Inheritance of Cross-sensitivity in Sweet Corn to Herbicides Applied Postemergence

Pataky, J. K.; Nordby, Jonathan N.; Williams, Martin M.; Riechers, Dean E.

doi:10.21273/jashs.131.6.744

Cited by 19 publications

(39 citation statements)

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“…Weed management in North American sweet corn ( Zea mays L.) production is characterised by reliance on soil applications of triazine and chloroacetamide herbicides (Anonymous, 2003) and risk of crop injury from several post‐emergence herbicides (Pataky et al. , 2006).…”

Section: Introductionmentioning

confidence: 99%

Crop competitive ability contributes to herbicide performance in sweet corn

2008

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Summary Crop variety effects on herbicide performance is not well characterised, particularly for sweet corn, a crop that varies greatly among hybrids in competitive ability with weeds. Field studies were used to determine the effects of crop competitive ability on season‐long herbicide performance in sweet corn. Two sethoxydim‐tolerant sweet corn hybrids were grown in the presence of Panicum miliaceum and plots were treated post‐emergence with a range of sethoxydim doses. Significant differences in height, leaf area index and intercepted light were observed between hybrids near anthesis. Across a range of sub‐lethal herbicide doses, the denser canopy hybrid Rocker suppressed P. miliaceum shoot biomass and fecundity to a greater extent than the hybrid Cahill. Yield of sweet corn improved to the level of the weed‐free control with increasing sethoxydim dose. The indirect effect of herbicide dose on crop yield, mediated through P. miliaceum biomass reduction, was significant for all of the Cahill’s yield traits but not Rocker. These results indicate that a less competitive hybrid requires relatively more weed suppression by the herbicide to not only reduce weed growth and seed production, but also to maintain yield. Sweet corn competitive ability consistently influences season‐long herbicide performance.

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Section: Introductionmentioning

confidence: 99%

Crop competitive ability contributes to herbicide performance in sweet corn

2008

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“…However, certain sweet corn hybrids are injured by applications of HPPD‐inhibitors applied alone (Williams and Pataky, 2010; Pataky et al, 2008, 2009; Meyer et al, 2010). Studies have determined that a single gene in sweet corn is responsible for sensitivity to multiple herbicides including HPPD‐inhibitors and other CYP‐metabolized herbicides (Pataky et al, 2006; Nordby et al, 2008; Williams and Pataky, 2008). Moreover, degree of sensitivity to these herbicides is driven by the number of mutant CYP alleles in the hybrid and environmental conditions influencing the plant growth (Pataky et al, 2008; Williams and Pataky, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…Sweet corn sensitivity to mesotrione, tembotrione, and possibly topramezone is conditioned by a single recessive gene (Williams et al, 2005; Williams and Pataky, 2008, 2010). This is apparently the same gene that conditions sensitivity to several other cytochrome P450 (CYP) metabolized herbicides from different chemical families (Pataky et al, 2006; Nordby et al, 2008). The gene in herbicide‐sensitive sweet corn inbred Cr1 was mapped to the region on the short arm of chromosome 5 as a previously sequenced CYP gene (Nordby et al, 2008), referred to as the nsf1 or ben1 gene, which is one of two genes also responsible for bentazon sensitivity (Kang, 1993; Williams et al, 2006; Dam et al, 2010).…”

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Photosystem II‐Inhibitors Play a Limited Role in Sweet Corn Response to 4‐Hydroxyphenyl Pyruvate Dioxygenase‐Inhibiting Herbicides

