Nicosulfuron, mesotrione, dicamba plus 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 F3 : 4families (F4plants) derived from of a cross between Cr1 (sensitive inbred) and 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 herbicide response. Families cosegregated for responses to these herbicides. In field studies with 60 F3 : 5families in 2005 and 120 F3 : 5families in 2007, responses to these herbicides and foramsulfuron and primisulfuron were associated. Responses to bentazon in field trials were similar to the aforementioned herbicides for tolerant families, but differences were noted for families that were sensitive or segregated for responses to nicosulfuron, foramsulfuron, primisulfuron, mesotrione, dicamba plus diflufenzopyr, and carfentrazone. The gene(s) affecting herbicide sensitivity in Cr1 maps to the same region of chromosome 5S as a previously sequenced cytochrome P450 gene, where alleles previously designatednsf1andben1were associated with sensitivity to nicosulfuron and bentazon and appear to be the result of a 392–base-pair insertion mutation. This work supports the hypothesis that a single recessive gene or closely linked genes in the sweet corn inbred Cr1 condition sensitivity to multiple cytochrome P450 enzyme-metabolized herbicides.

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).

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.

Gibberella ear rot, caused by Gibberella zeae, has increased in prevalence recently on lateseason processing sweet corn grown in North America. Little information is available about the development of Gibberella ear rot on processing sweet corn hybrids over extended periods of harvest. In five trials from 2003 to 2005, 12 processing sweet corn hybrids were inoculated with G. zeae and evaluated for severity of Gibberella ear rot on sequential harvest dates from 19 to 27 days after midsilk. Ear rot severity was assessed using a rating scale based on the percentage of kernels with visible symptoms of G. zeae colonization including kernel rot and mycelial growth. Severity ranged from 1.6 to 47.8% over the five trials. None of the hybrids was highly resistant to Gibberella ear rot, although some appeared to be less susceptible. Gibberella ear rot was less severe on three hybrids (GH 2690, GG 147, and Sprint) and more severe on three hybrids (GG 42, GG 145, and Jubilee). Other hybrids had moderate levels of ear rot or responses that varied among years. The relative response of hybrids did not change substantially during the extended period of harvest; however, the rate at which Gibberella ear rot developed on hybrids differed in 2003 and 2005 as reflected by a significant hybrid by harvest interaction. The interaction was primarily the result of Gibberella ear rot developing more severely on susceptible hybrids than on the less susceptible hybrids. The difference in Gibberella development could be exploited to limit losses due to this disease under certain circumstances. If a sweet corn processor had several fields ready to harvest at the same time, and some fields were planted with hybrids that are more susceptible while other fields were planted with hybrids that are less susceptible, losses due to Gibberella ear rot might be minimized by harvesting the most susceptible hybrids first. Other hybrids that might be best suited for early or late harvest can be identified from Gibberella ear rot ratings 28 days after silk channel inoculation at the midsilk growth stage.