Genetic Relationships of Alleles for Tolerance to Sethoxydim Herbicide in Maize

Autor: Gengenbach, B. G., VanDee, K. L., Egli, M. A., Hildebrandt, K. M., Yun, S. J., Lutz, S. M., Marshall, L. C., Wyse, D. L., Somers, D. A.
Zdroj: Crop Science; May 1999, Vol. 39 Issue: 3 p812-818, 7p
Abstrakt: Maize (Zea maysL.) and most other grasses are naturally susceptible to graminicides represented by the herbicides sethoxydim (211‐(ethoxyimino) butylJ‐5‐[2‐( ethylthio)propyl~‐3‐hydroxy‐2‐cyclohexen‐1‐one) and haloxyfop (2‐(4‐[3‐chIoro‐5‐(trifluorom ethyl)‐2‐pyridin‐yl]oxy)phenoxy‐methyl ester) because of the presence of a susceptible form of the target site enzyme, acetyl‐coA carboxylase. However, tolerant maize mutants have been obtained by tissue culture selection. Five selected mutant lines (S1, S2, S3, H1, H2) were previously shown to he allelic for the same tolerance gene (Acc1) and to express graminicide‐ tolerant acetyl‐coA carboxylase (ACCase) activity. The ohjectives of this study were to determine the genetic relationships among three additional mutants (S4, S5, S6) and the original five mutants and to examine the graminicide susceptibility of ACCase activity. Herbicide tolerance in 3‐wk‐old seedlings segregated as a single‐gene, partially dominant trait for all mutants. Crosses between mutants revealed that S1, S2, S3, S4, H1, and H2 were allelic for mutations at the Acc1locus and that S5 and S6 were allelic for mutations at a second locus designated Acc2. ACCase activity from the S2 mutant expressed a high level of sethoxydim tolerance while ACCase activity from the S5 mutant expressed a much lower level of herbicide tolerance. These data suggest that Acc1contributes a higher proportion of the total ACCase activity than the Acc2locus. Acc1and Acc2were mapped to chromosome 2 and chromosome 10, respectively, on the basis of RFLP and seedling phenotype markers. The S3 allele of Acc1cosegregated with a polymorphism on chromosome 2 identified by a maize ACCase cDNA probe indicating that the herbicide tolerance trait is conditioned by a structural gene for ACCase.
Databáze: Supplemental Index