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In this way, less reliance is placed on herbicides and so selection pressure should be reduced. Optimising herbicide input to the economic threshold level should avoid the unnecessary use of herbicides and reduce selection pressure. Herbicides should be used to their greatest potential by ensuring that the timing, dose, application method, soil and climatic conditions are optimal for good activity. In the UK, partially resistant grass weeds such as Alopecurus myosuroides blackgrass and Avena spp. Patch spraying, or applying herbicide to only the badly infested areas of fields, is another means of reducing total herbicide use.

When resistance is first suspected or confirmed, the efficacy of alternatives is likely to be the first consideration.

The use of alternative herbicides which remain effective on resistant populations can be a successful strategy, at least in the short term. The effectiveness of alternative herbicides will be highly dependent on the extent of cross-resistance. If there is resistance to a single group of herbicides, then the use of herbicides from other groups may provide a simple and effective solution, at least in the short term.

For example, many triazine-resistant weeds have been readily controlled by the use of alternative herbicides such as dicamba or glyphosate. If resistance extends to more than one herbicide group, then choices are more limited. It should not be assumed that resistance will automatically extend to all herbicides with the same mode of action, although it is wise to assume this until proved otherwise. In many weeds the degree of cross-resistance between the five groups of ALS inhibitors varies considerably.

Much will depend on the resistance mechanisms present, and it should not be assumed that these will necessarily be the same in different populations of the same species. These differences are due, at least in part, to the existence of different mutations conferring target site resistance. Consequently, selection for different mutations may result in different patterns of cross-resistance. Enhanced metabolism can affect even closely related herbicides to differing degrees.

For example, populations of Alopecurus myosuroides blackgrass with an enhanced metabolism mechanism show resistance to pendimethalin but not to trifluralin, despite both being dinitroanilines. This is due to differences in the vulnerability of these two herbicides to oxidative metabolism. Consequently, care is needed when trying to predict the efficacy of alternative herbicides.


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The use of two or more herbicides which have differing modes of action can reduce the selection for resistant genotypes. Ideally, each component in a mixture should:. No mixture is likely to have all these attributes, but the first two listed are the most important. There is a risk that mixtures will select for resistance to both components in the longer term.

One practical advantage of sequences of two herbicides compared with mixtures is that a better appraisal of the efficacy of each herbicide component is possible, provided that sufficient time elapses between each application. A disadvantage with sequences is that two separate applications have to be made and it is possible that the later application will be less effective on weeds surviving the first application. If these are resistant, then the second herbicide in the sequence may increase selection for resistant individuals by killing the susceptible plants which were damaged but not killed by the first application, but allowing the larger, less affected, resistant plants to survive.

This has been cited as one reason why ALS-resistant Stellaria media has evolved in Scotland recently , despite the regular use of a sequence incorporating mecoprop, a herbicide with a different mode of action. Rotation of herbicides from different chemical groups in successive years should reduce selection for resistance. This is a key element in most resistance prevention programmes.

The value of this approach depends on the extent of cross-resistance, and whether multiple resistance occurs owing to the presence of several different resistance mechanisms. A practical problem can be the lack of awareness by farmers of the different groups of herbicides that exist. In Australia a scheme has been introduced in which identifying letters are included on the product label as a means of enabling farmers to distinguish products with different modes of action. Herbicide resistance became a critical problem in Australian agriculture, after many Australian sheep farmers began to exclusively grow wheat in their pastures in the s.

Introduced varieties of ryegrass , while good for grazing sheep, compete intensely with wheat. Ryegrasses produce so many seeds that, if left unchecked, they can completely choke a field. Herbicides provided excellent control, while reducing soil disrupting because of less need to plough. Within little more than a decade, ryegrass and other weeds began to develop resistance. In response Australian farmers changed methods. Ryegrass populations were large, and had substantial genetic diversity, because farmers had planted many varieties. Ryegrass is cross-pollinated by wind, so genes shuffle frequently.

To control its distribution farmers sprayed inexpensive Hoegrass, creating selection pressure. In addition, farmers sometimes diluted the herbicide in order to save money, which allowed some plants to survive application. When resistance appeared farmers turned to a group of herbicides that block acetolactate synthase. Once again, ryegrass in Australia evolved a kind of "cross-resistance" that allowed it to rapidly break down a variety of herbicides.

