|Pataky, Jerald - UNIVERSITY OF ILLINOIS|
|Norby, Jon - UNIVERSITY OF ILLINOIS|
|Riechers, Dean - UNIVERSITY OF ILLINOIS|
Submitted to: Journal of the American Society for Horticultural Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 13, 2006
Publication Date: December 15, 2006
Citation: Pataky, Jerald K., Norby, John N., Williams, M., Riechers, D.E. 2006. Inheritance of cross-sensitivity in sweet corn to herbicides applied postemergence. Journal of the American Society for Horticultural Science. 131:744-751. Interpretive Summary: Many herbicides registered or being considered for use in sweet corn lack selectivity in certain hybrids. Previous research found associations, hereafter called ‘cross-sensitivity’, between crop response to nicosulfuron and mesotrione. Studies were conducted to determine if there was a common genetic basis for cross-sensitivity to these and other herbicides. Results indicate a single recessive gene conditioned sensitivity to four ALS-inhibiting herbicides (foramsulfuron, nicosulfuron, primisulfuron, and rimsulfuron), an HPPD-inhibiting herbicide (mesotrione), a growth regulator herbicide combination (dicamba+diflufenzopyr), and a PPO-inhibiting herbicide (carfentrazone). This research was the first to provide evidence that a single recessive gene conditions sensitivity to herbicides with unique modes of action in corn, leading to a novel hypothesis for eliminating herbicide-sensitive hybrids in breeding programs.
Technical Abstract: Some sweet corn 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 S1 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, BC1S1, BC2S1 and F3 families and 143 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 ALS-inhibiting herbicides (foramsulfuron, nicosulfuron, primisulfuron, and rimsulfuron), an HPPD-inhibiting herbicide (mesotrione), a growth regulator herbicide combination (dicamba+diflufenzopyr), and a PPO-inhibiting herbicide (carfentrazone). Based on highly significant positive correlations of phenotypic responses among S2:3, BC1S1, BC2S1 and F2 (S1:2) 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 inhibiting herbicide) although another gene(s) also appeared to affect bentazon tolerance.