Plant environmental stress tolerance enhancer and method for enhancing environmental stress tolerance

Abstract

To provide an agent for enhancing environmental stress tolerance that effectively improves the environmental stress tolerance of plants.SOLUTION: An agent for enhancing environmental stress tolerance of plants comprises, as an active ingredient, a compound represented by formula (I) in the figure or a tautomer thereof, or an agriculturally acceptable salt of them. (In formula (I), R1 and R2 each independently represent a hydrogen atom or an alkyl group having 1 to 4 carbon atoms, and R3 to R5 each independently represent an alkyl group having 1 to 4 carbon atoms.)SELECTED DRAWING: None

Description

[Technical Field]

[0001] The present invention relates to an agent for improving the environmental stress tolerance of plants and a method for improving environmental stress tolerance. [Background technology]

[0002] Environmental stresses such as global warming, drought, and salinization negatively impact plant survival, causing significant damage to agriculture. Because eliminating environmental stresses is difficult or prohibitively expensive, there has long been a need for herbicides that improve the environmental stress tolerance of a wide range of plants.

[0003] Here, ergothioneine is known as a compound that can affect plant growth.

[0004] Patent Document 1 discloses a fertilizer containing ergothioneine and a culture of microorganisms capable of biosynthesizing ergothioneine.

[0005] Patent Document 2 reports that applying ergothioneine alone to plants can promote plant growth or increase yield.

[0006] Patent document 3 reports that nitrogenase activity is improved by applying a microbial extract containing ergothioneine as a fertilizer.

[0007] Furthermore, Patent Documents 4 and 5 report that applying glycine betaine to plants controls plant stress and related conditions, and promotes plant growth. [Prior art documents] [Patent Documents]

[0008] [Patent Document 1] Japanese Patent Publication No. 2018-130091 [Patent Document 2] Patent Application No. 2019-128636 [Patent Document 3] European Patent Application Publication No. 3696154 [Patent Document 4] International Publication No. 96 / 14749 [Patent Document 5] International Publication No. 96 / 23413 [Summary of the Invention] [Problems to be Solved by the Invention]

[0009] As described above, various agents for improving environmental stress tolerance have been developed. However, an agent for improving environmental stress tolerance that exhibits a more excellent effect is still required. However, Patent Documents 1, 2, and 3 do not specify the effect of improving the environmental stress tolerance of plants. In Patent Documents 4 and 5, in addition to glycine betaine, 2-mercaptohistidine betaine (ergothioneine) is also described, but there are no examples regarding ergothioneine and its effect has not been confirmed.

[0010] Therefore, one aspect of the present invention aims to realize an agent for improving environmental stress tolerance and a method for improving environmental stress tolerance of plants that can effectively improve the environmental stress tolerance of plants. [Means for Solving the Problems]

[0011] In order to solve the above problems, an agent for improving environmental stress tolerance of plants according to one aspect of the present invention contains, as an active ingredient, a compound represented by the following formula (I) or a tautomer thereof, or an agriculturally acceptable salt thereof. [Chemical Formula] (In formula (I), R 1 and R 2 each independently represent a hydrogen atom or an alkyl group having 1 to 4 carbon atoms, and R 3 to R 5 each independently represent an alkyl group having 1 to 4 carbon atoms).

[0012] Also, in order to solve the above problems, a method for improving the environmental stress tolerance of plants according to one aspect of the present invention includes treating the above-described environmental stress tolerance improver to plants.

Effect of the Invention

[0013] According to one aspect of the present invention, it is possible to provide an environmental stress tolerance improver and a method for improving environmental stress tolerance capable of effectively improving the environmental stress tolerance of plants.

Mode for Carrying Out the Invention

[0014] 〔Environmental Stress Tolerance Improver〕 (Active Ingredient) The environmental stress tolerance improver according to the present embodiment contains, as an active ingredient, a compound represented by the following formula (I) (hereinafter simply referred to as "compound (I)"), a tautomer thereof, or an agriculturally acceptable salt thereof.

Chemical formula

[0015] The alkyl group may be linear or branched, that is, it may be a methyl group, an ethyl group, a propyl group, an isopropyl group, a butyl group, an isobutyl group, a sec-butyl group or a tert-butyl group.

[0016] R 1 and R 2 It is preferable that at least one of them is a hydrogen atom, and more preferably both are hydrogen atoms. R 1 and R 2If it is an alkyl group, it is preferably a methyl group, an ethyl group, or a propyl group, more preferably a methyl group or an ethyl group, and even more preferably a methyl group.

[0017] R 3 ~R 5 R is preferably independently a methyl group, an ethyl group, or a propyl group, more preferably a methyl group or an ethyl group, and even more preferably a methyl group. 3 ~R 5 Preferably, at least one of the groups is a methyl group, more preferably at least two are methyl groups, and even more preferably all are methyl groups.

[0018] "That tautomer" refers to the tautomer of compound (I). Compound (I) contains R 1 and R 2 If at least one of them is a hydrogen atom, then a tautomer exists. More specifically, in formula (I), R 2 If is a hydrogen atom, a compound represented by the following formula (II) (hereinafter simply referred to as "compound (II)") may exist as a tautomer. Also, in formula (I), R 1 If is a hydrogen atom, a tautomer represented by the following formula (III) (hereinafter simply referred to as "compound (III)") may exist. Hereinafter, compound (II) and compound (III) will be simply referred to as "tautomers". [ka] In equations (II) and (III), R 1 ~R 5 R in equation (I) 1 ~R 5 It is identical to [the other one].

[0019] The preferred compound as compound (I) or its tautomer is specifically ergothioneine, and more preferably L-(+)-ergothioneine.

[0020] These compounds may be commercially available, or synthesized using techniques well known to those skilled in the art, such as those described in Patent Publication No. 2013-506706 or Patent Publication No. 2006-160748. Furthermore, ergothioneine is known to be produced by bacteria and fungi. Examples of production methods using such microorganisms include those described in Patent Publication Nos. 2012-105618, 2014-223051, WO2016 / 104437, WO2016 / 121285, WO2015 / 168112, and WO2017 / 150304. As ergothioneine, the culture containing ergothioneine obtained from these microorganisms may be used as is, or the ergothioneine may be concentrated or purified before use.

[0021] "Agriculturally acceptable" generally means that a substance is safe, non-toxic, and not biologically or otherwise undesirable, and is acceptable for use as a pesticide, particularly for use in pesticides that improve plants' tolerance to environmental stress.

[0022] An "agriculturally acceptable salt" of compound (I) or its tautomer means an agriculturally acceptable salt as defined above, which provides the action and effects of compound (I) or its tautomer. Examples of such salts include hydrates, solvates, acid addition salts, salts formed when an acidic proton (proton acide) present in compound (I) or its tautomer is substituted with a metal ion, and salts formed when the acidic proton coordinates with an organic or inorganic base.

[0023] The acid addition salt may be formed with an inorganic acid or an organic acid. Examples of inorganic acids include hydrochloric acid, hydrobromic acid, sulfuric acid, nitric acid, and phosphoric acid. Examples of organic acids include acetic acid, benzenesulfonic acid, benzoic acid, camphorsulfonic acid, citric acid, ethanesulfonic acid, fumaric acid, glucoheptonic acid, gluconic acid, glutamic acid, glycolic acid, hydroxynaphthoic acid, 2-hydroxyethanesulfonic acid, lactic acid, maleic acid, malic acid, mandelic acid, methanesulfonic acid, muconic acid, 2-naphthalenesulfonic acid, propionic acid, salicylic acid, succinic acid, dibenzoyl-L-tartaric acid, tartaric acid, p-toluenesulfonic acid, trimethylacetic acid, and trifluoroacetic acid.

