Modes of Herbicide Action

Abstract

Weed Management is one of the most important crop intervention practice to counter crop loss. Different physical, mechanical, biological, and chemical methods are employed for the successful management of weeds. Among these chemical weed management practices focus on managing weeds using several chemical formulations which are commonly known as herbicides. Herbicides control the weed species through interference, mitigation, and disruption of the biochemical and physical processes of a cell. When herbicides are applied to a plant, it gets absorbed through plant surfaces and gets translocated to the specific site of action where it produces toxicity in the physiological and biochemical processes and ultimately check the growth and development of plant species. The sequential process from the introduction of herbicides to till it kills a plant is known as herbicides modes of action. The herbicides modes of action can be studied on nine different headings where the chemical group present in each herbicide acts on specific sites and interferes with the normal functioning of such sites ultimately checking the growth and development of a plant. This chapter is aimed at decoding the specific herbicide action in relation to its chemical family, translocation, action mechanism, and injury produced in the weed species.

1. Introduction

The global demand for food crops is rapidly increasing with the increase in the world’s population, on other hand production of crops is constrained by several factors such as weeds pest, insects, and diseases, among these all weeds are one of the major factors that can cause loss of productivity of field crops. Weeds are any plants that are grown in undesirable places and compete with crops plants for nutrients, sunlight, moisture, and other growth factors. Anything that grows in unintended places are generally referred to as weeds. According to Gharde [1], weeds are notorious yield reducer than pests, disease, and insects, which are thought to cause an estimated loss of 11billion USD in 10 major crops, which causes 31.4% loss in soybean, 30.8% in green grams, 25.3% in maize, 21.4% in mustard, 18.6% in wheat and 21.4% in direct-seeded rice. Reduction of crop yield in crops is due to competition between crops and weeds for space and other growth factors. Yield loss of crops due to weeds depends on several factors such as weed emergence time, weed density, types of weeds, competition ability of crops, and if left uncontrolled, they can cause 100% loss in crop production [2]. The successful and strategic management of weeds can decrease the yield loss significantly, which can ensure more grain harvest. The management of weeds has become one of the most researched aspects in the field of crop science. In small farm size, it can be managed through hand weeding or mechanical weeding machines like cono-weeder and weed-roller whereas its management in the large farms has become a problematic issue. Mostly in the case of commercial cultivation weeds species are mostly managed by using different pre-emergence and post-emergence herbicides. With the increase in the weed resistance towards these herbicides, there is a need for weed science research focusing on herbicide resistance and herbicide mode of action. In a study carried out by Heap [2], it was observed a total of 511 unique cases of herbicide resistance belonging to 266 weed species (153 dicot and 133 monocots) have been reported globally out of which major herbicide-resistance weed species were reported in wheat followed by maize, rice, soybean, spring barley, and cotton. Herbicide-resistant weed populations are rapidly evolving as the process of natural selection and development of traits by weeds to escape the action of herbicides. The graphs show that, herbicide resistance has been steeply increasing from 7 cases in 1975 to 509 cases at the end of 2020. The major herbicide resistant traits were observed in the weed family belonging to Poaceae or grass. The five major weed families Poaceae, Asteraceae, Brassicaceae, Amaranthaceae, and Chenopodiaceae account for 70% of total herbicide resistance cases though they only include 50% of total principal weeds [3]. More weed species are resistant to ALS inhibitors, with the reported 160 species, which is followed by Photosystem II inhibitors. Glyphosate one of the most common post-emergence herbicide used as broad broad-spectrum control of weeds has become less effective due to intensive use of herbicide leading to the quick emergence of glyphosate-resistant biotypes [4]. Mitigating herbicide resistance has become one of the most important things to consider during crop production. The herbicide resistance in plants can be somehow coped with by introducing different herbicides of the varied mode of action, crop rotation, and using integrated weed management practices in crops. The successful management of herbicide resistance in input-intensive agriculture can be combated by diversifying the herbicide products, cultivating crops with combined herbicide resistance, increasing reliance on pre-emergence herbicides than post-emergence herbicide, breeding weed-competitive crop cultivars, and advances in site-specific and precision weed management [5].

