Glyphosate behavior was examined in Italian ryegrass plants from Chile that were sensitive (S) and resistant (R) to this herbicide. In order to explain the resistance to glyphosate, contact angles, spray retention, foliar uptake, herbicide translocation, and target enzyme activity were studied. Contact angles of glyphosate solutions at a field concentration were 40° to 45° on the abaxial surface of R leaves as compared to 70° on S. Glyphosate spray retention by R plants was 35% lower than by S plants. Glyphosate uptake by the abaxial leaf surface of R plants was about 40% lower than that of S plants. In addition, in the R plants more glyphosate migrated to the tip of the treated leaves. The target enzyme in R and S plants was sensitive to the herbicide. Based on these and previous results, it is concluded that resistance in this Italian ryegrass biotype results from lower spray retention, lower foliar uptake from the abaxial leaf surface, and altered translocation pattern. The decreases in spray retention and foliar uptake constitute new mechanisms of glyphosate resistance.

The evolution of glyphosate-resistant weeds has recently increased dramatically. Six suspected glyphosate-resistant Amaranthus tuberculatus populations were studied to confirm resistance and determine the resistance mechanism. Resistance was confirmed in greenhouse for all six populations with glyphosate resistance factors (R/S) between 5.2 and 7.5. No difference in glyphosate absorption or translocation was observed between resistant and susceptible individuals. No mutation at amino acid positions G101, T102, or P106 was detected in the EPSPS gene coding sequence, the target enzyme of glyphosate. Analysis of EPSPS gene copy number revealed that all glyphosate-resistant populations possessed increased EPSPS gene copy number, and this correlated with increased expression at both RNA and protein levels. EPSPS Vmax and Kcat values were more than doubled in resistant plants, indicating higher levels of catalytically active expressed EPSPS protein. EPSPS gene amplification is the main mechanism contributing to glyphosate resistance in the A. tuberculatus populations analyzed.

Fenoxaprop-p-ethyl (FE), 2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy] propanoate, ethyl ester (R), is an aryloxyphenoxypropionate herbicide for postemergence control of annual and perennial grasses in paddy fields; its site of action is acetyl-coenzyme A carboxylase (ACCase), an enzyme in fatty acids biosynthesis. The possible mechanism(s) of resistance to FE in a resistant biotype of Echinochloa phyllopogon was examined, namely, absorption, translocation, and metabolism of FE and ACCase susceptibility to fenoxaprop acid (FA). Studies of the in vitro inhibition of ACCase discounted any differential active site sensitivity as the basis of resistance to FE. There were differences in absorption rates between biotypes from 3 to 48 h after application (HAA). Biotypes did not differ in either the amounts or the rates of FE translocated; 98% of applied [14C]FE remaining in the treated leaf. However, there was a good correlation between the rate of herbicide metabolism and the plant resistance. The R biotype produced 5-fold less FA and approximately 2-fold more nontoxic (polar) metabolites 48 HAA than the S biotype. Moreover, the higher rate of GSH conjugation in the resistant biotype as compared to the susceptible one indicates that GSH and cysteine conjugation is the major mechanism of resistance of the R biotype against FE toxicity.