[0024] Examples of metal ions that can substitute for acidic protons present in compound (I) or its tautomers include alkali metal ions, alkaline earth metal ions, and aluminum ions.

[0025] Examples of organic bases that can coordinate with acidic protons present in compound (I) or its tautomers include diethanolamine, ethanolamine, N-methylglucamine, triethanolamine, and tromethamine. Examples of inorganic bases include aluminum hydroxide, calcium hydroxide, potassium hydroxide, sodium carbonate, and sodium hydroxide.

[0026] The environmental stress tolerance enhancer according to this embodiment contains compound (I) or its tautomer, or an agronomically acceptable salt thereof, as an active ingredient, thereby improving the tolerance to environmental stress in plants treated with it compared to plants that were not treated with it.

[0027] In this specification, "improved tolerance to environmental stress" means that plants treated with the environmental stress tolerance enhancer according to this embodiment show less physiological damage caused by environmental stress compared to plants that were not treated with it.

[0028] An indicator of the suppression of physiological disorders caused by environmental stress is, for example, the environmental stress suppression rate. The "environmental stress suppression rate" is the percentage by which physiological disorders occurring in plants after growing for a predetermined period under environmental stress are suppressed by treating them with the environmental stress tolerance enhancer according to the embodiment, compared to plants that were not treated. For example, if the physiological disorders occurring in plants that have not been treated with the environmental stress tolerance enhancer under environmental stress are set at 100%, and the physiological disorders occurring in plants treated with the environmental stress enhancer are 20%, then the environmental stress suppression rate is 80%. Regarding the "environmental stress suppression rate," "improved tolerance to environmental stress" means that the environmental stress suppression rate is high.

[0029] Indicators of physiological disorders include, for example, wilting, chlorosis (whitening or yellowing), necrosis (death), and wilting in plants, and for example, wilting, chlorosis (whitening or yellowing), necrosis (death), and wilting in leaves. However, these are not the only examples; other indicators include a decrease in plant height, root length, number of flowers, number of fruits, and seed yield.

[0030] For example, "plant mortality rate" refers to the ratio of the number of plants that die after growing under predetermined conditions for a predetermined period to the total number of plants tested. For example, if 80 out of 100 plants die after growing under predetermined conditions for a predetermined period, the mortality rate is 80%. Regarding "plant mortality rate," "improved tolerance to environmental stress" means that plants treated with the environmental stress tolerance enhancer according to this embodiment have a lower mortality rate under environmental stress compared to plants that were not treated.

[0031] For example, "leaf mortality rate" is the ratio of the number of leaves that withered and died after the plant was grown under predetermined conditions for a predetermined period to the total number of leaves of the plant tested. For example, if 8 out of 10 leaves withered and died after the plant was grown under predetermined conditions for a predetermined period, the leaf mortality rate is 80%. Regarding "leaf mortality rate," "improved tolerance to environmental stress" means that plants treated with the environmental stress tolerance enhancer according to this embodiment have a lower mortality rate under environmental stress compared to plants that were not treated.

[0032] For example, "leaf whitening rate" is the ratio of the number of leaves that have turned white after growing the plant under predetermined conditions for a predetermined period to the total number of leaves of the plant tested. For example, if 8 out of 10 leaves have turned white after growing the plant under predetermined conditions for a predetermined period, the leaf whitening rate is 80%. Regarding "leaf whitening rate," "improved resistance to environmental stress" means that plants treated with the environmental stress tolerance enhancer according to this embodiment have a lower whitening rate under environmental stress compared to plants that were not treated.

[0033] One example is "leaf necrosis rate," which is the ratio of the leaf area that became necrotic after the plant was grown under specified conditions for a specified period to the total leaf area of ​​the plant tested. For example, after the plant was grown under specified conditions for a specified period, the total leaf area was 100 cm². 2 Of which, 80cm 2 The necrosis rate of leaves when necrosis is present is 80%. Regarding the "leaf necrosis rate," "improved tolerance to environmental stress" means that plants treated with the environmental stress tolerance enhancer according to this embodiment have a lower necrosis rate under environmental stress compared to plants that were not treated.

[0034] For example, "leaf wilting rate" is the ratio of the number of wilted leaves to the total number of leaves of the tested plant after it has been grown under predetermined conditions for a predetermined period. For example, if 8 out of 10 leaves of a plant have wilted after it has been grown under predetermined conditions for a predetermined period, the leaf wilting rate is 80%. Regarding "leaf wilting rate," "improved resistance to environmental stress" means that plants treated with the environmental stress tolerance enhancer according to this embodiment have a lower wilting rate under environmental stress compared to plants that have not been treated.

[0035] Regarding "plant height," as another example, "improved tolerance to environmental stress" means that plants treated with the environmental stress tolerance enhancer according to this embodiment have a greater plant height under environmental stress compared to plants that were not treated. Similarly, regarding "root length," as another example, "improved tolerance to environmental stress" means that plants treated with the environmental stress tolerance enhancer according to this embodiment have a longer root length under environmental stress compared to plants that were not treated. Similarly, regarding "number of flowers," as another example, "improved tolerance to environmental stress" means that plants treated with the environmental stress tolerance enhancer according to this embodiment have a greater number of flowers under environmental stress compared to plants that were not treated. Similarly, regarding "number of fruits," as another example, "improved tolerance to environmental stress" means that plants treated with the environmental stress tolerance enhancer according to this embodiment have a greater number of fruits under environmental stress compared to plants that were not treated. Furthermore, regarding the example of "seed yield," the statement "improved tolerance to environmental stress" means that plants treated with the environmental stress tolerance enhancer according to this embodiment yield more seeds under environmental stress compared to plants that were not treated.

[0036] In particular, a preferred embodiment is an environmental stress tolerance enhancer for suppressing the death, chlorosis (whitening or yellowing), necrosis (death), or wilting of plants or leaves caused by environmental stress.

[0037] In this specification, "environmental stress" refers to environmental factors that plants may experience that inhibit normal growth. Examples include high temperature stress, low temperature stress, frost stress, salt stress, excess nutrient stress, drought stress, excess water stress, ultraviolet stress, low light stress, and high light stress.

[0038] These factors are basically conditions under which normal growth is difficult if the plant is not treated with the environmental stress tolerance enhancer according to this embodiment. Here, "normal growth" refers to the degree of growth when these factors are not present and the plant is not treated with the environmental stress tolerance enhancer according to this embodiment. Furthermore, "difficulty in normal growth" includes not only cases where growth is difficult, but also cases where the degree of growth is worse than normal growth.

[0039] The environmental stress tolerance enhancer according to this embodiment preferably contains compound (I) or an agriculturally acceptable salt thereof as an active ingredient. The environmental stress tolerance enhancer according to this embodiment may contain a plurality of compounds from compound (I) and its tautomers or agriculturally acceptable salts thereof as an active ingredient.

[0040] Normally, in solution, compound (I) and compound (II) or compound (III) can exist in equilibrium. The ratio of compound (I) to compound (II) or compound (III) can vary depending on the solvent, temperature, pH, etc.