The advancement in the field of genetics, plant physiology, chemistry, and plant science has made open to many researchers to understand the basis and mechanism of herbicide resistance. Herbicide resistance mechanisms can be target site resistance, non-target site resistance, cross-resistance, and multiple resistance [6]. The target site herbicide resistance is due to the mutation in genes encoding herbicide enzymes, non-target herbicide resistance is due to the reduced amount of herbicide active ingredients through reduced absorption or translocation. The cross-resistance is due to the use of several herbicides with the same mode of action and multiple resistance is due to two or more herbicide resistance mechanisms in response to a sequential selection of herbicides with a different mode of action. The herbicide mode of action explains how the active ingredients present in commercial herbicide formulation act on plants. The mode of action of herbicide is variable based on the chemical composition of their active ingredients and the weeds species in which they act on. Some herbicides act on plants through the root system, some act on photosynthesis and photosystem, and some herbicides are found to act on the cell membrane and enzymatic pathways. Understanding the mode of action of herbicides is important for the management, classification, organization, and hierarchy of the herbicides as it also provides an insight into herbicide resistance, which has become a problem in sustainable agricultural management [7].

Herbicide enters into a plant system through several different mechanisms. These acting mechanism differs in between the herbicide in relation to the chemical nature that is present in the active ingredients of the herbicide. The herbicide mode of action discusses on the sequence of events from the introduction of herbicide in the environment till its kills the plant through toxicity produced by the chemicals presents in the active ingredients of the herbicide, whereas the herbicide mechanism of action discusses on physiological and biochemical changes caused by the herbicide within plant system. Understanding the mode of herbicide action helps to relate the chemistry of herbicide and the physiology that exists within a plant. The knowledge of acting mechanisms helps to cope with the problem of herbicide resistance and helps to maximize the efficacy of herbicide during weed management. The study incorporates the parts of how herbicide gets absorbed in the plant surface and how they act on the physiology of weed plant and injure them to eliminate them from the competition with crop species. The knowledge on general chemistry, plant physiology, genetics, and plant science can help to decipher the roles that lie beyond the herbicide mode of action. In general herbicides are classified as pre-emergence and post-emergence herbicides. In pre-emergent herbicide the mode of action is principally through absorption from root zones, whereas in the case of post-emergent herbicide the mode of action is mainly through absorption from foliar parts. In general, to acts as an herbicide on a plant, it must pass through certain sequential stages of contact, absorption, movement, toxicity, and death of weed species and the mode of herbicide action to produce injury includes inhibition, disruption, interruption, and mitigation of regular growth of weed species [8]. The exploration of the mode of herbicide action is dynamic and new modes of action of herbicide has been constantly adding, which is helping for the discovery of new herbicide. Based on the site of action of herbicide and mode of action altogether 22 types of herbicide action have been developed. Therefore, understanding the mode of herbicide action can substantially help in understanding the mechanism of herbicide resistance and exploring new strategies to cope with herbicide resistance. So, the chapter focuses on different herbicide mode of action in relation to their chemical family, mechanism of action, translocation, and toxicity. In recent years, a perennial weed of Roegneria genus commonly known as wild rye, which is widely distributed in China has shown tolerance to ACCase inhibitor herbicides like fenoxaprop, clodinafop and pinoxaden [9]. It was observed that the ACCase activity were increased by 1.46 and 1.34-fold in wild rye and wheat plant after 72 hours of fenoxaprop treatment than at 0 hrs of treatment as shown in Figure 1. It was suggested that the enhanced activity of ACCase is due to enhanced metabolism of herbicide, leading to herbicide tolerance.

Figure 1.

Increase in the enzymatic activity of ACCase with increase in treatment time in wild oat and wheat plant depicting tolerance to fenoxaprop [9].