et al. 2014

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Postemergence (POST) application of 4-hydroxyphenyl pyruvate dioxygenase (HPPD) inhibitors in combination with a photosystem II (PSII) inhibitor, such as atrazine [6-chloro-N-ethyl-N9-(1-methylethyl)-1,3,5-triazine-2,4-diamine], is common practice in sweet corn (Zea mays L.) production. Given the sensitivity of sweet corn to HPPD-inhibiting herbicides, the objective of this work was to determine the extent to which cytochrome P450 (CYP) genotype and PSII-inhibitors affect crop sensitivity to HPPD-inhibiting herbicides. Greenhouse experiments were used to identify PSII-inhibitors that were least injurious when combined with the HPPD-inhibitors,Subsequently, HPPD-inhibitors were tested individually with PSII-inhibitors atrazine, or bentazon [3-(1-methylethyl)-(1H)-2,1,3benzothiadiazin-4(3H)-one2,2-dioxide], or alone in field experiments on all three CYP genotypic classes; hybrids homozygous for mutant CYP alleles (cypcyp), hybrids homozygous for functional alleles (CYPCYP), and heterozygous hybrids (CYPcyp). Leaf bleaching within 1 wk of herbicide application increased when a PSII-inhibitor was combined with an HPPD-inhibitor; however, the relatively low level of injury was short-lived. Tank mixing atrazine to mesotrione, tembotrione, or topramezone in sweet corn did not increase risk of yield loss compared to HPPD-inhibitor applied alone. The synergistic effect on weed control between certain PSII-and HPPD-inhibitor combinations reported previously does not hold true regarding sweet corn sensitivity to these herbicides. Among three HPPD-inhibitors tested in sweet corn, topramezone was the safest, regardless of PSII combination. Mutant CYP alleles, namely CYPcyp and cypcyp hybrids, are the main cause of sweet corn sensitivity to mesotrione, tembotrione, and other CYP-metabolized herbicides; therefore, breeding efforts to eliminate mutant CYP alleles should remain a high priority.

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“…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).…”

mentioning

confidence: 99%

“…Cross-sensitivity to multiple P450metabolized 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).…”

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confidence: 99%

Further Evidence of a Genetic Basis for Varied Levels of Injury to Sweet Corn Hybrids from Cytochrome P450-metabolized Herbicides Applied Postemergence

Williams¹,

Wax²,

Pataky³

et al. 2008

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Over the last two decades, sweet corn injury from postemergence herbicides has resulted in routine screening of combinations of new and existing hybrids and herbicides. Sensitivity of sweet corn to several cytochrome P450-metabolized herbicides is simply inherited and has a common genetic basis, a single P450 locus that may account for a large amount of the variation in sweet corn injury commonly observed among screening trials. Using data from 13 hybrid-herbicide screening trials, the objective of this work was to determine the extent to which injury from P450-metabolized herbicides was associated with the genotypes of hybrids at a locus affecting herbicide sensitivity. Of the 703 hybrids evaluated in the University of Illinois sweet corn hybrid nurseries from 2002 to 2007, previous work showed that a total of 104, 70, and nine of the hybrids were known to be homozygous-tolerant, heterozygous, or homozygous-sensitive, respectively, for an allele affecting herbicide response. Nurseries from 2002 to 2007 included six trials with mesotrione, three trials with nicosulfuron, and one trial each with foramsulfuron, tembotrione, halosulfuron, and carfentrazone. When means of hybrids in genotypic classes were compared, homozygous-sensitive hybrids were consistently injured more severely than homozygous-tolerant and heterozygous hybrids. When environmental conditions favored crop injury, heterozygous hybrids had an intermediate response that was closer to homozygous-tolerant hybrids than homozygous-sensitive hybrids. These data are further evidence that the probability of injury from several P450-metabolized herbicides, including mesotrione, nicosulfuron, foramsulfuron, tembotrione, halosulfuron, and carfentrazone, is highest in homozygous-sensitive hybrids and least in homozygous-tolerant hybrids and that variability of responses among sweet corn hybrids to these P450-metabolized herbicides can be explained largely by the genotype of a hybrid at a single locus.

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Inheritance of Cross-sensitivity in Sweet Corn to Herbicides Applied Postemergence

Cited by 19 publications

References 32 publications

Crop competitive ability contributes to herbicide performance in sweet corn

Crop competitive ability contributes to herbicide performance in sweet corn

Photosystem II‐Inhibitors Play a Limited Role in Sweet Corn Response to 4‐Hydroxyphenyl Pyruvate Dioxygenase‐Inhibiting Herbicides

Further Evidence of a Genetic Basis for Varied Levels of Injury to Sweet Corn Hybrids from Cytochrome P450-metabolized Herbicides Applied Postemergence

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