[0041] (Applicable to) The environmental stress tolerance enhancer in this embodiment generally exhibits an effect of improving environmental stress tolerance in all plants, but examples of applicable plants are listed below. Grasses such as rice, wheat, barley, rye, oats, rye grass (trichi kale), corn, sorghum, sugarcane, turfgrass, bentgrass, Bermuda grass, fescue and ryegrass; legumes such as soybeans, peanuts, kidney beans, peas, adzuki beans and alfalfa; morning glory family such as sweet potato; nightshade family such as chili peppers, bell peppers, tomatoes, eggplants, potatoes and tobacco; buckwheat family such as buckwheat; daisy family such as sunflower; Araliaceae family such as ginseng; brassica family such as rapeseed, broccoli, Chinese cabbage, turnips, cabbage, arugula, radishes and radishes; amaranth family such as sugar beets; mallow family such as cotton; rusaceae family such as coffee plants; This includes plants from the Malvaceae family such as kao, Camellia family such as tea, Cucurbitaceae family such as watermelon, melon, cucumber and pumpkin, Liliaceae family such as onion, leek and garlic, Rosaceae family such as strawberry, apple, almond, apricot, plum, cherry, Japanese apricot, peach and pear, Apiaceae family such as carrot, Araceae family such as taro, Anacardiaceae family such as mango, Bromeliaceae family such as pineapple, Papaya family such as papaya, Ebenaceae family such as persimmon, Ericaceae family such as blueberry, Juglandaceae family such as pecan, Musaceae family such as banana, Oleaceae family such as olive, Arecaceae family such as coconut and date palm, Rutaceae family such as mandarin orange, orange, grapefruit and lemon, Vitaceae family such as grape, flowers and ornamental plants, trees other than fruit trees, and other ornamental plants.

[0042] Furthermore, examples include wild plants, plant cultivars, plants and plant cultivars obtained through conventional biological breeding methods such as crossbreeding or plasmofusion, and genetically modified plants and plant cultivars obtained through genetic manipulation. Examples of genetically modified plants and plant cultivars include herbicide-resistant crops, pest-resistant crops incorporating genes that produce insecticidal proteins, disease-resistant crops incorporating genes that produce disease-resistant substances, crops with improved taste, crops with increased yield, crops with improved shelf life, and crops with increased yield. Examples of genetically modified plant cultivars approved in various countries include those stored in the database of the International Service for Agri-Biotechnology (ISAAA). Specifically: AgriSure, AgriSure 3000GT, AgriSure 3122 EZ Refuge, AgriSure 3122 Refuge Renew, AgriSure Artesian 3030A, AgriSure Artesian 3011A, AgriSure Duracade, AgriSure Duracade 5222 EZ Refuge, AgriSure GT, AgriSure GT / CB / LL, AgriSure RW, AgriSure Viptera 3110, AgriSure Viptera 3111, AgriSure Viptera 3220 EZ Refuge, AgriSure Viptera 3220 Refuge Renew, BiteGard, Bollgard, Bollgard II, Bollgard II / Roundup Ready, Bollgard 3 XtendFlex Cotton, Bollgard Cotton, Bollgard / Roundup Ready Cotton, Bt, Bt / BXN Cotton, Bt Maize, BtXtra, BXN, BXN Canola, BXN Cotton, Clearfield, DroughtGard, Enlist, Enlist Cotton, Enlist WideStrike 3 Cotton, Genuity, Genuity Bollgard II XtendFlex, Genuity Intacta RR2 Pro, GenuitySmartStax、Genuity SmartStax RIB Complete、Genuity VT Double Pro、Genuity VT Double Pro RIB Complete、Genuity VT Triple Pro、Genuity VT Triple Pro RIB Complete、GlyTol、GlyTol Cotton、Herculex、Herculex 1、Herculex RW、Herculex XTRA、IMI、IMI Canola、InVigor、KnockOut、Liberty Link、Liberty Link Conola、Liberty Link cotton、NatureGard、Newleaf、Nucotn、Optimum、Optimum AcreMax、Optimum AcreMax I、Optimum AcreMax-R、Optimum AcreMax RW、Optimum AcreMax RW-R、Optimum AcreMax Xtra-R、Optimum AcreMax Xtreme-R、Optimum AcreMax Xtreme、Optimum Intrasect、Optimum Intrasect Xtra、Optimum Intrasect Xtreme、Optimum Leptra、Optimum TRIsect、Poast Compatible、Powercore、Powercore Corn、Powercore Corn Refuge Advanced、Protecta、Roundup Ready、Roundup Ready 2、Roundup Ready Conola、Roundup Ready Cotton、Roundup Ready Xtend、Roundup Ready / YieldGard、RR Flex / Bollgard II、SCS、SmartStax、SmartStax Refuge Advanced、StarLink、Twinlink、VipCot、VipCot Cotton、WideStrike、WideStrike 3、YieldGard、YieldGard Corn Borner、YieldGard Rootworm、YieldGard PlusおよびYieldGardExamples include those containing registered trademarks such as VT Triple.

[0043] (formulation) In this embodiment, the environmental stress tolerance enhancer is generally formulated and used in various forms such as powders, granules, powder-granules, wettable powders, aqueous solvents, emulsions, liquids, oils, aerosols, microencapsulated formulations, pastes, coatings, fumigants, vaporizers, and trace sprays by mixing the active ingredient compound (I) or its tautomers, or mixtures thereof, with a carrier, surfactant, and other formulation aids.

[0044] Examples of carriers used as formulation aids include solid carriers and liquid carriers. Solid carriers include powder carriers and granular carriers, and examples include minerals such as clay, talc, diatomaceous earth, zeolite, montmorillonite, bentonite, kaolinite, kaolin, pyrophyllite, pyrophyllite, pyrophyllite, acid clay, activated clay, attapulgite, attapulga clay, limestone, calcite, marble, vermiculite, perlite, pumice, silica, silica sand, sericite, and pottery stone; synthetic organic substances such as urea; salts such as calcium carbonate, sodium carbonate, magnesium carbonate, sodium sulfate, ammonium sulfate, potassium chloride, slaked lime, and baking soda; and amorphous silica (white Examples of carriers include synthetic inorganic materials such as carbon, fumed silica, and titanium dioxide; plant-based carriers such as wood flour, corn stalks (cob), walnut shells (nut exoskeleton), fruit seeds, rice hulls, coconut hulls, sawdust, bran, soybean flour, powdered cellulose, starch, dextrin, and sugars (lactose, sucrose, etc.); and various polymer carriers such as cross-linked lignin, cationic gels, gelatin that gels with heating or polyvalent metal salts, water-soluble polymer gels (agar, etc.), chlorinated polyethylene, chlorinated polypropylene, polyvinyl acetate, polyvinyl chloride, ethylene / vinyl acetate copolymers, and urea / aldehyde resins.

[0045] Examples of liquid carriers include aliphatic solvents such as paraffins (normal paraffin, isoparaffin, naphthene); aromatic solvents such as xylene, alkylbenzene, alkylnaphthalene and solvent naphtha; mixed solvents such as kerosene; machine oils such as refined high-boiling-point aliphatic hydrocarbons; alcohols such as methanol, ethanol, isopropanol, butanol and cyclohexanol; polyhydric alcohols such as ethylene glycol, diethylene glycol, propylene glycol, dipropylene glycol, hexylene glycol, polyethylene glycol and polypropylene glycol; polyhydric alcohol derivatives such as propylene glycol ethers; acetone, acetophenone, Examples include ketones such as cyclohexanone, methylcyclohexanone, and γ-butyrolactone; esters such as fatty acid methyl esters (coconut oil fatty acid methyl ester), ethylhexyl lactate, propylene carbonate, and dibasic acid methyl esters (dimethyl succinate, dimethyl glutamate, dimethyl adipate); nitrogen-containing solvents such as N-alkylpyrrolidones and acetonitrile; sulfur-containing solvents such as dimethyl sulfoxide; oils and fats such as coconut oil, soybean oil, and rapeseed oil; amide solvents such as dimethylformamide, N,N-dimethyloctanamide, N,N-dimethyldecanamide, methyl 5-(dimethylamino)-2-methyl-5-oxovalerate, and N-acylmorpholine solvents (CAS No. 887947-29-7, etc.); and water.