2. Lipids synthesis inhibitors

These kinds of herbicides are those which cause disruption in lipid synthesis and check the growth of plants through rupture of the cell wall and cell oozing. The herbicide having group 1 site of action falls under these categories, where herbicide inhibits Acetyl CoA Carboxylase (ACCase) enzyme which is required for fatty acids synthesis that forms a part of phospholipid bilayer in the cell membrane of plant cells. The inhibition of (ACCase) enzymes restricts the formation of cell wall in meristematic regions and ultimately kills the plant cell. The (ACCase) inhibitors herbicides are used for the selective control of weed species, which are found to have resistance with glyphosate herbicide [10]. The mechanism begins when the herbicide comes in contact with plant species and it gets translocated in the meristematic region through phloem where it inhibits the meristematic activity producing necrotic symptoms in the growing tissues after one week of application [10, 11]. The chemical family of this herbicide includes aryloxyphenoxylpropinate, cyclohexanedione, and phenylpyrazole which are applied as post-emergence herbicides to control grassy weeds in broadleaf crops [11]. The common herbicides include fenoxaprop, fluazifop, diclofop, quizalofop, clethodim, sethoxydim, and Pinoxaden. These groups of herbicides are applied through foliar spay and translocated through phloem in meristematic regions. The major injury includes plants turn brown, chlorotic symptoms can been seen in the leaves, and vein browning and purpling can be seen after 3-4 days of herbicide application. (ACCase) inhibitor herbicides are short-lived in soil, relatively low solubility in soil, and used relatively in low rates. They have low leaching potential and are found to be less hazardous to the environment. (ACCase) inhibitors herbicides are found to have resistance against 43 grass weeds species [12].

3. Amino-acid synthesis inhibitors

These kinds of herbicide are found to have two sites of action. They belong to group 2 Acetolactate Synthetases (ALS) that catalases the synthesis of branched-chain amino acids, such as leucine, isoleucine, and valine. The inhibition of these enzymes restricts the biosynthesis of these amino acids, which are the essential part of protein necessary for cell membrane formation. The ALS inhibitors are found to have effect on the reproduction of some plant species such as inducing male sterility and their potency, which can act extremely at low concentrations, and the rapid evolution of resistance to these herbicides in some plants [13, 14]. They are the largest group of herbicides that are post-emergence selective in nature. The chemical ingredients are of these herbicides are absorbed through roots and foliage and translocated through both xylem and phloem. The major injury of ALS inhibiting herbicide includes interveinal chlorosis, purpling and root pruning. The major chemical family includes sulphonyl urea, Imidazolinone, Sulfonylurea, and Triazolopyrimidine [15]. The common herbicides include imazamox, imazapic, imazaquin, imazethapyr, nicosulfuron, metsulfuron, triasulfuron, chlorsulfuron, rimsulfuron, prosulfuron, pyroxsulam, diclosulam, and flumetsulam. In a study conducted by Dor [16], the tissue culture of broomrape was found to be more sensitive to imazapic in which a concentration of 0.05μM significantly decreased the biomass and a concentration of 10μM caused blackening of died callus, which suggests that free amino acid content increased with the increased in the concentration of imazapic as shown in Figure 2.

Figure 2.

The control of callus biomass is more effect in lower concentration than in higher concentration of amino acid inhibitor herbicide imazapic [16].

The second group of herbicides that causes amino-acid synthesis inhibition are group 9 herbicides, which causes blockade in the production of enzymes from 5- enoylpuruvyl Shikimate-3-phosphate (EPSP) pathway. The enzymes in EPSP pathway catalyze the biosynthesis of aromatic amino acids like phenylalanine, tyrosine, and tryptophan. These amino are essential for protein synthesis and the absence of them causes cell membrane disintegration. The broad-spectrum herbicide glyphosate belongs to the chemical family which checks the EPSP pathway [17]. Herbicides having this mode of action is non-selective and absorbed through phloem tissues. They produce major injury in foliage, causing foliage discolorations stunting and killing the plant ultimately. The growth and development of the plant is check right after the herbicide application; the major symptoms appear only after a few days of application.

