Maize (Zea maps L.) and most other grasses are naturally susceptible to gra
minicides represented by the herbicides sethoxydim (2[1-(ethoxyimino)butyl]
-5-[2-(ethylthio)propyl]-3-hydroxy-2-cyclohexen-1-one) and haloxyfop (2-{4-
[3-chloro-5-(trifluoro methyl)-2-pyridin-yl]oxy}phenoxy-methyl ester) becau
se of the presence of a susceptible form of the target site enzyme, acetyl-
CoA carboxylase. However, tolerant maize mutants have been obtained by tiss
ue culture selection. Five selected mutant lines (S1, S2, S3, H1, H2) were
previously shown to be allelic for the same tolerance gene (Acc1) and to ex
press graminicide-tolerant acetyl-CoA carboxylase (ACCasc) activity. The ob
jectives of this study were to determine the genetic relationships among th
ree additional mutants (S4, S5, S6) and the original five mutants and to ex
amine the graminicide susceptibility of ACCase activity. Herbicide toleranc
e in 3-wk-oId seedlings segregated as a single-gene, partially dominant tra
it for all mutants. Crosses between mutants revealed that S1, S2, S3, S4, H
1, and H2 were allelic for mutations at the Acc1 locus and that S5 and S6 w
ere allelic for mutations at a second locos designated Acc2. ACCase activit
y from the S2 mutant expressed a high level of sethoxydim tolerance while A
CCase activity from the S5 mutant expressed a much lower level of herbicide
tolerance. These data suggest that Acc1 contributes a higher proportion of
the total ACCase activity than the Acc2 locus. Acc1 and Acc2 were mapped t
o chromosome 2 and chromosome 10, respectively, on the basis of RFLP and se
edling phenotype markers. The S3 allele of Acc1 cosegregated with a polymor
phism on chromosome 2 identified by a maize ACCase cDNA probe indicating th
at the herbicide tolerance trait is conditioned by a structural gene for AC
Case.