[0046] Examples of surfactants used as formulation aids include nonionic surfactants, anionic surfactants, cationic surfactants, amphoteric surfactants, silicone surfactants, fluorinated surfactants, and biosurfactants. Examples of nonionic surfactants include sorbitan fatty acid esters, polyoxyethylene sorbitan fatty acid esters, sucrose fatty acid esters, polyoxyethylene fatty acid esters, polyoxyethylene resin acid esters, polyoxyethylene fatty acid diesters, polyoxyethylene alkyl ethers, polyoxyethylene alkylphenyl ethers, polyoxyethylene dialkylphenyl ethers, polyoxyethylene alkylphenyl ether formalin condensates, polyoxyethylene / polyoxypropylene block polymers, alkylpolyoxyethylene / polyoxypropylene block polymer ethers, alkylphenyl polyoxyethylene / polyoxypropylene block polymer ethers, polyoxyethylene alkylamines, polyoxyethylene fatty acid amides, polyoxyethylene fatty acid bisphenyl ethers, polyoxyethylene benzylphenyl (or phenylphenyl) ethers, polyoxyethylene styrylphenyl (or phenylphenyl) ethers, polyoxyethylene castor oil, polyoxyethylene hydrogenated castor oil, and alkyl glycosides.

[0047] Examples of anionic surfactants include sulfates such as alkyl sulfates, polyoxyethylene alkyl ether sulfates, polyoxyethylene alkylphenyl ether sulfates, polyoxyethylene benzyl (or styryl) phenyl (or phenylphenyl) ether sulfates, and polyoxyethylene / polyoxypropylene block polymer sulfates; paraffin (alkane) sulfonates, α-olefin sulfonates, dialkyl sulfosuccinates, alkylbenzene sulfonates, mono or dialkylnaphthalene sulfonates, naphthalene sulfonate-formaldehyde condensates, alkyldiphenyl ether disulfonates, lignin sulfonates, and poly Examples include sulfonates such as oxyethylene alkylphenyl ether sulfonates and polyoxyethylene alkyl ether sulfosuccinate half-esters; carboxylates such as fatty acids, resin acids, polycarboxylic acids, alkyl ether carboxylates, alkenyl succinic acid, N-acyl amino acids, and naphthenic acid; and phosphates such as polyoxyethylene alkyl ether phosphates, polyoxyethylene mono or dialkylphenyl ether phosphates, polyoxyethylene benzyl (or styryl) phenyl (or phenylphenyl) ether phosphates, polyoxyethylene / polyoxypropylene block polymer phosphates, and alkyl phosphates.

[0048] Examples of cationic surfactants include salts of amines such as alkylamines and alkylpentamethylpropylenediamine; and salts of ammonium compounds such as alkyltrimethylammonium, methylpolyoxyethylenealkylammonium, alkylpyridinium, mono- or dialkylmethylated ammonium, alkyldimethylbenzalkonium, and benzethonium (octylphenoxyethoxyethyldimethylbenzylammonium).

[0049] Examples of amphoteric surfactants include dialkyldiaminoethyl betaine, alkyldimethylbenzyl betaine, and lecithin (such as phosphatidylcholine and phosphatidylethanolamine).

[0050] Examples of silicone-based surfactants include trisiloxane ethoxylate.

[0051] Examples of fluorinated surfactants include perfluoroalkyl carboxylates, perfluoroalkyl sulfonates, and perfluoroalkyltrimethylammonium salts.

[0052] Examples of biosurfactants include sophorolipid, rhamnolipid, trehaloselipid, mannosyl alditollipid, cellobioselipid, glucoselipid, oligosaccharide fatty acid esters, spiculosporic acid, corinomicolic acid, agaritic acid, surfactant, cerauetchin, viscosine, lichensine, arsolofactin, emulsan, and alasan.

[0053] Other pharmaceutical additives include inorganic salts (sodium, potassium, etc.) used as pH adjusters; water-soluble salts such as sodium chloride; xanthan gum, guar gum, carboxymethylcellulose, polyvinylpyrrolidone, carboxyvinyl polymers, acrylic polymers, polyvinyl alcohol, starch derivatives, water-soluble polymers (polysaccharides, etc.), alginic acid and its salts used as thickeners; metal stearate, sodium tripolyphosphate, sodium hexametaphosphate used as disintegrating and dispersing agents; benzoic acid and its salts, sorbic acid and its salts, propionic acid and its salts, p-hydroxybenzoic acid, methyl p-hydroxybenzoate, 1,2-benzothiazolin-3-one used as preservatives; and other additives. Examples of chemicals used include: sodium polyphosphate, sodium polyacrylate, sodium ligninsulfonate, sodium citrate, sodium gluconic acid / glucoheptanoate, ethylenediaminetetraacetic acid and its disodium or ammonium salts; pigments and dyes used as colorants; fluorine-based defoamers, silicone-based defoamers, ethylene oxide / propylene oxide copolymers used as defoamers; phenol-based antioxidants, amine-based antioxidants, sulfur-based antioxidants, phosphoric acid-based antioxidants used as antioxidants; salicylic acid-based UV absorbers, benzophenone-based UV absorbers used as UV absorbers; quicklime, magnesium oxide, etc. used as drying agents; and other agents such as spreading agents and phytotoxicity reducers.

[0054] The formulations include those that are used as is and those that are used after dilution with a diluent such as water to a specified concentration. When used after dilution, the concentration of compound (I) should preferably be in the range of 0.0001 to 1% by weight. The same applies to tautomers of compound (I).

[0055] These formulations contain compound (I) as the active ingredient in an amount of 0.1 to 90% by weight, more preferably 0.2 to 50% by weight. The amount of compound (I) used is 0.005 to 50 kg, more preferably 0.03 to 30 kg, per hectare of agricultural land such as fields, paddies, orchards, and greenhouses. The same applies to tautomers of compound (I). These concentrations and amounts can be increased or decreased without being bound by the above ranges, as they vary depending on the dosage form, timing of use, method of use, location of use, and target plant.

[0056] (Other active ingredients) The environmental stress tolerance enhancer in this embodiment can be used in combination with other known active ingredients to enhance its performance as an environmental stress tolerance enhancer, or to impart effects other than environmental stress tolerance enhancement. Examples of other known active ingredients include active ingredients contained in known environmental stress tolerance enhancers, known plant growth regulators, fungicides, insecticides, acaricides, nematicides, and herbicides.

[0057] Known active ingredients in environmental stress tolerance enhancers include, for example, seaweed extracts, corn extracts, microalgae, mycorrhizal fungi, humic acid, fulvic acid, oxidized glutathione, L-proline, glycine betaine, 5-aminolevulinic acid, 2-hexenal, trehalose, silicic acid, nicotinic acid, acetic acid, and ethanol.