4. Growth regulators

Growth regular mode of mechanisms of herbicide checks the growth of plant by modulating the balances of growth hormones and regulators within the plant system. The herbicide having this mode of action belongs to two different group of the site of action. Which consists of group 4 herbicides which are generally synthetic auxins such as 2,4-D. The synthetic auxins imbalance the Indole Acetic Acid level and causes growth abnormalities in plants and leading plants to ultimate death. The major chemical family includes Phenoxy, benzoic acids, and carboxylic acids. The common herbicides in use are 2,4-D, 2,4-DB, Dichlorprop, MCPA, MCPB, Dicamba, Clopyralid, and Picloram. These herbicides are commonly used to control broadleaf weeds in plant species, having narrow leaves as post-emergence herbicides [18]. The action of herbicide is controlled by multiple factors rather than a single factor, which disturb the nucleic acid metabolism and cell wall integrity. During recent years, the herbicide efficacy and use of synthetic auxin herbicides has been decreased due to the problem of herbicide resistance and the evolution of other herbicides. Figure 3 depicts the research status on synthetic auxin herbicides from 2011 to 2019 published by WSSA [19].

Figure 3.

Distribution of Synthetic Auxin Research from 2011 to 2013. Adapted from Todd [19].

The group of herbicides belonging to the growth regulators mode of action are chemicals that check the transport of auxin in the meristematic regions. Through the mode of action of these herbicides remain elusive, the majority of these classes of herbicide are found to check the bi-directional flow of auxin by inhibiting vesicle trafficking in plants [20]. The major chemical family of this herbicide are semicarbazone which checks the growth of broadleaf weed in grass crops. The herbicide is absorbed through roots and foliage and they translocate through xylem and phloem. The application of these herbicide during pre-post emergence gives better control of broad leaf weeds. They produce injuries in growth and reproduction abnormalities, leaf malformation, cupping of leaves, abnormal outgrowths of tissues, brittleness in stem, and stalk.

5. Photosynthesis inhibitors

Photosynthesis inhibitors disturbs the process of photosynthesis by binding with the specific binding sites in photosystem II present in the chloroplast of plant cells. Inhibition of photosynthesis could result in slow starvation of the plant and cessation of starch translocation; however rapid death occurs perhaps from the production of secondary toxic substances. Herbicides of photosystem II belong to the following chemical classes: s-triazines, triazinone, uracil, urea, phenyl carbamates, anilide, cyanophenols, dinitrophenol, which are classified into three different groups 5, 6, and 7 on the basis of site of action [21]. The commonly used herbicides having this mode of action are atrazine, simazine, metribuzin, hexazinone, terbacil, bromoxynil, bromacil, pyrazone, bentazon, diuron, and linuron. The group 5 herbicides inhibit photosynthesis by binding within serine in PSII and are absorbed through roots and shoots and translocated through xylem and phloem, group 6 herbicide inhibits photosynthesis by binding with histidine, these herbicide acts as post-emergence contact herbicide, so through spraying of herbicide is recommended. The group 7 herbicides bind with protein complex present in the thylakoid membrane, which checks the transport of electron in the Electron transport Chain. The blocking of electron causes reduced carbon dioxide fixation and production of ATP and NADPH2, which are known as energy packets of respirations. These herbicide controls both narrow and broadleaf weeds. The action of these herbicides is greater during the daytime when there is full sunlight as the herbicide gets activated in presence of light. The herbicides show symptoms of chlorosis and necrosis of leaf margins which progresses towards the base of the leaves after a few hours of application.