Four classes of herbicides become ineffective within a few years. In only two herbicide classes, called Photosystem II and long-chain fatty acid inhibitors, were effective against ryegrass. Recently, the term "organic" has come to imply products used in organic farming. Under this definition, an organic herbicide is one that can be used in a farming enterprise that has been classified as organic. Depending on the application, they may be less effective than synthetic herbicides [ citation needed ] and are generally used along with cultural and mechanical weed control practices.

From Wikipedia, the free encyclopedia. Chemical used to kill unwanted plants. This article may be unbalanced towards certain viewpoints. Please improve the article by adding information on neglected viewpoints, or discuss the issue on the talk page. October Main articles: Rainbow herbicide and Herbicidal warfare. This section needs expansion.

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Bioherbicide Index of pesticide articles Integrated pest management List of environmental health hazards Rainbow herbicides and Herbicidal warfare Soil contamination Surface runoff Weed Weed control Defoliant. February Pesticides Industry.

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Summary in press release here Main page for EPA reports on pesticide use is here. CBC News. Halifax Examiner. Encyclopedia of environment and society. Robbins, Paul, , Sage Publications. Thousand Oaks. Cobb; John P. Reade Herbicides and Plant Physiology. Agricultural Control Chemicals. Advances in Chemistry. In Lichtfouse, E. Sustainable Agriculture Reviews Springer International Publishing.

Pesticide Biochemistry and Physiology. Biochemistry, 4th Edition. Genetic Nature of Resistance Resistance may occur in plants naturally due to selection as the result of random and infrequent mutations or it may be induced through genetic engineering Gressel, ; Devine and Preston, Through selection, where the herbicide is the selection pressure, susceptible plants are killed while resistant plants survive to reproduce without competition from susceptible plants. If the herbicide is continually used, resistant plants successfully reproduce and become dominant in the population Pedersen et al.

In the absence of herbicide treatment, resistant species to an herbicide are not as fit as are susceptible plants. This is because the efficiency of some physiological processes such as photosynthesis is reduced in resistant plants by the alteration of a specific protein that is also the herbicide binding site, so conferring resistance. Since resistant plants are less fit, they reproduce at lower rates and consequently represent a smaller fraction of the number of individuals within a population.

In contrast, some resistance traits do not have the same fitness cost. In those cases, resistant individuals often represent a larger fraction of a population. Consequently, increased tolerance to most herbicides is generally inherited in a polygenic fashion; more than one allele on many genes gives additive tolerance. Some increases in tolerance are due to gene duplications Gressel and Rotteveel, This could give rise to higher levels of detoxifying enzymes.

Resistance is usually inherited on one or at most two major nuclear genes in species where newly resistant biotypes or varieties have appeared Cole and Rodgers, ; Devine and Preston, ; Gressel, Therefore, herbicide resistance is the inherited ability of a plant to survive and reproduce following exposure to a dose of herbicide that would normally be lethal to the wild type. The mutation theory postulates that a genetic mutation occurs within a plant following the application of an herbicide and that this mutation confers resistance to the plant Daniell, Repeated use of herbicides that target the same site of action, or are broken down in plants through similar biochemical pathways, can lead to the selection of individuals with a genetic endowment to survive lethal doses of the herbicide.

On the other hand, Jander et al. Different mutations on the target ALS enzyme can lower its affinity for a wide range of ALS inhibitors, resulting in various patterns of resistance to these herbicides. However, Fischer et al.

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In accordance, tolerance of rice to bispyribac-sodium can be abolished by the simultaneous application of P inhibitors suggesting the involvement of P as a mechanism of selectivity to this herbicide in rice Osuna et al. The natural selection theory is widely regarded as the most plausible explanation for the development of resistance. The theory states that herbicide-resistant species have always occurred at extremely low numbers.

Most herbicides affect a single specific site of action and that site is usually under the control of a single gene, or at most a few genes Gressel, With a single gene mutation, even minor changes in gene expression can confer resistance by modifying the site where an herbicide has its toxic effect; the site of action. The evolution of a resistant population in a species comes about in response to selection pressure imposed by that herbicide or by another herbicide that shares the same site of action.

When a herbicide exerts selection pressure on a population, plants possessing the resistance trait have a distinct advantage Daniell, When an herbicide effectively controls the majority of susceptible members of a species, only those possessing a resistance trait can survive and produce seeds for future generations.