[0058] Known plant growth regulators include, for example, aminoethoxyvinylglycine, chlormecoat, chlorprofam, cyclanilide, dikeglac, daminozite, etephon, flurprimidol, flumetraline, forchlorfenuron, gibberellin, mepicote chloride, methylcyclopropene, benzylaminopurine, paclobutrazol, prohexadione, thidiazuron, tributylphosphoritrithioate, trinexapac-ethyl, uniconazole, and 1-naphthaleneacetate sodium Examples include lium, 1-naphthylacetamide, 1-methylcyclopropene, 4-CPA (4-chlorophenoxyacetic acid), MCPB (2-methyl-4-chlorophenoxybutyrate ethyl), isoprothiolane, indolebutyric acid, etichlozate, calcium formate, chlormecoat, choline, cyanamide, dichlorprop, decyl alcohol, sorbitan trioleate, nicosulfuron, pyraflufen ethyl, butruarin, prohydrojasmon, anisifruprine, and pendimethalin.

[0059] Suitable effective ingredients for fungicide applications include, for example, nucleic acid synthesis and metabolism inhibitors, fungicides acting on the cytoskeleton and motor proteins, respiratory inhibitors, amino acid and protein biosynthesis inhibitors, signal transduction inhibitors, lipid biosynthesis or transport / cell membrane structure or function inhibitors, cell membrane sterol biosynthesis inhibitors, cell wall biosynthesis inhibitors, melanin biosynthesis inhibitors, host plant resistance inducers, multi-point fungicides, and biopesticides / biologically derived pesticides with multiple mechanisms of action.

[0060] Specifically, nucleic acid synthesis and metabolism inhibitors include venalaxyl, venalaxyl M or quilaraxyl, flalaxyl, metalaxyl, metalaxyl M or mefenoxam, ofrace, oxadixyl, bupirimate, dimethyrimole, ethyrimole, hydroxyisoxazole, octylinone, and oxolinic acid.

[0061] Furthermore, bactericides that act on the cytoskeleton and motor proteins include benomyl, carbendazim, fuberidazole, thiabendazole, thiophanate, thiophanate-methyl, diethofencarb, etaboxam, pencyclon, zoxamide, fluopicolide, fluopimomid, phenamacryl, metraphenone, and pyriophenone.

[0062] Additionally, respiratory inhibitors include diflumetrim, phenazaquine, tolfenpyrad, benodanil, benzovindiflupir, bixafen, boscalid, carboxyne, fenflam, flubeneteram, fluindapir, fluopyram, flutolanil, fluxapiroxad, flametopir, impilfluxam, isofetamide, isoflucipram, isopyrazam, mepronil, oxycarboxyne, penflufen, penthiopyrad, pidflumetofen, pyrapropoin, pyraziflumid, sedaxane, tifluzamide, azoxystrobin, chemoxystrobin, dimoxystrobin, enestrobin, enoxastrobin, famoxadone, and phenamide. Examples include phenaminestrobin, fluphenoxystrobin, fluoxastrobin, kresoximmethyl, mandestrobin, metminostrobin, methyltetraprole, orysastrobin, picoxystrobin, pyraclostrobin, pyrametostrobin, pyroxystrobin, pyribencarb, triclopyricarb, trifloxystrobin, amisulbrom, cyazofamide, fenpicoxamide, florylpicoxamide, metharylpicoxamide, binapacril, dinocap, fluazinam, meptyldinocap, triphenyltin acetate, triphenyltin chloride, triphenyltin hydroxide, silthiofam, and ametoctrazine.

[0063] Furthermore, examples of amino acid and protein biosynthesis inhibitors include cyprodinil, mepanipyrim, pyrimethanil, blastosidine S, kasugamycin, streptomycin, and oxytetracycline.

[0064] Other examples of signal transduction inhibitors include proquinazide, quinoxyfen, fludioxonil, clozolinate, dimethacron, fenpiclonil, iprodione, procymidone, and vinclozoline.

[0065] Furthermore, examples of lipid biosynthesis or transport / cell membrane structure or function inhibitors include edifenphos (EDDP), ipropenphos (IBP), isoprothiolane, pyrazophos, biphenyl, chloreneb, dichloran (CNA), etridiazole, quintozen (PCNB), technazen (TCNB), tolclophosmethyl, iodocarb, propamocarb, prothiocarb, extract of tea tree (Goseikajupte), vegetable oil mixtures (eugenol, geraniol, thymol), natamycin (pimaricin), fluoxapiproline, and oxathiapiproline.

[0066] Inhibitors of cell membrane sterol biosynthesis include azaconazole, vitertanol, bromconazole, cyproconazole, difenoconazole, diniconazole, epoxyconazole, etaconazole, fenbuconazole, fluoxythioconazole, fluquinconazole, flusilazole, flutriafole, hexaconazole, imazalil, imibenconazole, ipconazole, ipfentrifluconazole, mefentrifluconazole, metconazole, mycrobutanil, oxpoconazole, pefurazoate, penconazole, prochloraz, propiconazole, prothioconazole, simeconazole, tebuconazole, tetraconazole, triadimefon, triadimenol, triflumizole, triticonazole, phenalimol, nualimol, and pyrifenoc. Examples include pyrisoxazole, triforine, methyl(2RS)-2-[2-chloro-4-(4-chlorophenoxy)phenyl]-2-hydroxy-3-(1H-1,2,4-triazole-1-yl)propanoate, 1-((1H-1,2,4-triazole-1-yl)methyl)-5-(4-chlorobenzyl)-2-(chloromethyl)-2-methylcyclopentan-1-ol, methyl2-((1H-1,2,4-triazole-1-yl)methyl)-3-(4-chlorobenzyl)-2-hydroxy-1-methylcyclopentan-1-carboxylate, algimorph, dodemorph, fenpropimorph, tridemorph, fenpropidine, piperalin, spiroxamine, fenhexamide, fenpyrazamine, pyributicarb, naphthifine, and terbinafine.

[0067] Examples of cell wall biosynthesis inhibitors include polyoxin, bentheavalicarb (bentheavalicarb isopropyl), dimethomorph, flumorph, iprovalicarb, mandipropamide, pyrimorph, and valifenarate.

[0068] Examples of melanin biosynthesis inhibitors include phthalide, pyroquilon, tricyclazole, carpropamide, diclocimet, phenoxanil, and tolprocarb.

[0069] Examples of resistance-inducing agents for host plants include acibenzolar-S-methyl, probenazole, thiadinyl, isothianil, laminarin, knotweed extract, Bacillus mycoides isolate J, cell wall of Saccharomyces cerevisiae LAS117 strain, fosetyl (fosetyl-aluminum, fosetyl potassium, fosetyl sodium), phosphate, phosphates, and diclobentiazox.

[0070] Examples of multi-point bactericides include Farbam, Mancozeb, Maneb, Methylam, Propineb, Thiuram, Thiazole zinc, Zineb, Ziram, Ambam, Anilazine, Dithianone, Diclofluanide, Tolfluanide, Guazatin, Iminoctadine acetate, Iminoctadine albesylate, copper or various copper salts (e.g., basic copper chloride, cupric hydroxide, basic copper sulfate, copper sulfate, organocopper (oxine copper), nonylphenolsulfonate copper, DBEDC, etc.), sulfur, Captan, Captahol, Holpet, TPN (chlorothalonil), quinoxalines (quinomethionate), fluorimide, and metasulfocarb.

