated in this study. Most of the hybrids and inbreds were previously identified as having had some adverse response to P450-metabolized herbicides. F2 progeny of hybrids and progeny from crosses of hybrids and inbreds with Cr1, Cr2 (a nicosulfuron- and mesotrione-tolerant inbred), or one of five herbicide-sensitive field corn inbreds were evaluated for responses to nicosulfuron and mesotrione in six field trials in 2006 and 2007. Also, the chromosomal location of the gene(s) in Cr1 conditioning sensitivity to multiple P450-metabolized herbicides was mapped from a population of 121 F3:4 families derived from a cross of Cr1 with Cr2. Based on our results, a common genetic basis for sensitivity to nicosulfuron and mesotrione is prevalent in commercially-adapted sweet corn. Simply-inherited cross-sensitivity in the sweet corn inbred Cr1 maps to a region of the short arm of chromosome 5 where a non-functional mutant of a cytochrome P450 gene, previously was designated as the nsf1 gene or the ben1 gene, was recently located and sequenced. Forty-five sweet corn hybrids and 29 sweet corn inbreds evaluated in our study appear to be either homozygous or heterozygous for an allele that is the same as or very closely linked to the allele in Cr1 that condition sensitivity. These hybrids and inbreds come from 12 different seed and food processing companies and include sugary, sugary enhancer and shrunken-2 endosperm types. Hybrids in this group are grown commercially for processing and fresh consumption in nearly every market in North America and in many regions throughout the world. Seven field corn inbreds, including several with the same mutation as the nsf1 and ben1 alleles, also were classified as sensitive with alleles that appear to be the same as or very closely linked to those in Cr1. This information provides a basis from which the issue of herbicide sensitivity in sweet corn can be addressed, improved, and possibly, solved by elimination of alleles that render germplasm sensitive to multiple herbicides.