As known, plants exhibit a wide range of diversity. The plants in a population with characteristics enabling them to survive under a wide range of environmental and other adverse conditions will be the ones to produce seeds that maintain these survival characteristics. The plants less adapted do not survive and hence only the fittest plants produce seeds. Plants that possess characteristics, such as resistance to herbicides that are not common to the entire species are referred to as biotypes.

When most of the susceptible members of a population are controlled, those resistant biotypes are able to continue growing and eventually to produce seeds. The seed from the resistant biotypes ensures that the resistance trait carries into future seasons. If the same herbicide is used year after year, or several times during a single season, the resistant biotypes continue to thrive, eventually out-numbering the normal susceptible population Powles et al. Consequently, relying on the same herbicide or herbicides with the same mode of action for weed control creates selection pressure that favors the development of herbicide-resistant biotypes.

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Contributing Factors for Plant Resistance Three mechanisms have been identified that account for herbicide resistance Devine and Preston, The first deals with alterations in the target site of the herbicide. An herbicide has a specific site within the plant where it acts to disrupt a particular plant process or function. If this target site is somewhat altered, the herbicide molecule may be unable to exert its phytotoxic action effectively.

Target site insensitivity is the most commonly reported mechanism of herbicide resistance. Herbicide resistance caused by target site changes often provides high levels of resistance Preston, and is often dominant. Dinelli et al. They further indicated differences in glyphosate uptake, translocation, or metabolism were disregarded as potential resistance mechanisms in L. Further, the mechanism of resistance in L. The second mechanism is the enhanced metabolism of the herbicide. Metabolism within the plant is one mechanism a plant uses to detoxify foreign compounds such as herbicides.

A plant with an enhanced ability to metabolize an herbicide can potentially inactivate it before it can reach its site of action within the plant. Compartmentation of the herbicide represents the third mechanisms for herbicide resistance. Plants are capable of sequestering foreign compounds within their cells or tissues to prevent the compounds from causing harmful effects. When an herbicide is placed within a restricted compartment, it cannot reach its site of action and thus is unable to kill the plant.

The proposed mechanism for this resistance is that the resistant biotypes restrict the movement of the herbicides within themselves and do not allow the herbicides to reach their sites of action. A high rate of seed production with most seed germinating within a year can accelerate the evolution of resistance. When susceptible plants are removed from the population by the herbicide, prolific seed production by resistant plants rapidly shifts the population toward resistance.

High seed production coupled with genetic variation increases the probability that resistance will evolve. Herbicides with prolonged soil residual activity exert selection pressure for a longer time period since they kill most of the susceptible plants that germinate over a growing season. An herbicide with a single target site controlled by few genes is more likely to encounter plants with mutations for resistance than is an herbicide with several modes of action Gronwald, A high effective kill rate rapidly depletes susceptible genes from the population and the result is a rapid increase in resistance among the progeny of a few initial resistant plants Orson and Oldfield, Like target site changes, selection for enhanced metabolism can also occur in response to repeated applications of the same herbicide or of a group of herbicides that are vulnerable to the same detoxification enzymes.

Selection with enhanced metabolism is more rapid when an herbicide is used continuously at or below the low recommended rate. This allows a gradual increase of the biotypes that are more able to metabolize the compound. It is well established that persistent herbicide application to a plant population is a strong selection pressure for individuals carrying genes conferring herbicide resistance.

Biotypes with enhanced metabolism have a lower level of resistance than those expressing resistance through site of action changes. Plants expressing any genetically-endowed traits enabling survival in the presence of the herbicide have a strong advantage and may come to dominate the population. The severity and time-period over which resistance can develop varies dependent upon the herbicide s used and biological, agro-ecological and managerial factors Powles and Holtum, Cross Resistance to Herbicides Cross resistance is defined as the expression of a genetically-endowed mechanism conferring the ability to withstand herbicides from different chemical classes.

There are two broad cross resistance categories; target site cross resistance and non target site cross resistance Hall et al. Target Site Cross Resistance It occurs when a change at the biochemical site of action of one herbicide also confers resistance to herbicides from different chemical classes that inhibit the same site of action in the plant. Target site cross resistance does not necessarily result in resistance to all herbicide classes with a similar mode of action or indeed all herbicides within a given herbicide class.

