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  • Author or Editor: Dean E. Riechers x
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Mutation of a cytochrome P450 (CYP) gene on the short arm of chromosome five, referred to as nsf1 or ben1, conditions sensitivity to certain P450-metabolized herbicides in corn (Zea mays L.). Previous research has shown that the sweet corn inbred Cr1 is sensitive to nicosulfuron, mesotrione, and at least seven other P450-metabolized herbicides with five different modes of action. Although the nsf1/ben1 CYP gene has not been sequenced from Cr1, a QTL that conditions cross-sensitivity to P450-metabolized herbicides was detected in a segregating population of Cr1 × Cr2 (herbicide tolerant) on the short arm chromosome five in tight linkage disequilibrium with the nsf1/ben1 CYP locus. Sweet corn hybrid cultivars and inbreds that had been identified in previous research as being susceptible to injury from P450-metabolized herbicides were tested in this study to determine if they were allelic with Cr1 for cross-sensitivity to nicosulfuron and mesotrione. These cultivars and inbreds were developed by 12 independent commercial breeding programs. These cultivars include sugary, sugary enhancer, and shrunken-2 endosperm types that are grown for processing and fresh consumption in markets throughout North America and in other temperate climates throughout the world. Each hybrid cultivar, their F2 progeny, and progeny from testcrosses of cultivars with Cr1 and Cr2 were evaluated for responses to mesotrione and nicosulfuron. Each inbred line, progeny from crosses of inbreds with Cr1 and Cr2, and F2 progeny from crosses of inbreds with Cr1 were also tested. Based on segregation of progeny from testcrosses with Cr1 and Cr2 and the F2 generation, 45 sweet corn hybrid cultivars and 29 sweet corn inbreds, including lines from each of the 12 breeding programs, appeared to be sensitive to nicosulfuron and mesotrione as the result of a gene that is the same as or very closely linked to the gene in Cr1. None of the cultivars or inbreds appeared to be sensitive to these herbicides as a result of other independent genes; however, additional genes that modify responses to these herbicides may be present in a few cases. The presence of a gene conditioning sensitivity to nicosulfuron and mesotrione, and probably to several other P450-metablolized herbicides, provides an explanation for varied levels of injury and inconsistent responses of sweet corn hybrid cultivars under differing environmental conditions. This information provides a basis from which an industry-wide concern with herbicide sensitivity in sweet corn can be addressed by various methods, including the elimination of an allele rendering germplasm sensitive.

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Some sweet corn (Zea mays L.) hybrids and inbreds can be severely injured by applications of postemergence herbicides. An association was observed between the responses of sweet corn hybrids and inbreds to nicosulfuron and mesotrione, and F2 families derived from a cross of a sensitive (Cr1) and a tolerant (Cr2) sweet corn inbred segregated for response to these two herbicides. These observations prompted us to examine the inheritance of sensitivity in sweet corn to multiple postemergence herbicide treatments with different modes of action and to determine if there was a common genetic basis for cross-sensitivity to these herbicides. The sensitive and tolerant inbreds, progeny in the F1, F2, BC1, and BC2 generations, and BC1S1, BC2S1, F2:3 (S1:2) and F3:4 (S2:3) families were screened for responses to eight herbicide treatments. Based on segregation of tolerant and sensitive progeny and segregation of family responses, our data indicate that a single recessive gene in Cr1 conditioned sensitivity to four acetolactate synthase (ALS)-inhibiting herbicides (foramsulfuron, nicosulfuron, primisulfuron, and rimsulfuron), a 4-hydroxyphenylpyruvate dioxygenase (HPPD)-inhibiting herbicide (mesotrione), a growth regulator herbicide combination (dicamba + diflufenzopyr), and a protoporphyrinogen oxidase (PPO)-inhibiting herbicide (carfentrazone). Based on highly significant positive correlations of phenotypic responses among BC1S1, BC2S1, F2:3, and F3:4 families, the same gene (or closely linked genes) appeared to condition responses to each of these herbicide treatments. The dominant allele also conditions tolerance to bentazon [a photosystem II (PSII)-inhibiting herbicide] although another gene(s) also appeared to affect bentazon tolerance.

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Nicosulfuron and mesotrione are herbicides from different chemical families with different modes of action. An association between the sensitivity of sweet corn (Zea mays L.) to nicosulfuron and mesotrione was observed when hybrids, inbreds, and S1 families (S2 plants) were evaluated for herbicide sensitivity in field trials. In 2003 and 2004, 50% and 53% of mesotrione-sensitive hybrids were sensitive to nicosulfuron compared with only 6% and 1% of mesotrione-tolerant hybrids that were sensitive to nicosulfuron. In trials with inbreds in 2003 and 2004, 88% and 78% of nicosulfuron-sensitive inbreds had some injury from mesotrione but 0% and 5% of nicosulfuron-tolerant inbreds were injured by mesotrione. Among S1 families, 77% of the mesotrione-sensitive families were nicosulfuron-sensitive but only 5% of the mesotrione-tolerant families were sensitive to nicosulfuron. Segregation of S1 families for response to mesotrione was not significantly different from a 1:2:1 pattern of sensitive: segregating: tolerant families (chi square value = 2.25, P = 0.324) which would be expected if sensitivity was conditioned by a single recessive gene. Segregation of S1 families for response to nicosulfuron was 15:23:26 (sensitive: segregating: tolerant) which was slightly different from an expected 1:2:1 ratio (chi square value = 8.84, P = 0.012). Segregation of S1 families probably was affected by the relatively small number of S2 plants sampled from each family. Similar responses of the S1 families to nicosulfuron and mesotrione lead us to hypothesize that the same recessive gene is conditioning sensitivity to both herbicides. Possibly, this gene is common in the inbreds and hybrids that were sensitive in these trials. These hypotheses will be tested by examining segregation in S2 families and other segregating generations and by conducting tests of allelism among sensitive inbreds and inbred parents of sensitive hybrids. Chemical names: 2-(4-mesyl-2-nitrobenzoyl)-3-hydroxycyclohex-2-enone, (mesotrione); 2-[[[[(4,6-dimethoxy-2-pyrimidinyl)amino]carbonyl]amino]sulfonyl]-N,N-dimethyl-3-pyridinecarboxamide, (nicosulfuron).

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