[0071] Examples of biopesticides / biologically derived pesticides with multiple mechanisms of action include: Bacillus subtilis AFS032321 strain, Bacillus amyloriquefaciens QST713 strain, Bacillus amyloriquefaciens FZB24 strain, Bacillus amyloriquefaciens MBI600 strain, Bacillus amyloriquefaciens D747 strain, Bacillus amyloriquefaciens F727 strain, Chronostachys rosea CR-7 strain, and Gliocladium catenaratum J. Examples include 1446 strains, Pseudomonas chlororaffis AFS009 strain, Streptomyces glyceobilides K61 strain, Streptomyces riddix WYEC108 strain, Trichoderma atroviride I-1237 strain, Trichoderma atroviride LU132 strain, Trichoderma atroviride SC1 strain, Trichoderma asperelum T34 strain, extracts from Swaingrea glutinosa, and extracts from the cotyledons of Japanese bean seedlings.

[0072] Other compounds used as fungicides include chloroinconazide, seboctylamine, flumethylsulforim, fluphenoxadiazam, cyflufenamid, cymoxanil, diclomedin, dipimethitrone, dozin, fenitropan, ferimzon, flusulfamide, fluthianil, harbin, inorganic salts (bicarbonates (sodium bicarbonate, potassium bicarbonate), potassium carbonate), ibuflufenoquine, quinoprole, natural origins, machine oil, organic oils, picarbutrazox, pyridaclomethyl, quinofumerine, tebufloxin, tecrophthalam (bactericide), triazoxide, validamycin, aminopyriphene, and shiitake mushroom mycelium extract.

[0073] Suitable active ingredients for insecticide applications include, for example, acetylcholinesterase (AChE) inhibitors, GABAergic chloride ion channel blockers, sodium channel modulators, nicotinic acetylcholine receptor (nAChR) competitive modulators, nicotinic acetylcholine receptor (nAChR) allosteric modulators, glutamate-gated chloride ion channel (GluCl) allosteric modulators, juvenile hormone analogs, other nonspecific (multisite) inhibitors, choroidal organ TRPV channel modulators, mite growth inhibitors acting on CHS1, microbial insect midgut endothelial disruptors, mitochondrial ATP synthase inhibitors, oxidative phosphorylation uncoupling agents that disrupt the proton gradient, and nicotinic Examples include nAChR channel blockers, CHS1-acting chitin biosynthesis inhibitors, type 1 chitin biosynthesis inhibitors, molting inhibitors (Diptera insects), ecdysone receptor agonists, octopamine receptor agonists, mitochondrial electron transport chain complex III inhibitors, mitochondrial electron transport chain complex I inhibitors (METI), voltage-gated sodium channel blockers, acetyl-CoA carboxylase inhibitors, mitochondrial electron transport chain complex IV inhibitors, mitochondrial electron transport chain complex II inhibitors, ryanodine receptor modulators, chordosal organ modulators, GABAergic chloride ion channel allosteric modulators, and baculoviruses.

[0074] Acetylcholinesterase (AChE) inhibitors include alanicarb, aldicarb, bendiocarb, benfuracarb, butocarboxime, butoxycarboxime, NAC (carbaryl), carbofuran, carbosulfan, ethiofencarb, BPMC (phenobucarb), phenothiocarb, formentate, furathiocarb, MIPC (isoprocarb), methiocarb, methomyl, MTMC (metholcarb), oxamyl, pyrimicarb, PHC (propoxul), thiodicarb, thiophanox, triazamate, trimetacarb, XMC, MPMC (xylylcarb), Acephate, Azamethiphos, Adinphos-ethyl, Adinphos-methyl, Kazsaphos, Chloretoxyphos, CVP (Chlorfenvinphos), Chlormephos, Chlorpyrifos, Chlorpyrifos-methyl, Coumaphos, CYAP (Cyanophos), Dimeton-S-methyl, Diazinon, DDVP (Dichlorvos), Diclotophos, Dimethoate, Dimethylvinphos, Ethylthiometon (Disulfone), EPN, Ethion, Etoprophos, Fanflu, Phenamiphos, MEP (Fenitrothion), MPP (Fenthion), Fostiazate, Heptenophos, Imisiaphos, Isofenphos, Isopropyl Examples include O-(methoxyaminothiophosphoryl) salicylate, isoxathion, malathion, mecarbam, methamidophos, DMTP (methidathion), mevinphos, monoclotophos, BRP (naled), omethoate, oxydimeton methyl, parathion, methylparathion (parathion methyl), PAP (fenthoate), phorate, phosalon, PMP (phosmet), phosphamidone, foxim, pyrimiphos methyl, profenophos, propetamphos, prothiophos, pyraclophos, pyridaphenthion, quinalphos, sulfotep, tebupyrimphos, temephos, terbuphos, CVMP (tetrachlorvinphos), thiometon, triazophos, DEP (trichlorfon), and bamidothion.

[0075] Examples of GABAergic chloride ion channel blockers include chlordane, benzoepine (endosulfan), dienochlor, ethiprole, fipronil, pyriprol, and nicoflurprole.

[0076] Examples of sodium channel modulators include acrinatrin, allethrin (allethrin, d-cis-trans- and d-trans-isomers), bifenthrin, bioallethrin (bioallethrin, S-cyclopentenyl-isomer), violethmetrin, chloroprarethrin, chlorfensone, cycloprothrin, cyfluthrin (cyfluthrin, β-isomer), cyhalothrin (cyhalothrin, λ- and γ-isomers), cypermethrin (cypermethrin, α-, β-, θ- and ζ-isomers), cyphenothrin [(1R)-trans isomer], deltamethrin, dimefluthrin, empenthrin [(EZ)-(1R)-isomer], esfenvalerate, etofenprox, and fe Examples include propatrin, fenvalerate, flubrocitrinate, flucitrinate, flumethrin, fluvalinate (τ-fluvalinate), halfenprox, imiprothrin, cadesrin, metofluthrin, monfluorothrin, epsilon-metofluthrin, epsilon-monfluorothrin, permethrin, phenothrin [(1R)-trans isomer], prallethrin, profluthrin, pyrethrin, resmethrin, silafluofen, tefluthrin, phthalthrin (tetramethrin), tetramethrin [(1R)-isomer], tralomethrin, transfluthrin, DDT, methoxychlor, aldrin, dieldrin, and linden.

[0077] Examples of competitive modulators of nicotinic acetylcholine receptors (nAChRs) include acetamiprid, clothianidin, dinotefuran, imidacloprid, nitenpyram, thiacloprid, thiamethoxam, nicotine sulfate (nicotine), sulfoxaflor, flupyradiflon, dichloromesothiaz, fenmesoditiaz, and triflumesopyrim.

[0078] Nicotinic acetylcholine receptor (nAChR) allosteric modulators include spinetram, spinosad, flupyrimin, and GS-omega / kappa HXTX-Hv1a peptide.

[0079] Examples of glutamate-gated chloride ion channel (GluCl) allosteric modulators include abamectin, emamectin benzoate, lepimectin, and milbemectin.

[0080] Examples of juvenile hormone analogs include hydroprene, quinoprene, methoprene, phenoxycarb, and pyriproxyfen.

[0081] Other nonspecific (multisite) inhibitors include methyl bromide, other alkyl halides, chloropicrin, sodium aluminum fluoride, sulfuryl fluoride, borax, boric acid, disodium octaborate, sodium metaborate, tartaric acid, dazomet, carbam (metham ammonium salt), metam sodium salt (carbam sodium salt), and methyl isothiocyanate (methyl isothiocyanate).