Herbicides are active at one or more target sites within a plant. Target sites are enzymes, proteins, or other places in the plant where herbicides bind and thereby disrupt normal plant functions Saari et al. One example is ALS that is involved in synthesizing branched-chain amino acid s, valine, leucine and isoleucine. Several classes of herbicides are known to inhibit ALS, such as the sulfonylureas, imidazolinones, triazolopyrimidine sulfonanilides and pyrimidinyl oxybenzoates, by binding to a relic quinone-binding site Tan and Medd, , causing dysfunction of the enzyme and reducing the synthesis of certain amino acid s that are necessary for protein synthesis Nemat Alla and Hassan, ; Devine and Preston, These highly selective ALS-inhibiting herbicides are very valuable for weed management in a wide range of crops worldwide.

These ALS-inhibiting herbicides differ in chemical structure but are active at the same target site. When a plant expressing resistance to an herbicide also demonstrates resistance to other herbicides that target the same plant process even though the plant has not been exposed to the other herbicides, the resistance is termed cross-resistance on a target-site basis target-site cross-resistance. Consequently, cross-resistance refers to resistance to an herbicide the plant has not been previously exposed to but that has a mode of action similar to the original herbicide.

They detected the involvement of Ps in E. The dose-response studies confirmed cross-resistance in resistant E. ALS assays demonstrated that, unlike resistant E. Thus, binding differences between both herbicides at the target site are suggested. The study of Osuna et al. The considerable variation in the level of resistance across and within various ALS-inhibiting herbicide chemistries is likely to be due to subtly different binding by particular herbicides on the ALS enzyme and different mutations of ALS.

Evidences from competitive binding studies show that ALS-inhibiting herbicides bind to the same or closely overlapping sites on ALS Devine and Preston, The wide variation in target site cross resistance amongst biotypes with resistant ALS enzyme implies that there are a number of different functional mutations of the ALS gene. Resistant biotypes in many cases have modified ALS genes with one or more point mutations causing reduced sensitivity to the ALS-inhibiting herbicides Tan and Medd, In addition, Holtum et al.

Substitutions of threonine, alanine, serine, histidine and glutamine for this proline residue have been observed in some species. There are several possible mutations of the ALS gene, which will confer resistance to these herbicides and yet retain enzyme function. It is likely that these different mutations in the ALS gene provide different levels of target site cross resistance within and between ALS-inhibiting herbicide chemistries.

A Rotala indica accession was tested for resistance to the sulfonylurea herbicide, imazosulfuron Kuk et al. The accession was confirmed to be resistant and was cross-resistant to other sulfonylurea herbicides, bensulfuron-methyl, cyclosulfamuron and pyrazosulfuron-ethyl, but not to imidazolinone herbicides, imazapyr and imazaquin. The resistance mechanism of R. Since the level of resistance to other sulfonylurea herbicides in the enzyme assay was much lower than that in the whole plant assay, other mechanisms of resistance, such as herbicide metabolism, or reduced absorption and translocation may be involved.

Many researchers have shown that the mechanism of resistance to ALS inhibitors is alteration of the target enzyme Saari et al. A number of different mutations can endow resistance to various ALS-inhibiting herbicides without any significant impairment of enzyme function in vivo. Two chemically dissimilar herbicide groups, the aryloxyphenoxypropionic acid and cyclohexanedione herbicides target the enzyme ACCase Devine and Shimabukuro, These herbicides are lethal to many Graminaceae but are harmless to dicot species and have therefore become widely employed for grass weed control.

Varying levels of resistance to haloxyfop-R-methyl and sethoxydim, the Accase inhibitors, were found in itchgrass Rottboellia cochinchinensis biotypes and cross-resistance among graminicides was confirmed Avila et al. No differences in the translocation or metabolism of sethoxydim were observed between resistant and susceptible biotypes. These results suggest that cross resistance in itchgrass biotypes is conferred by a reduced sensitivity of the target enzyme.

Selection either with an aryloxyphenoxypropionic acid herbicide, or a cyclohexanedione herbicide, has led to target site cross resistance to both classes. Two biotypes of Alopecurus myosuroides have been documented as highly resistant to the aryloxyphenoxypropionic herbicides as a result of resistant ACCase Hall et al. The ACCase from these biotypes is also resistant to cyclohexanedione herbicides. Resistance to aryloxyphenoxypropionic acid herbicides in several biotypes of the wild oat species Avena fatua and Avena sterilis is also endowed by resistant forms of the ACCase enzyme Devine and Preston, Herbicides from different chemical classes bind to overlapping, but not identical sites on the target enzyme.