6. Nitrogen metabolism inhibitors

This mode of mechanism belongs to herbicide of group 10 having site of action at glutamate synthesis pathway. These herbicide inhibits the production of glutamate syntheses enzymes, which is essential for the conversion of ammonia to other nitrogenous compounds [22]. The blocking causes the accumulation of ammonia ions in the plant leading to increase in PH of the surrounding tissues. This causes protein disintegration, breakage of fatty acids, rupturing of cells, and overall imbalance of ion within cell sap. The major chemical family of herbicides having this mode of action are Phosphorylated Amino Acids commonly traded in the chemical name of glufosinate. These are the broad-spectrum, postemergence herbicide having limited translocation within plant systems so that through spraying of this herbicide is recommended for maximum efficiency. The major injury produced by this herbicide is foliar injury in the plant. The injury symptoms are more prevalent in the younger leaves, in contrast to the deficiency symptoms and plant stress symptoms.

7. Pigment inhibitors

Pigment inhibitors are those herbicides that cause blocking in pigment formation such as anthocyanins, carotene, retinol, and chlorophyll. These herbicides belong to group 12 site of action which blocks the enzymatic activity of 4-hydrooxy phenyl Pyruvate dehydrogenase (HPPD), which plays a role in the synthesis of pigments like chlorophyll, anthocyanin, and carotene. The another group comprises of herbicides from group 13, which causes inhibition of determine synthesis that causes inhibition of synthesis of retinol and degradation of phytin pigments [23]. The major chemical family of these herbicides includes Pyrazole, Pyrazolone, and Pyridazinone. The commonly used herbicides are amitrole, clomazone, isoxaflutole, and mesotrione. The level of pigments is highly reduced leading presence of unbound lipid radicles which causes lipid oxidation, make some protein dysfunctional, and ruptures of the cell membrane. The injury produced by these herbicides is prominent as they show white or bleaching coloration right after the application. In prolonged symptoms expression of translucent leaves, and rapid wilting of weeds species can be seen in the applied area.

8. Cell membrane disrupter

These herbicides interfere with the cell membrane activity, causing them to distort in their structure and functions. The site of action of these herbicides comprises of herbicides belonging to group 14, which causes inhibition of Protoporphyrinogen Oxidase (PPO) enzymes which catalyzes the conversion of ProtoporphyrinogenIX (PPGIX) to Protoprophyrin (PPX). The accumulation of PPGIX causes interbonding to form triplet PPGIX which in the presence of light can disrupt the hydrogen bond, break the bond between fatty acids, and degradation of protein structures. Likewise, triplet PPGIX can obstruct the biosynthesis of chlorophyll and haeme pigments [24]. The chemical family under this group of herbicides are Diphenyl Ether, Thiadiazole, Triazolinone, and Trifluro Methyl Uracil, which includes commonly used herbicides like lactofen, oxyfluorfen, acifluorfen, fomesafen, flumiclorac, and sulfentrazone.

The other group of herbicides, which acts as cell membrane disrupters are chemical belonging to Group 22, which causes inhibition of Photosystem I during photosynthesis. The major chemical family of this group are bipyridylium, which comprises of commercialized herbicides such as diquat and paraquat. These chemical causes the diversion of the electron from the PSI and generate herbicide radicals, which on reacting with oxygen form hydrogen peroxide and hydroxyls radical that causes the breaking of unsaturated fatty acids, chlorophyll, lipids, and proteins in the cell membrane [25]. These herbicides are post-emergence herbicides that get activated under bright light and have a contact mode of action. These herbicides are found to control weeds well under the maturity period too. The major injury system appears in the plant after 1–2 hours of application with evident water-soaked foliage, browning, and necrosis.

