Contents
2.1. Chemistry and Mode of Action
2.1.1. Inhibition of Fatty Acid Biosynthesis
2.1.2. Perturbation of the Trans-membrane Proton Gradient 2.2.
Mechanisms Endowing Selectivity in
Resistant Species 2.3. Evolution and
Development of Resistance 2.4.
Mechanism of Resistance in Weeds 2.5. Cross-resistance |
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APP (aryloxyphenoxy propanoate)
and CHD (cyclohexanedione) herbicides are used to control grass weeds allover
the world. These herbicides act as acetyl coenzyme A carboxylase (ACCase)
inhibitors. Table 1 shows the ACCase inhibitors resistant weeds by species and
country.
The 3-hydroxy group in the CHD herbicides can
deprotonate, conferring weak acid characteristics, but they are generally very
labile and subject to rapid photolysis.
Table 1. The ACCase inhibitors most important two
resistant weeds by species and country (WSSA 2004).
Herbicide resistance in weeds:
http://www.weedscience.org/Summary/UspeciesMOA.asp?lstMOAID=2
Both APP and CHD herbicides are
used for the selective control of grass weeds in cereal and dicot crops. Most of
these two herbicidal groups are particularly active on annual grass weeds.
The meristems (apical and
intercalary) are the primary sensitive sites responsible for ultimate plant
death in susceptible species (Shimabukuro, 1990). Growth of meristems is inhibited
shortly after contact with diclofop-methyl
and other APP and CHD herbicides, and chlorosis of emerged leaves is observed 3
to 4 days after herbicide application.
Two
mechanism of action have been proposed for APP and CHD herbicides: 1) a biochemical
mechanism involving the inhibition of acetyl-CoA carboxylase (ACCase) and
subsequent fatty acid biosynthesis in plastids, and 2) a biophysical mechanism
involving the perturbation of the transmembrane proton gradient cross the
plasma membrane (Powles and Holtum, 1994).
2.1.1. Inhibition of Fatty Acid
Biosynthesis
Biosynthesis
of fatty acids and lipids is essential to the normal growth and development of
plants. Lipids are involved in the biogenesis and function of various
membranes, cellular signal transduction and other physiological functions
(Browse and Somerville, 1991). Fatty acid biosynthesis is localized in the
chloroplasts and plastids of non-green tissues. The synthesis of malonyl-CoA
catalyzed by acetyl-coenzyme A carboxylase (ACCase) (the key enzyme that
regulates this biosynthesis) is the first committed step in fatty acid
biosynthesis. The antibiotic cerulenin inhibits the condensation of the initial
products in this biosynthesis giving similar end results to APP and CHD herbicides.
Inhibition
experiments also indicated that APP and CHD herbicides might act at the same
site on ACCase (Rendiana et al, 1990). Collectively, the enzyme
inhibition data indicated that APP and CHD herbicides are potent inhibitors of
ACCase from grass species, and that selectivity between grass and dicot species
is due to the relative insensitivity of dicot ACCase to these herbicides.
2.1.2. Perturbation of the
Transmembrane Proton Gradient
It is demonstrated that all plant
cells establish and maintain a transmembrane proton gradient that is vital to
their growth and development (Serrano, 1985). The proton gradient is
established (inside negative and outside positive at the plasma membrane) by an
electrogenic (energy required) proton pump (H+– ATPase) that is
driven by the hydrolysis of ATP.
The
free acids diclofop and haloxyfop depolarize the
membrane potential or dissipate the transmembrane proton gradient in parenchyma
cells of wild oat and other plants (Wright and Shimabukuro, 1987), while
resistant dicots such as mung bean and sunflower are insensitive to membrane
depolarization by APP herbicides.
Sethoxydim
does not affect H+–
ATPase activity, but inhibits the plasma membrane-bound transmembrane redox
potential (Weber and Luttge, 1988), an alternative mechanism for the
establishment of the transmembrane proton gradient.
It is found
that two mechanisms confer selectivity on grass and dicot crops that are
resistant to APP and CHD herbicides. ACCase from dicot species is much less
sensitive to in vitro inhibition by these herbicides than is ACCase from grasses.
Many dicots crops do exhibit a substantial capacity for APP detoxification
(Shimabukuro, 1990) and might be insensitive to membrane depolarization.
Selectivity
in different grass species is based upon at least on other mechanism. Grass
crops such as wheat rapidly metabolize some APP herbicides to inactive products
(Shimabukuro et al, 1987). Since the ester forms of these herbicides are
nonphytotoxic, the first step in the metabolism of APP herbicides in both R and
S species is usually deesterification of the nonphytotoxic ester to the parent
acid. There is evidence that this bioactivation reaction is catalyzed by a
carboxylesrease.
The
metabolism pathway for diclofop-methyl
in wheat and wild oat has been investigated. Following deesterification, possibly
outside the plasma membrane, diclofop
acid is subject to aryl hydroxylation. The hydroxylated product is usually
found in only very small quantities, due to rapid glycosylation of the hydroxyl
group (Jacobson and Shimabukuro, 1984). Thus, the parent acid is depleted and
the aryl glycoside accumulates rapidly in resistant grasses. The same process
can occur in susceptible grasses, such as wild oat; however, less of the aryl
glycoside is formed, and more of the glucose ester of diclofop. The latter product can be
hydrolyzed in the tissue to release the parent acid again thus prolonging the
presence of the herbicidally active compound.
