These herbicides, similar to auxin hormones, cause rapid changes in cell walls as a result of increased ac-
tivity of plasma membrane adenosinetriphosphatase (ATPase) [118,119].
The herbicides belonging to this group selectively kill broadleaf plants and weeds. They tend to be
absorbed by leaves, although to a lesser extent they can enter through the roots. They can move via either
phloem or xylem toward the zones of the plant that are growing; therefore they are as effective in peren-
nial plants as in annual broadleaf plants.
RESISTANCE Many monocotyledon crops and weeds are naturally resistant to these herbicides. It has
been shown that arylhydroxylation by some monooxygenases confers resistance to these herbicides [120].
Some of these genes from bacteria are being used to make resistant crop plants [121].
VII. SEEDLING GROWTH INHIBITORS
Within this group there are three herbicide families: dinitroanilines, acetanilides, and thiocarbamates.
These herbicides reduce the ability of seedlings to develop normally in soil. Plants take up these herbi-
cides after germinating until the seedling emerges from the soil.
Dinitroanilines act as root inhibitors, affecting division, elongation, and cellular differentiation. They
bind to the heterodimers of tubulin, inhibiting polymerization, and stop mitosis in prometaphase. Thus,
chromosomes are found to be condensed and cannot migrate to the poles. This causes an abnormal nu-
cleus because the nuclear membrane is reconstituted with condensed chromosomes [122–125]. As a rule,
it is believed that these compounds affect multiple sites, fundamentally lipid and protein synthesis.
Acetanilides and thiocarbamates are inhibitors of shoots. Their action site is not known, but they
probably have multiple action sites.
Dinitroanilines are effective against annual weeds, less against annual dicotyledons, but they have lit-
tle effect on perennial species. In cultivation, seeds must be located below the contaminated soil layer or
planted after the herbicide degradation. Susceptibility is associated with especially small seeds, low lipid
content, or a high proportion of meristematic tissue with low protection in the soil where the herbicide acts.
Acetanilide derivatives are generally used for preemergence control of annual grasses and broadleaf
weeds in agronomic and vegetable crop production [126].
RESISTANCE The principal resistance mechanisms are related to decreased absorption of the herbi-
cide and poor movement of the herbicide through the most superficial caps of cells. Some species can de-
grade dinitroanilines, and in others the resistance may be associated with high levels of lipids. In other
cases, resistance has been associated with an increase of free amino acid levels [127]. Several biotypes
that have acquired great resistance to these herbicides produce a higher quantity of tubulin and tubulin
of greater molecular weight [122]. Researchers have found that in a biotype of goosegrass, resistance to
dinitroaniline is inherited in a single recessive nuclear gene [123].
Acetanilide herbicides are detoxified in biological systems by the formation of glutathione-ac-
etanilide conjugates. This conjugation is mediated by glutathione-S-transferase, which is present in mi-
croorganisms, plants, and animals [128].
ACKNOWLEDGMENTS
We are thankful for the financial help of Ministerio de Educación y Cultura (PB96-1358) and Plan An-
daluz de Investigación.
REFERENCES
- JS Holt. Mechanisms and agronomic aspects of herbicide resistance. Annu Rev Plant Physiol Plant Mol Biol.
44:203–229, 1993. - A Díaz, M Lacuesta, A Muñoz-Rueda. Comparative effects of phosphinothricin on nitrate and ammonium as-
similation and on anaplerotic CO 2 fixation in N-deprived barley plants. J Plant Physiol 149:9–13, 1996. - BJ Mazur, SC Falco. The development of herbicide resistant crops. Annu Rev Plant Mol Biol 40:441–470,
1989. - DE Moreland. Mechanisms of action of herbicides. Annu Rev Plant Physiol 31:597–638, 1980.
- G Sandmann, P Böger. Sites of herbicide inhibition at the photosynthetic apparatus. In: LA Staehelin, CJ
Arntzen, eds. Encyclopedia of Plant Physiology. Vol 19. Berlin: Springer-Verlag, 1986, pp 596–602.
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