The patterns of resistance of ACCase to herbicides can be strikingly different even among resistant biotypes of the same species. Moreover, aryloxyphenoxypropionic acid and cyclohexanedione herbicides cause also a rapid depolarization of plant cell membrane potentials by allowing the influx of protons Shimabukuro, This ability to depolarize the membrane potential following removal of the herbicide is not observed with susceptible biotypes.

Powles and Holtum recorded the occurrence of repolarisation of the membrane potential in resistant L. DiTomaso claimed a direct connection between the differential abilities of the resistant L. However, the changes of the enzyme appear to be less frequent than changes in glyphosate translocation processes Duke, ; Koger et al. Multiple biochemical factors appear to contribute to resistance and an incompletely dominant single locus nuclear gene has been linked to glyphosate resistance Zelaya et al. Biochemical studies point to reduced translocation of glyphosate as a major reason for resistance Vaughn, ; Feng et al.

Resistance to glyphosate has been reported in Eleusine indica Lee and Ngim, and in Conyza canadensis Main et al. The primary mode of action of glyphosate is the competitive inhibition of the plant enzyme EPSPS which catalyses the penultimate step in the shikimate pathway Franz et al. Studies of the molecular and genetic basis of evolved resistance to glyphosate in biotypes of E.

Feng et al. Another target site is the photosynthetic electron transfer at Photosystem-II PSII , which is inhibited by numerous chemically dissimilar herbicide classes such as triazines and substituted ureas Mengistu et al. PSII is an essential component of the photosynthetic apparatus in plants that uses light energy to split water, releasing oxygen, protons and electrons. The electron flow from PSII is essential to plant life. The D1 protein has an extraordinarily high rate of turnover, faster than any other known thylakoid protein. Continual synthesis of D1 protein is necessary to replace photo-damaged D1, which is then quickly degraded by proteolysis Rintamaki et al.

Classical PSII inhibitors, such as the herbicides triazines and phenylureas, bind to the D1 protein in a stoichiometric fashion. Upon herbicide binding, the electron flow from PSII is disrupted and carbon dioxide fixation ceases. Since the electron acceptor in the inhibited PSII is now not able to accept electrons from photo-excited chlorophyll, free radical s are generated and chlorosis develops Rutherford and Krieger-Liszkay, Herbicide resistance is due to target site resistance endowed by a modification at the herbicide target site, the D1 protein of PSII Gronwald, It is noteworthy that biotypes highly resistant to triazine herbicides as a result of a modified D1 protein are not resistant to the chemically distinct substituted urea herbicides, despite the fact that the substituted urea herbicides are also potent PSII inhibitors Gronwald, A plausible explanation is that the substituted urea and triazine herbicides probably bind to overlapping, but not identical, sites in PSII Trebst, Non Target Site Cross Resistance It is defined as cross resistance to dissimilar herbicide classes conferred by a mechanism s other than resistant enzyme target sites.

Heap and Knight elucidated that many L.

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Similarly, Matthews showed that an initially susceptible L. Thus selection with an ACCase-inhibiting herbicide can lead to resistant populations that display non target site cross resistance to ALS-inhibiting herbicides without exposure to these herbicides. The resistance of these biotypes is probably resulted from an enhanced rate of herbicide metabolism by Ps. Sweetser et al. Malathion which inhibits the Pdependent detoxification of primisulfuron, a sulfonylurea herbicide, in microsome preparations from maize can inhibit chlorsulfuron metabolism and reduce chlorsulfuron resistance in the cross-resistant biotype Christopher et al.

This reversal of resistance by malathion confirms that detoxification plays a major role in chlorsulfuron resistance in this biotype. On the other hand, the rate of metabolism of diclofop-acid in a resistant L. The location of this remaining herbicide might be sequestered away from the metabolizing enzymes and the active site.

It appears likely that enhanced metabolism is the common mechanism of herbicide resistance operating in the resistant biotype. Similarly, a L. The mechanism endowing triazine and substituted urea herbicide resistance has been identified in these biotypes as due to enhanced rates of herbicide metabolism Burnet et al. The triazine herbicide simazine is metabolized in the resistant biotypes 2 to 3 times the rate of metabolism attained by the susceptible biotype Burnet et al.