[0082] Examples of TRPV channel modulators for chordal organs include pymetrozine, pyrifluquinazone, and afidopiropene.

[0083] Examples of mite growth inhibitors that act on CHS1 include clofentedine, diflovidazine, hexythiazox, and etoxazole.

[0084] Examples of microbial-derived insect midgut endometrial disruptors include Bacillus thuringiensis subsp. israelensis, Bacillus thuringiensis subsp. aizawai, Bacillus thuringiensis subsp. kurstaki, Bacillus thuringiensis subsp. tenebrionis, proteins contained in Bt crops (Cry1Ab, Cry1Ac, Cry1Fa, Cry1A.105, Cry2Ab, Vip3A, mCry3A, Cry3Bb, Cry34Ab1 / Cry35Ab1), and Bacillus sphaericus.

[0085] Examples of mitochondrial ATP synthase inhibitors include diafenthiurone, azocyclotin, tricyclohexyltin hydroxide (cyhexatine), fenbutatin oxide, BPPS (propargit), and tetradiphon.

[0086] Examples of oxidative phosphorylation uncoupling agents that disrupt the proton gradient include chlorfenapyr, DNOC, and sulfuramide.

[0087] Examples of nicotinic acetylcholine receptor (nAChR) channel blockers include bensultap, cartap hydrochloride, thiocyclam, thiosultap sodium, and monosultap.

[0088] Examples of chitin biosynthesis inhibitors that act on CHS1 include bistriflurone, chlorfluazurone, diflubenzuron, flucycloxurone, flufenoxurone, hexaflumurone, lufenuron, novaron, nobiflumuron, teflubenzuron, and triflumuron.

[0089] Examples of chitin biosynthesis inhibitors (Type 1) include buprofezin.

[0090] Examples of molting inhibitors (for flies) include cyromazine.

[0091] Examples of molting hormone (ecdysone) receptor agonists include chromafenozide, halofenozide, methoxyfenozide, and tebufenozide.

[0092] Examples of octopamine receptor agonists include amitraz.

[0093] Examples of mitochondrial electron transport chain complex III inhibitors include hydramethylnon, acequinosyl, fluacrypyrim, flupyroxystrobin, and bifenazate.

[0094] Examples of mitochondrial electron transport chain complex I inhibitors (METIs) include phenazaquine, fenpyroximate, pyridaben, pyrimidifene, tebufenpyrad, tolfenpyrad, and Delis (rotenone).

[0095] Examples of voltage-gated sodium channel blockers include indoxacarb and metaflumisone.

[0096] Examples of acetyl-CoA carboxylase inhibitors include spirodiclofen, spiromesifen, spiropidione, spidoxamato, spirobudifen, and spirotetramat.

[0097] Examples of mitochondrial electron transport chain complex IV inhibitors include aluminum phosphide, calcium phosphide, hydrogen phosphide, zinc phosphide, hydrogen cyanide (calcium cyanide / sodium cyanide), and potassium cyanide.

[0098] Examples of mitochondrial electron transport chain complex II inhibitors include cyenopyrafen, cyetopyrafen, cyflumetofen, piflubumi, and cyclobutrifluram.

[0099] Examples of ryanodine receptor modulators include chlorantraniliprole, cyantraniliprole, cyclaniliprole, flubendiamide, tetraniliprole, flchlordiniliprole, thiolantraniliprole, tetrachlorantraniliprole, cyhalodiamids, and cyprofuranilide.

[0100] Examples of string organ modulators include flonicamide.

[0101] Examples of GABAergic chloride ion channel allosteric modulators include broflanilide, fluxamethamide, and isocycloceram.

[0102] Examples of baculoviruses include codling moth (Cydia pomonella GV), codling moth (Thaumatotibia leucotreta GV), velvet bean caterpillar (Anticarsis gemmatalis MNPV), and tobacco budworm (Helicoverpa armigera NPV).

[0103] Other insecticides, acaricides, and nematicides include azadirachtin, benzomate (benzoximate), phenisobromolate (bromopropylate), quinoxaline (quinomethionate), kelthane (dicofol), lime sulfur mixture, mancozeb, pyridaryl, sulfur, acinonapyr, amidoflumet, benzpyrimoxane, fluazaindridine, fluensulfone, fluhexaphon, flupentiophenox, flomethin, metaldehyde, ticlopyrazoflor, zinpropylidaz, trifluenflonate, indazapiroxamet, sulfiflumin, and Burkhold Examples include Lya species, Wolbachia pipeientis (Zap), Aralia elata extract, fatty acid monoesters containing glycerin or propanediol, neem oil, machine oil, rapeseed oil, blended oils, starch, reduced starch saccharides, sodium oleate, ferric phosphate, nemadectin, Beauveria bassiana strain, Metaridium anisopria strain (F52), Pesilomyces fumosoroseus apopka strain (97), diatomaceous earth, DCIP (dichlorodiisopropyl ether), DD (1,3-dichloropropene), levamisole hydrochloride, morantel tartrate, and thioxazafen.

[0104] Suitable effective ingredients for herbicidal applications include, for example, acetolactate synthesis (ALS) inhibitors, amino acid compounds, cyclohexanedione compounds, acetamide compounds, bipyridilium compounds, allyloxyphenoxypropionic acid compounds, carbamate compounds, pyridine compounds, urea compounds, dinitroaniline compounds, protoporphyrinogen oxidase (PPO) inhibitors, phenoxyacetic acid compounds, hydroxyphenylpyruvate dioxygenase (HPPD) inhibitors, and triazine compounds.

[0105] Examples of acetolactic acid synthesis (ALS) inhibitor compounds include imazametabenz and imazametabenzmethyl, imazamox, imazapic, imazapyr, imazakine, imazetapyr, amidosulfuron, azimsulfuron, bensulfuron and bensulfuronmethyl, chlorimuron and chlorimuronmethyl, chlorimuronethyl, chlorsulfuron, cinosulfuron, cyclosulfamuron, etamethosulfuron and etamethosulfuronmethyl, eto Xysulfuron, flazasulfuron, flucetosulfuron, flupyrsulfuron, flupyrsulfuron methyl and its salts, horamsulfuron, halosulfuron, halosulfuron methyl, imazosulfuron, iodosulfuron and its salts, iodosulfuron methyl and its salts, mesosulfuron, mesosulfuron methyl, metazosulfuron, metosulfuron, metosulfuron methyl, nicosulfuron, oxasulfuron, primisulfuron, primisulfuron Examples include flonmethyl, propyrisulfuron, prosulfuron, pyrazosulfuron, pyrazosulfuron ethyl, limsulfuron, sulfomethuron, sulfomethuron methyl, sulfosulfuron, thifensulfuron, thifensulfuron methyl, triasulfuron, tribenulon, tribenulon methyl, trifloxysulfuron and its salts, triflusulfuron, triflusulfuron methyl, tritosulfuron, imizametabenzmethyl, bispyribac sodium, chloranslam, chloranslam methyl, dicloslam, floraslam, fulcarbazone and its salts, flumethoslam, metoslam, orthosulfamuron, penoxulam, piroxulam, propoxycarbazone and its salts, pyribenzoxime, pyrifthalide, pyriminobac methyl, pyrimisulfan, pyrithiobac and its salts, pyroxyslam, thiencarbazone, thiencarbazone methyl, and triafamone.

