|Pataky, Jerald - UNIV OF ILLINOIS|
|Nordby, Jonathon - UNIV OF ILLINOIS|
|Riechers, Dean - UNIV OF ILLINOIS|
|Sprague, Christy - MICHIGAN STATE UNIV|
|Masiunas, John - UNIV OF ILLINOIS|
Submitted to: HortScience
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 10, 2005
Publication Date: October 1, 2005
Citation: Williams, M., Pataky, J.K., Nordby, J.N., Riechers, D.E., Sprague, C.L., Masiunas, J.B. 2005. Cross-sensitivity in sweet corn to nicosulfuron and mesotrione applied postemergence. Hortscience. 40(6):1801-1805. Interpretive Summary: Weed management in sweet corn relies heavily on older herbicide chemistries with significant ecological shortcomings. More recently developed herbicides with better environmental profiles are slow to be registered for use in sweet corn because, in part, some hybrids are susceptible to herbicide-induced injury. Study was undertaken to determine if there was an association between sensitivity of sweet corn to nicosulfuron and mesotrione. Responses of hybrids, inbreds, and S1 families to these two herbicides lead us to hypothesize the same recessive gene conditions sensitivity to both herbicides. The impact of this research is a potential breakthrough in the fundamental understanding of sensitivity of sweet corn to postemergence herbicides, which would ultimately result in improved technology for weed management in sweet corn.
Technical Abstract: Abstract. 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.