Similarly, the substituted urea herbicide chlortoluron is also metabolized at an enhanced rate Burnet et al. The developed resistance of Alopecurus myosuroides biotypes following selection with substituted urea herbicides, particularly chlortoluron is not due to a resistant PSII target site but due to an enhanced rate of metabolism of chlortoluron and isoproturon Hall et al. Similarly 1-aminobenzotriazole inhibits simazine metabolism and reduces the level of simazine resistance Burnet et al. Microsomal membrane preparations isolated from a resistant and a susceptible population displayed low intrinsic rates of chlortoluron metabolism Holtum et al.

Nemat Alla found that 1-aminobenzotriazole increased phytotoxicity of alachlor, metolachlor and atrazine concluding greater persistence in contact with their target sites. Moreover, greater persistence of these herbicides was concluded as a result of P blockage, which would retract their degradation. Therefore, the enzymic basis for the enhanced metabolism resistance mechanism in these biotypes is likely to be due to increased activity of Ps, which have the capacity to either de-alkylate or ring-hydroxylate these herbicides.

Multiple Resistance to Herbicides Multiple resistance is the expression-within individuals or populations- of more than one resistance mechanism. Multiple resistant plants may possess from two to many distinct resistance mechanisms and may exhibit resistance to a few or many herbicides. When a plant that has been exposed to herbicides that attack different target sites expresses resistance to more than one of these herbicides, that is termed multiple resistance Hall et al.

The simplest cases are where an individual plant or population possesses two or more different resistance mechanisms which provide resistance to a single herbicide, or class of herbicides. More complicated are situations where two or more distinct resistance mechanisms have been selected either sequentially or concurrently by different herbicides and endow resistance to the classes of herbicide to which they had been exposed. The most complicated and difficult to control situations are where a number of resistance mechanisms, involving both target site and non target site resistance mechanisms, are present within the same individual Powles and Holtum, Most cases of herbicide resistance in plants involve a single mutation or modification in some function so that the species is resistant or cross-resistant.

Rarely does a single plant express resistance to several herbicides that affect different target sites. Consequently, multiple-resistance refers to resistance to more than one class of herbicides with very different modes of action in which more than one basis for resistance is involved. Multiple resistance has been reported on a number of occasions when herbicides of different chemical classes have been applied to a population either as a mixture, or sequentially, following the development of resistance to the first herbicide Hall et al.

A biotype of Amaranthus retroflexus was developed target site resistance to triazine herbicides and when diuron was applied to this resistant population, resistance developed to diuron Lehoczki et al. Molecular Biology for Herbicide Resistance The emerging field of molecular ecology aims to improve the ecological predictability of transgenic crop plants Sandermann, Selectivity between crop and weed are due to catabolic degradation of the herbicide by the crop, closely related weeds are to be expected to have similar catabolic pathways as the crop.

Herbicides can interfere with many different plant processes, usually acting at a single molecular site, generating profound metabolic consequences that lead eventually to the death of the plant. Herbicide resistance can be conferred by several mechanisms, the most important of which are target site insensitivity and rapid metabolic transformation of the herbicide to inactive products Devine and Preston, The ability to transform any major crop with herbicide tolerance genes means that new uses for individual herbicide chemicals can be created, maximizing selectivity between weeds and the crop by manipulating the properties of the crop plant, rather than chemistry.

Selectivity is enhanced by inserting exogenous resistance genes into the crops or by selecting natural mutations. Biotechnologically-Derived Herbicide Resistant Crops The real values of biotechnologically-derived herbicide resistant crops come from instances where there really are no viable weed control methods e. The easiest way to obtain selectivity among closely related species is to engineer resistance to a general herbicide into the crop Sankula et al. The calibrational use of antisense and knockout techniques with known herbicide targets yields inhibited or dead plants Haake et al.

So, biotechnology has been used to generate target site herbicide resistant crops by transfer of field or laboratory generated mutants into crop varieties. As all the mutations were found at a low frequency; one in a million or less, the resistant traits are not of near neutral fitness. The csr gene encodes an enzyme only insensitive to sulfonylureas whereas the imr1 mutant ALS gene also isolated from Arabidopsis thaliana is insensitive to imidazolinones Sathasivan et al. By creating suitable hybrid ALS gene from both of these mutants, transgenic tobacco biotypes could be generated displaying high level resistance to both classes of herbicides.

