bicide [2,88]. In Chlamydomonas reinhardtii, resistance is due to lack of phosphinothricin transport into
the cells [89]. An alternative approach was to introduce the gene bar, which produces a detoxifying en-
zyme, into plants. The bargene is from Streptomyces hygroscopicus, which produces bialaphos, the
tripeptide precursor of PPT. The protein encoded by the bargene protects these bacteria from the action
of their own antibiotics by metabolizing PPT to an inactive derivative [90,91].
IV. LIPID SYNTHESIS INHIBITORS
These compounds are formed by two herbicide families: phenoxypropionates (diclofop, haloxyfop, and
trifop) and cyclohexanediones (alloxydim, sethoxydim, and dethodim). These herbicides inhibit fatty acid
synthesis, which is fundamental for the biosynthesis of lipids. The lipids are also fundamental for the in-
tegrity of the cellular membranes and for the growth of plants.
All of these herbicides inhibit a key enzyme, the acetyl–coenzyme A (CoA) carboxylase, in the path-
way of fatty acid synthesis [92–94]. This enzyme produces the carboxylation of acetyl-CoA, using ATP
and HCO 3 , giving malonyl-CoA (Figure 6). Cyclohexanediones and phenoxypropionates probably bind
the same region, but in different sites, of the target enzyme [94–96].
Also, it is believed that these herbicides dissipate the transmembrane proton gradient [97,98]. They
are absorbed by leaves and move by phloem to the rest of the plant.
RESISTANCE Perennial as well as annual weeds are susceptible to these inhibitors, but most of the
broadleaf plants are tolerant. Dicotyledon and monocotyledon (except graminaceous) crops are resistant
to these herbicides. Dicotyledons have an acetyl-CoA carboxylase resistant to these herbicides, and many
of them also have the capacity for cyclohexanedione and phenoxypropionate detoxification. Most grass
crops are susceptible, but wheat is tolerant to diclofop. Wheat rapidly detoxifies diclofop with a demethy-
lation produced by an active esterase [99,100].
Resistance to acetyl-CoA carboxylase inhibitors in crop plants was investigated [101]. In one case,
mutants with increased expression of susceptible acetyl-CoA carboxylase were obtained [102]; in another
case plants with a resistant acetyl-CoA carboxylase were found [103].
There are examples of weeds that are naturally tolerant to diclofop [104]. Many weeds are develop-
ing resistance to these herbicides by evolving a resistant acetyl-CoA carboxylase [105,106] or by induc-
tion of this protein to compensate for the inactivated enzyme [103,107].
PHYSIOLOGICAL MECHANISMS OF HERBICIDE ACTIONS 781
Figure 6 Scheme of fatty acid metabolism with the enzymes that are targets for herbicides. Dashed arrow in-
dicates site of action of main herbicides. ACC, acetyl-CoA carboxylase; FAS, fatty acid synthetase cycle.