9. Seedling root growth inhibitors

These group of herbicides belong to group 3 of the site of action which inhibits the root development in young seedlings by interfering with the cell wall microtubules. Due to this mode of action of herbicides they are commonly called microtubules inhibitors. These chemicals inhibit cell division and cause the blocking of root growth and extension due to the assembly of herbicide-tubulin complex inside microtubules. The complex inhibits the polymerization of microtubules disturbing root cell wall formation [26]. These herbicides are used as pre-emergence herbicides their application through direct soil incorporation gives the best result. The chemical family of these herbicides is dinitroaniline, which is commercialized in the chemical form of pendimethalin. Other commonly used herbicides include trifluralin, ethafluralin, cycloate, and butylate. The major injury of this herbicide is swollen coleoptile, swollen hypocotyl, callus formation, brittle stem, and formation of short secondary roots.

10. Seedling shoot growth inhibitors

Seedling shoot growth inhibitors are the herbicides belonging to group 8 site of action, which interfere with the activity of lipid synthesis through chemical thiocarbamate. These chemical inhibits the biosynthesis of protein, fatty acids, flavonoids, and gibberellins. The other group of herbicides acting as seedling shoot growth inhibitors is long chain fatty acids inhibitors. These herbicide conjugates with Acetyl CoA to form thiocaramate sulfoxide which inhibits long-chain fatty acids during seedling seed growth [27]. The chemical family chloroacetamide, which comprises of chemical herbicides like alachlor, butachlor, and metolachlor are herbicides belonging to this mode of action. They are used as pre-emergence herbicides, soil incorporation of these herbicides give better efficiency. These herbicides are volatile in nature, which are absorbed through roots and emerging shoots and only translocated through xylem vessels in plants. The major injury produced by these groups of chemicals are stunting and enlarged cotyledons.

11. Some novel modes of herbicide action

The problem of herbicide resistance has led the researcher to explore on new modes of herbicide action. Exploring herbicides with a new mode of action can potentially be effective for those weed species which are resistant to conventional herbicides. Several methods are being employed to explore herbicide that acts on new site of action. Major focus has been put on the exploration of phytotoxic primary and secondary metabolites such as protoporphyrin IX and sphingoid bases. The next approach commonly used for the study is identifying the potential site of action with very low-level enzyme level [28]. The herbicide with the target site, Dihydrodipiconitae Sythetase (DHDPS), which catalase the first and rate-limiting step in lysine synthesis is found to be effective in Arabidopsis thaliana conformed by using high throughout the chemical screen. The class of inhibitors are found to bind with the novel and unexplored packets within DHDPS, which produces the symptoms of retarded growth and germination [29]. Another novel herbicide with the chemical form tetflupyrolimet belonging to Weed Science Society of America (WSSA) group 28 is found to be effective against the control of long-season grass weeds in rice fields. The herbicide acts on homogentiosata solanesyltransferase (HST) and dihydroorotate dehydrogenase (DHODH) inhibition [30]. The use of tetflupyrolimet has been under research on several other crops like sugarcane, wheat, soybean, and corn. The herbicide is expected to launch commercial in the year 2023, especially recommended for transplanted and direct-seeded rice.

12. Conclusion

Herbicides have become one of the indispensable parts of commercial agriculture to control the weed species efficiently. The continuous and excessive use of herbicides has evolved the problem of herbicide resistance in many weed species. The new exploration of herbicide mode of action has provided new insights on the target action of herbicides and their acting mechanism along with providing solutions for herbicide resistance. A sound knowledge on the mode of herbicide action help farmer to select the herbicide based on degree of weed infestation, a suitable method for herbicide application, and understand the action mechanism involved to check the growth of weeds in field crops. The study of the mode of action interrelates with the study of the site of action, active chemical involved, and injury produced by such chemicals in the growth and development of weed crops which is equally useful for herbicide formulation. Hence, from the discussions in this chapter, it is evident that different herbicides have their own mode of action to kill the field weeds. Knowing the herbicide mode of action can help for the tactical management of weed species and cope with the resistance trait that lies within plant species.

Acknowledgments

The author acknowledges Mr. Roshan Subedi, Assistant Professor of the Institute of Agriculture and Animal Science, Tribhuvan University for his constant guidelines and support during the preparation of this book chapter.

Conflict of interest

The authors declare no conflict of interest.