It is a key pathway linking photosynthetic carbon reduction to the synthesis of aromatic amino acid s, auxin and diverse secondary products in plants. A fitness penalty with any target site herbicide resistant crops could be assumed due to the fact that if the resistant mutation was neutral there would be naturally-resistant populations pre-existing. Also, glufosinate resistance was similarly achieved in tissue culture by over-expression of the gene encoding its target site with overproduction of glutamine synthase Sankula et al.

Additionally, transgenic tobacco plants overexpressing protoporphyrinogen IX oxidase protox five-fold in chloroplasts are resistant to a discriminatory dose of 20 mM acifluorfen, which severely inhibited the wild type Lermontova and Grimm, The results of incomplete suppression of gene expression achieved by antisense or overexpressive co-suppression have an advantage over the knockout or deletion of genes for elucidating potential targets. Biotechnologically-derived herbicide resistant wheat and rice are obtained from the insertion of a gene into wheat or rice conferring resistance to a broad spectrum herbicide Gressel, a, b.

The transgenes will allow problems of resistance to be overcome. Two types of gene have been used to generate herbicide-resistant crops; where the gene product detoxifies the herbicide and where the herbicide target has been modified such that it no longer binds the herbicide. Nevertheless, there have been more problems with the transgenics than the mutants. The magnitude of resistance with transgenics is not as high as it is with the natural mutations Gruys et al.

Transgenics will be less resistant than target site mutants bearing the same transversion. Recurrent selection of a natural mutant will select for homozygous resistant individuals. This cannot happen with the generation of transgenics, which bear and express both the native and transgenic enzymes. Thus, transgenic plants with target site resistance are functionally heterozygous and will remain so despite recurrent selection.

When the herbicide is applied, target site of biotechnologically-derived herbicide resistant crops must depend on the transgenic derived enzyme while the native is inhibited; perhaps even causing phytotoxic precursors to accumulate Lee et al. So, problems with some resistant crops still found, suggesting that the critical balance of transgenic and native enzymes is not optimal.

Andrew detected stem brittleness and cracking in untreated glyphosate-resistant soybean suggesting an overproduction of product leading to increased lignin formation when both the native and transgene derived enzymes are operative. The problems arising from the functional heterozygote status of transgenic target site resistant plants could be overcome by enhancing the metabolism of the herbicide through gene coding for an enzyme degrading herbicide together with target-site resistance Mannerlof et al.

Metabolically-Resistant Biotechnologically-Derived Herbicide Resistant Crops More genes for catabolic resistance to several herbicides could be able to rapidly generate herbicide-resistant crops with metabolic resistance. In addition to genes encoding insensitive target sites, some detoxification genes were also identified. Many crops bearing transgenes coding for highly specific enzymes that metabolically catabolize herbicides have been generated Cole and Rodgers, The expression of plant P transgenes conferred phenylurea resistance Inui et al.

On the other hand, transgenes encoding maize GSTs increased the level of herbicide resistance in many plant species Jepson et al. Unlike the target site resistances, the crops generated with metabolic resistances seem to be problem-free, with little metabolic load conferred by generating the small amount of enzyme needed. Inhibitors of protox induce photodynamic death of plants within h in bright sunlight. A gene encoding the plastid-located protox of Arabidopsis has been introduced into the genome of tobacco Nicotiana tabacum plants Lermontova and Grimm, ; Cobb and Kirkwood, The transformants were screened for low protoporphyrin IX accumulation upon treatment with the diphenyl ether-type herbicide acifluorfen.

Leaf disc incubation and foliar spraying with acifluorfen indicated the lower susceptibility of the transformants against the herbicide. The resistance to acifluorfen is conferred by overexpression of the plastidic isoform of protox. The overproduction of protox neutralizes the herbicidal action, prevents the accumulation of the substrate protoporphyrinogen IX and consequently abolishes the light-dependent phytotoxicity of acifluorfen.

Similarly, strains of Conyza bonariensis contain a complex of enzymes capable of detoxifying the reactive oxygen species generated by the PSI blocker paraquat and keeping the plants alive until the paraquat is dissipated Ye et al. Nonetheless, like the native gene, the modified gene conferred a high level of resistance to the herbicide oxyfluorfen in a seedling growth test Yang et al.

