Nature (Vol. 435, No. 7041, 26 May 2005)
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The mechanism of action of quinclorac has intrigued scientists for over two decades Abdallah et al. There is a hypothesis that quinclorac acts as an auxin. ABP1 may act as a coordinator for the cell division and expansion, and its activity is influenced by the auxin levels on the plasmalemma Braun et al. The computer modeling of the TIR1 protein validated the hypothesis that quinclorac is perceived by the auxinic receptors, suggesting that this is the primary herbicide target Dharmasiri et al.
Only the auxinic effect of quinclorac, however, is arguable.
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Also, quinclorac did not acidify the growth medium of mung bean Vigna radiata tissues Mito et al. In relation to this point, it is also not known whether the family of TIR1 receptors responds to all the several signals from auxins and whether the biological activities that depend on the sensitivity of the tissue, physiological stage, biotype and species Grossman, It is possible that differences of auxin sensitivity on these receptors among plant species would explain the selectivity paterns of auxinic herbicides Grossman, ARFs activate the transcription of genes that respond to auxin, including those that create ACS 1-aminocyclopropanecarboxylate synthase acid and 9-cis-epoxycarotenoid dioxygenase McMahon et al.
These enzymes are fundamental on the biosynthesis pathways of ethylene and abscisic acid ABA , respectively Kraft et al. The increase on the ACC levels results in the action of ACO, leading to an accumulation of ethylene and cyanate Figure 2 on the tissues Sunohara et al. At 96 hours after spraying quinclorac, the concentration of cyanate increased from three up to nine times on the shoots of D.
After spraying quinclorac, the ethylene and cyanate levels on susceptible D. On plants that are resistant to the herbicide, no significant differences were observed Abdallah et al. This suggests that the possible insensitivity of the enzyme to the effects of quinclorac may contribute to the resistance in plants.
Studies with D. With the exogenous application of potassium cyanate KCN on D. Spraying the ACS aminoethoxyvinylglycine inhibitor on these plants, reduced the phytotoxic effects of quinclorac and the production of ethylene Abdallah et al. High HCN levels may block the electron flow on the chloroplast and mitochondria, and it may lead to the formation of ROS and cell damage Navrot et al. Spraying malation associated with quinclorac on E.
Dicotyledons sensitive to quinclorac show no changes on the cyanate levels Grossman, ABA accumulation leads to an excessive production of ROS, particularly hydrogen peroxide H 2 O 2 , causing cellular damage and leaf senescence van Eerd et al. Galium spurium plants that are resistant and susceptible to quinclorac showed no differences on the absorption, translocation, degradation and exudation of the herbicide. This indicates that other processes are involved on the resistance to these biotypes van Eerd et al.
After spraying quinclorac on G. On resistant biotypes, there was no increase on the ethylene levels, however, they showed a three fold increment on the ABA levels, in comparison to the plants that were not sprayed with quinclorac; however, these levels were not enough to cause plant injury van Eerd et al.
On susceptible G. The third hypothesis that would explain the quinclorac activity is related to its ability to induce the production of ROS, thus, suggesting that they would be responsible for the phytotoxic effects on susceptible grass plants Sunohara et al. The accumulation of ROS inhibits the electron transportat during photosynthesis, promotes damages to the chlorophyll, damages proteins, membrane lipids and nucleic acids Bowler et al.
High production of ROS and subsequent events were observed on E. These results indicate that the ethylene induced by quinclorac did not cause cell death or lipid peroxidation on corn roots cells of D. In addition, cyanate is produced on stoichiometrically similar amount than ethylene Peiser et al. The linear relation between the amount of the cyanate and ethylene contents were observed, for quinclorac and 2,4-D. It is theorized that the plant tolerance to quinclorac is due to the higher production of ROS detoxifying enzymes Sunohara et al.
Eleusine indica plants showed high activity on the enzymatic protection system to eliminate ROS, suggesting that this process may be responsible for the tolerance to herbicides that induce the overproduction of ROS, such as quinclorac Sunohara et al. Oryza sativa, Z.