In wheat,
the plasma membrane and plastid target sites are both sensitive to the action
of diclofop. Nevertheless, inhibition
of lipid biosynthesis and membrane depolarization are overcome by the rapid
metabolism and detoxification of diclofop
in intact tissues (Shimabukuro, 1990). However, wheat is susceptible to haloxyfop, fluazifop, and some other APP herbicides
because of its ability to rapidly detoxify these herbicides.
Since the
introduction of APP and CHD herbicides about 20 years ago, they have gained
widespread popularity for control of grass weeds in both cereal and dicot
crops. The practice of growing wheat in a monoculture, as is common in many
parts of the world, has led to continuous use of these herbicides to control
common weeds mainly Avena and Lolium species.
As the APP
and CHD herbicides provide control of grass weed only, evolution of resistance
to these herbicides is restricted to grasses. Several weed species in which
resistance to APP and/or CHD has been documented and that includes A. fatua and A. sterilis ((Devine and
Shimabukuro, 1994). In most instances, resistance has developed after repeated use
of herbicides from either or both chemical groups over several years. However,
the patterns of resistance and cross-resistance within a species are variable.
For example, although most of the resistant A. fatua lines from Canada
are resistant to both APP and CHD herbicides, the relative degree of resistance
to different products can vary among lines. In some cases there is a high level
of resistance to APP herbicides but no resistance to CHD herbicides (Heap et
al, 1993). Although it is often difficult to determine herbicide use
histories, it appears that selection fore more than 4 years is sufficient too
give rise to resistant populations. However, in situations where the herbicides
may be applied more than once a year, this period may be shortened. Other agronomic practices, such as the
use of tillage or other mechanical weed control measures, may delay the
development of resistance (Matthews, 1994).
APP
and CHD herbicides must reach the sensitive meristematic sites in their toxic
forms at sufficient concentrations to disrupt normal growth and development of
sensitive cells. In addition, herbicidal injury must be maintained at a
threshold level over a critical period, after which irreversible damage results
and death of cells becomes inevitable. Three key factors that influence the
above processes are herbicide absorption and translocation, herbicide
metabolism and detoxification, and sensitivity of the target sites (Devine and
Shimabukuro, 1994).
As previously mentioned, ACCase
is well characterized as the target site of these herbicides. ACCase from most
grasses is sensitive to both groups of herbicides. The fact that resistance to
APP and CHD herbicides is not correlated with reduced ACCase sensitivity in some
weeds, or with any other processes, often associated with herbicide resistance
(e.g., uptake, translocation, and metabolism), supports the idea of another
mechanism of resistance. The
evidence to occurrence of metabolism to the parent acid of these herbicides in
wild oat resistant populations was not found. The alteration in the target site
(ACCaes) was sufficient to give cause to resistant population as determined by
a few studies. Physiological evidence indicated that APP and CHD both are bound
to the same region of the target enzyme (Rendina et al., 1989).
Furthermore, alteration in the binding site on ACCase enzyme was described as
the mechanism of resistance in UM1 wild oat in Australia.
An altered ACCase enzyme confers
herbicide resistance in different wild oat populations. Many populations show a
high level of target site resistance (insensitive ACCase) (Murray et al.,
1996). In wild oat populations, the levels of resistance vary from 0- to
300-fold resistance to specific ACCase inhibitors (Heap et al., 1993).
Prior research on ACCase inhibitors resistant wild oat generally indicated
high levels of resistance, in some instances, (e.g., <100-fold resistance to sethoxydim for UM1) (Heap et al.,
1993).
Cross-resistance in grass weeds
such as wild oat was observed in many patterns, and the mechanism endowing
cross-resistance in that weed was recognized. It occurs when a change at the
site of action of one herbicide also confers resistance to herbicides from a different
class that inhibits the same site of action, as selection by APPs for
APP-resistant ACCase that is also less sensitive to inhibition by CHD (Powles
and Holtum, 1994).
It was found that resistance in
wild oat lines occurred primarily in area where APP and CHD herbicides were
used repeatedly. Only a few of these have been characterized based on
cross-resistance patterns (Heap et al., 1993). Cross-resistant
populations of wild oat were discovered to herbicides in Group 1 (ACCase
inhibitors), Group 2 (ALS inhibitors) and Group 8 herbicides, triallate and difenzoquat (Morrison et al.,
1995). All populations that lasted as resistant to triallate were also
resistant to difenzoquat. As
previously mentioned, physiological evidence indicated that APP and CHD both
are bound to the same region of the target enzyme (Rendina et al.,
1989).
However, different
cross-resistance patterns characterize ACCase inhibitor resistance in weed
(Moss, 1990; Heap et al., 1993). The clear differentiation between some
types indicates that binding of APP herbicides may be more sensitive to changes
in the ACCase than binding of CHD herbicides. Although unproven, it may well be
that some mutation or conformation changes in vicinity of the ACCase inhibitor
binding, but not CHD herbicides (Bourgeois et al., 1997). The first
known instance of wild oat population exhibiting cross-resistance to both APP
and CHD herbicides the <150–fold
resistance of UM1 to sethoxydim is much higher than reported for
ACCase–resistant maize mutants (Parker et al., 1993).
In Egypt, no literature are
available on the determination of resistant grass weed populations to APP and CHD herbicides
despite some of them are the principle compounds used to control these weeds
for many years.
Herbicide mode of action
important site :
http://ipcm.wisc.edu/uw_weeds/extension/articles/herbmoa.htm
http://www.agcom.purdue.edu/AgCom/Pubs/WS/WS-23.html
Global
distribution of weed resistant ACCase web site :
http://www.weedscience.org/ACCaseDist.GIF