Jung et al. When this gene is expressed in transgenic rice plants, the Mx Protox protein is dually targeted into plastids and mitochondria via ambiguous transit signals, increasing resistance to oxyfluorfen. Overexpression of the Mx Protox transgene in rice confers a fold level resistance to oxyfluorfen over the wild-type rice Ha et al.

Higher herbicide resistance in transgenic plants expressing Mx Protox is simply due to the overexpression of Mx Protox protein in both chloroplasts and mithochondria with 5- and fold increase in Protox activity, respectively, over the wild-type rice Jung et al. Oxidative stress. Statistical analysis In each experiment, four pots containing four plants were used per treatment.

Results Characterization of the nanocapsules containing atrazine The encapsulation efficiency, colloidal stability and physicochemical characteristics of the polymeric nanocapsules with and without atrazine have been described previously [ 20 ]. Download: PPT. Herbicidal activity assays Symptom evolution and weight analysis. Fig 2. Symptom evolution in B. Fig 3. Shoot dry weights of B. Physiological parameters. Fig 4. Maximum photosystem II quantum yields of B.

Fig 5. Leaf gas exchange parameters of B. Oxidative stress parameters. Fig 6. Oxidative stress parameters of B. Discussion The development of modified release systems for agrochemicals has increased in recent years, together with the need to evaluate the effectiveness of these systems in controlling target species [ 7 ]. References 1. Life in a contaminated world. Chen HD, Yada R. Nanotechnologies in agriculture: New tools for sustainable development. Trends Food Sci Tech. View Article Google Scholar 3. Perspectives for nano-biotechnology enabled protection and nutrition of plants.

Biotechnol Adv. Applications of nanomaterials in agricultural production and crop protection: A review. Crop Prot. View Article Google Scholar 5. Applications of controlled release systems for fungicides, herbicides, acaricides, nutrients, and plant growth hormones: a review. Adv Sci Eng Med. View Article Google Scholar 6.

Solid lipid nanoparticles co-loaded with simazine and atrazine: Preparation, characterization, and evaluation of herbicidal activity. J Agric Food Chem. Kah M, Hofmann T. Nanopesticide research: Current trends and future priorities. Environ Int. Quina F.

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Nanotecnologia e o meio ambiente: perspectiva e riscos. Quim Nova. View Article Google Scholar 9. Nanopesticides: state of knowledge, environmental fate, and exposure modeling. Crit Rev Environ Sci Technol. View Article Google Scholar Controlled pesticide release from biodegradable polymers. Cent Eur J Chem. Guia de herbicidas. Londrina, Livroceres; Hess DF. Light-dependent herbicides: An overview. Weed Sci. Impacts of atrazine in aquatic ecosystems.

Rev Bras Eng Agric Ambient. Dalton RL, Boutin C. Comparison of the effects of glyphosate and atrazine herbicides on nontarget plants grown singly and in microcosms. Environ Toxicol Chem. Influence of light intensity on the toxicity of atrazine to the submerged freshwater aquatic macrophyte Elodea canadensis. Ecotoxicol Environ Saf. Atrazine promotes biochemical changes and DNA damage in a Neotropical fish species.

A risk assessment of atrazine use in California: human health and ecological aspects. Pest Manag Sci. Characterization of atrazine-loaded biodegradable poly hydroxybutyrate-co-hydroxyvalerate microspheres. J Polym Environ. Poly epsilon-caprolactone nanocapsules as carrier systems for herbicides: Physico-chemical characterization and genotoxicity evaluation.

J Hazard Mater. Application of poly epsilon-caprolactone nanoparticles containing atrazine herbicide as an alternative technique to control weeds and reduce damage to the environment. The return of a forgotten polymer—Polycaprolactone in the 21st century. Prog Polym Sci. Ecotoxicological evaluation of poly epsilon-caprolactone nanocapsules containing triazine herbicides. J Nanosci Nanotechnol. Arbuscular mycorrhizas increase survival, precocity and flowering of herbaceous and shrubby species of early stages of tropical succession in pot cultivation.

J Trop Ecol. The water culture method of growing plants without soil. California Agricultural Experiment Station. Murchie EH, Lawson T. Chlorophyll fluorescence analysis: a guide to good practice and understanding some new applications.