Because certain sweet corn hybrids are sensitive to postemergence herbicides, new hybrids frequently are screened for responses to existing herbicides, and new herbicides are routinely tested for potential injury to existing hybrids (e.g., Diebold et al., 2003; Morton and Harvey, 1992; Stall and Bewick, 1992; Williams and Pataky, 2008). Although this type of screening identifies hybrids that may be injured from postemergence herbicides, a more comprehensive understanding of the genetic basis of herbicide sensitivity in sweet corn offers a mechanism by which this problem can be addressed and possibly solved by elimination of alleles that render sweet corn sensitive.
A sensitive or tolerant response of sweet corn to several cytochrome P450-metabolized herbicides is a simply inherited trait. Alleles at a single cytochrome P450 (CYP) locus (or a group of very closely linked loci) on the short arm of chromosome 5S condition response of corn to multiple, P450-metabolized herbicides, including: bentazon, carfentrazone, dicamba plus diflufenzopyr, foramsulfuron, imazethapyr, mesotrione, nicosulfuron, primisulfuron, rimsulfuron, and tembotrione (Barrett et al., 1997; Nordby et al., 2008; Pataky et al., 2006b; Williams and Pataky, 2008). A single gene conditioning sensitivity to nicosulfuron was identified from a field corn inbred W703a and designated as nsf1 (Kang, 1993). A single gene conditioning cross-sensitivity to bentazon and nicosulfuron was identified in the field corn inbred GA209 and designated as ben1 (Barrett et al., 1997; Bradshaw et al., 1994; Fleming et al., 1988). An allele at the Nsf1 locus on chromosome 5S from a nicosulfuron-tolerant field corn inbred, B73, contained the highly conserved heme-binding sequence FxxGxxCxG found in most cytochrome P450 genes (Williams et al., 2006). Alleles in the field corn inbreds, GA209 and W703a, contained identical 392 base pair insertions in this gene sequence relative to B73. Thus, it appears that this insertion mutation results in a nonfunctional P450 allele resulting in herbicide sensitivity and that the nsf1 and ben1 genes are the same mutant of a CYP gene.
Cross-sensitivity to multiple P450-metabolized herbicides also is simply inherited in the sweet corn inbred Cr1 (Nordby et al., 2008; Pataky et al., 2006b; Williams and Pataky, 2008). The allele (or closely linked alleles) in Cr1 that conditions the cross-sensitivity map to the same region of chromosome 5S as the Nsf1/Ben1 locus and progeny from crosses of Cr1 with GA209 and W703a have homogeneous responses to nicosulfuron and mesotrione (Nordby et al., 2008). Thus, cross-sensitivity in Cr1 appears to be the result of the same insertion mutation as nsf1/ben1, a similar mutation, or an allele at a very closely linked locus.
The common genetic basis for cross-sensitivity to several P450-metabolized herbicides is prevalent in sweet corn grown in nearly every market in North America and throughout the world. Forty-five sweet corn hybrids and 29 sweet corn inbreds were either homozygous or heterozygous for an allele that is the same as or very closely linked to alleles in Cr1 that condition cross-sensitivity (Pataky, unpublished data). This group of hybrids and inbreds represents sweet corn germplasm from 12 different commercial breeding programs and includes sugary, sugary enhancer, and shrunken-2 endosperm mutants. Some of these hybrids were among a group of 149 sweet corn hybrids evaluated for responses to foramsulfuron, mesotrione, and nicosulfuron in 12 trials in six states (Bollman et al., 2005). Those 149 hybrids differed genotypically for the presence or absence of alleles affecting herbicide metabolism and phenotypically for their response to the three P450-metabolized herbicides (Pataky et al., 2008). When trial mean levels of injury were above minimal levels (e.g., 1% to 6% depending on the herbicide), response of the three genotypic classes of hybrids followed a consistent pattern. Homozygous-sensitive hybrids were killed or severely injured. Heterozygous hybrids had intermediate responses that were more similar to homozygous-tolerant than homozygous-sensitive hybrids; however, injury to heterozygous hybrids was 1.5 to 2.3 times greater than injury to homozygous-tolerant hybrids. In another trial, homozygous-sensitive hybrids were killed by tembotrione plus the safener isoxadifen-ethyl applied at a standard use rate, whereas homozygous-tolerant and heterozygous hybrids were uninjured (Williams and Pataky, 2008).
Since 2002, 249 to 379 sweet corn hybrids were evaluated annually for responses to postemergence herbicides as part of the University of Illinois sweet corn hybrid nurseries (Pataky et al., 2002, 2003, 2004, 2005, 2006a, 2007). Hybrid responses to mesotrione were evaluated in each year. Other herbicides evaluated in at least 1 year included carfentrazone, foramsulfuron, halosulfuron, nicosulfuron, and tembotrione. Herbicide evaluations were added to the UI sweet corn hybrid nurseries at a time when little was known about the inheritance of herbicide sensitivity in sweet corn. Although these data have been used to report individual hybrid responses, further analysis would provide an independent test of the genetic basis for varied levels of injury to sweet corn from P450-metabolized herbicides. The objective was to determine the extent to which injury observed in these nurseries was associated with the genotypes of hybrids at a locus conditioning herbicide sensitivity.
Barrett, M. , Polge, N. , Baerg, R. , Bradshaw, R. & Poneleit, C. 1997 Role of cytochrome P450 in herbicide metabolism and selectivity and multiple herbicide metabolizing cytochrome P450 activities in maize 35 50 Hatzios K. Regulation of enzymatic systems detoxifying xenobiotics in plants Kluwer Academic Publishers Dordrecht, The Netherlands
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