Although there are several researches and studies conducted with quinclorac, there are still some uncertainties on its mechanism of action. On monocot plants, there are some controversies on its effect, and there is evidence of inhibition of the biosynthesis of the cellular wall Koo et al. On this review, we suggest an integrating hypothesis that associates all the processes described on the previous sections.
Integrative Theory of the Mode of Action of Quinclorac: Literature Review1
Our interpretation is that quinclorac is a herbicide with multiple mechanisms of actions, in such a way that the final result of its activity is a combined result not necessarily simultaneous or on the same vegetal tissues of the inhibition of the cell wall synthesis, the auxinic action and the overproduction of ROS Figure 3 , as previously described.
The black arrows indicate the mode of action on dicotyledons, and the gray arrows, the mode of action on monocots. The dotted grey arrows indicate action pathways that need further evidence. Some questions still need to be cleared by the research, such as: whether or not there are quinclorac receptors on the plasma membrane of cells; the determination of the transport mechanism of quinclorac inside the cell; and evidence that TIR1 receptors respond to quinclorac or whether there are other signaling proteins involved in the process.
Therefore, complementary studies may help to understand the biochemical and physiological activity of quinclorac, thus, providing evidence that the existing theories up to this moment are inter-related, as suggested here Figure 3. Understanding the sensitivity and the physiological responses of weeds to quinclorac may offer basic information for their management and the possibility of optimized use of this herbicide.
The resistance of plants to quinclorac may be associated to the sensitivity on the site of action on the cell wall synthesis Koo et al. Therefore, elucidating the mechanism and the mode of action of quinclorac is a fundamental step to elaborate resistance prevention and management strategies.
To professors M. Mechanism of resistance to quinclorac in smooth crabgrass Digitaria ischaemum. Habituation of bean Phaseolus vulgaris cell cultures to quinclorac and analysis of the subsequent cell wall modifications.
Receptors for auxin: will it all end in TIRs?. Trends Plant Sci. The endocytosis of cellulose synthase in Arabidopsis is dependent on mu2, a clathrin mediated endocytosis adaptin. Plant Physiol. BOND, J.
Effect of postflood quinclorac applications on commercial rice cultivars. Weed Technol. Superoxide-dismutase and stress tolerance. Plant Molec. That may be what happens as people age, according to Semenkovich. As cells try to compensate, more damage accumulates. There also is evidence that a similar process occurs in birds.
In a series of experiments in the s, researchers found that when pigeons develop atherosclerosis — and some do — their blood vessels have inefficient mitochondrial metabolism prior to developing blockages. One area of interest involves essential fatty acids, which regulate body functions such as blood pressure and blood clotting. Deficiency in essential fatty acids is thought to contribute to atherosclerosis. Armed with the results of this study, Semenkovich believes a deficiency in essential fatty acids may cause changes in the way metabolism occurs in the blood vessel wall.
Vascular respiratory uncoupling increases blood pressure and atherosclerosis, Nature ; vol. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked third in the nation by U. Through its affiliations with Barnes-Jewish and St. Plant Cell, v.
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Subcompartment localization of the side chain xyloglucan-synthesizing enzymes within Golgi stacks of tobacco suspensioncultured cells. Plant J.
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Wall structure and wall loosening. A look backwards and forwards. Nonmotile cellulose synthase subunits repeatedly accumulate within localized regions at the plasma membrane in Arabidopsis hypocotyl cells following 2,6-dichlorobenzonitrile treatment. The F-box protein TIR1 is an auxin receptor. Nature, v. Golgi-mediated synthesis and secretion of matrix polysaccharides of the primary cell wall of higher plants.
Frontiers Plant Sci. Cellulose biosynthesis inhibitors: comparative effect on bean cell cultures.
The mode of action of auxin herbicides: a new ending to a long, drawn out story. The mechanism of quinclorac selectivity in grasses. Auxin herbicides induce H2O2 overproduction and tissue damage in cleavers Galium aparine L. News from old compounds: the mode of action of auxin herbicides. Chemistry of crop protection: progress and prospects in science and regulation. Weinheim: Wiley, Auxin herbicides: current status of mechanism and mode of action. Pest Manage. Auxin-induced ethylene triggers abscisic acid biosynthesis and growth inhibition. A comparative analysis of the plant cellulose synthase CesA gene family.