[0106] Examples of amino acid-based compounds include bialaphos and its salts, glufosinate and its salts, glufosinate P and its salts, and glyphosate and its salts.

[0107] Examples of cyclohexanedione compounds include alloxidium, butroxidium, cretodymium, cloxoxidium, cycloxidium, prophoxidium, cethoxidium, tepraloxidium, and tralcoxidium.

[0108] Examples of acetamide compounds include napropamide, dimethachlor, petoxamide, acetochlor, alachlor, alidoclor (CDAA), butenachlor, delaclor, dietatylethyl, propisochlor, pyrinachlor, butachlor, dimethenamide, dimethenamide P, metazachlor, metrachlor, S-methochlor, pretilachlor, propachlor, tenylchlor, fluphenacet, and mefenacet.

[0109] Examples of bipyridilium compounds include cypercoat, morphamcoat, diquat, and paraquat.

[0110] Examples of allyloxyphenoxypropionic acid compounds include clodinafop, clodinafoppropargyl, clofop, cyhalofopbutyl, diclofop, diclofopmethyl, diclofopPmethyl, phenoxaprop, phenoxapropethyl, phenoxapropPethyl, fluadifop, fluadifopbutyl, fluadifopPbutyl, haloxyfop, haloxyfopmethyl, haloxyfopPmethyl, isoxapirihop, metamihop, propaxifop, quizalohop, quizalohopethyl, quizalohopPethyl, and quizalohopPtefuryl.

[0111] Examples of carbamate compounds include ashram, carbetamide, desmedifam, chlorprocarb, phenisocarb, cycloate, dimepiperate, pevlate, thiocarbasil, burnalate, barban, chlorbuffam, chlorprofam, profam, suep, fenmedifam, butyrate, EPTC, esprocarb, molinate, olbencarb, prosulfocarb, pyributicarb, thiobencarb (benchiocarb), and trialate.

[0112] Examples of pyridine compounds include aminopyralide, clopyralide, diflufenican, dithiopyr, flulidone, fluroxypyr, halouxifene, florpyrauxifene, picloram and its salts, picolinafene, thiazopyr, and triclopyr and its salts.

[0113] Examples of urea compounds include benzthiazolon, bromulone, buturone, chlorbromulone, chloroxurone, diphenoxrone, dimeflon, ethidimulone, fenulon, fluothirone, metobenzulon, metobromulone, metoxrone, monolinurone, mononulon (CMU), nevlon, paraflulon, sideurone, thiazaflulon, chlorotolurone, dimuron, diurone (DCMU), fluomethurone, isoproturone, linurone, metabenzthiazulon, tebuthiurone, cumylon, carbchylate, and isourone.

[0114] Examples of dinitroaniline compounds include benfluralin (veslodin), butruarin, dinitramine, ethalfluralin, fluroralin, isopropaline, nitralin, profluralin, oryzaline, pendimethalin, prodiamine, and trifluralin.

[0115] Examples of protoporphyrinogen oxidase (PPO) inhibitors include asifluorphen, acroniphen, azaphenidine, bifenox, clomethoxyl, ethoxyphen, ethoxyphenethyl, homesaphen, fluazolate, fluoroglycofen, fluoroglycofenethyl, halosaphen, lactofen, oxyfluorphen, butaphenacil, epiriphenacil, chlornitrofen (CNP), fluorodiphen, fluoronitrofen (CFNP), nitrofen (NIP), oxyflufen, chlorphthalim, flumipropine, carfentrazone, carfentrazone ethyl, synidone ethyl, flumicrolacpentyl, flumioxazine, fluthiaset, fluthiaset methyl, oxaziargyl, oxadiazone, pentoxazone, pyraclonil, pyraflufen, pyraflufenethyl, saflufenacil, sulfentrazone, tidiazimine, benzfenzizone, profluazole, and flufenpyruethyl.

[0116] Examples of phenoxyacetic acid compounds include 2,4,5-T, 2,4-D and their salts, 2,4-DB and its salts, clomeprop, dichlorprop, phenoprop, MCPA and its salts, MCPB and its salts, mecoprop (MCPP) and its salts, and mecoprop P and its salts.

[0117] Examples of hydroxyphenylpyruvate dioxygenase enzyme (HPPD) inhibitors include benzobicyclon, benzofenap, bicyclopyrone, isoxaflutol, mesotrione, pyrasulfolol, pyrazolinate, pyrazoxyfen, sulcotrione, tefuryltrione, tembotrione, toprameson, fenquinotrione, and tolpyrate.

[0118] Examples of triazine compounds include atlatone, adiprothrin, chlorazine, siprazine, desmethrin, dipropetrin, eglinadine ethyl, ipazine, metoprotrin, procyazin, proglinadine, prometone, propazine, sebutyrazine, sebutyrazine, terbumetone, trietadine, ametrin, atrazine, cyanazine, dimethametrin, hexazinone, indadiflame, metamitron, metrivudine, promethrin, simazine (CAT), simetrin, terbutyrazine, terbutrin, and triaziflame.

[0119] In addition, other compounds used as herbicides include amicarbazone, ethidine, isomethiodin, aminocyclopyrachlor, aminotriazole, anirofos, piperofos, beflubutamide, benazoline, benfresate, bentazon, bromacil, isocyl, bromobutide, bromophenoxime, bromoxynil, butamiphos, DMPA, TCTP (chlortal dimethyl), cafenstrol, chloridazone (PAC), brompyrazone, chlortal, chromazon, cumilon, dicamba (MDBA) and its salts, chloramben, TCBA (2,3,8-TBA), benazoline ethyl, chlorfenac, chlorfenprop, diclobenyl (DBN), chlorthiamide (DCBN), scinmethiline, methiozoline, amitorol, flamprop M, hosamin, methyl dimuron, monalid, MSMA, diphenzocort, diflufenzopyr, endotal and its salts, etofumesate, etobenzanide, phenoxasulfone, phentrazamide, flupoxam, fluorochloridone, flu Lutamon, Indanophan, Tridiphan, Ioxinil, Ipfencarbazone, Isoxaben, Triazifuran, Renacil, Methylarsonic acid, Naptalam, Flurochloridone, Norflurazone, Oxadiclomefone, Pinoxadene, Chloranocryl-Dicryl, Pentanocrol (CMMP), Propanil, Propyzamide, Pyridate, Pyroxasulfone, Promacil, Quinclorac, Kinmelac, Quinoclamine, Terbasil, Cyclopyri Molate, Florpyrauxifen-benzyl, Lancotrione and its salts, Cyclopyranil, Bixrozone, Tetoflupyrrolimet, Dimesulfazet, Dinosum, Dinoseb (DNBP), DNOC, Dinoterb, Ethinofen, Medinoterb, DSMA, Cacodylic acid, Diphenamide, Naproanilide, Tebutam, Benslide, Darapone, TCA, Mefluidide, Pe Examples include fluidone, CAMA, thiafenacil, trifludimoxazine, limisoxafen, fenpyrazone, dioxopyritrone, cypirafluone, bipirazone, benkitrone, fluchloraminopir, pyriflubenzoxime, fluphenoximacil, iptriazopyride, flusulfinum, broclozone, indolauxipir, icaforin, pyrakinate, tetrapion (flupropanate) and its salts, as well as d-limonene.

[0120] [Methods to improve plant tolerance to environmental stress] The environmental stress tolerance enhancer in this embodiment can be used, for example, in agricultural or non-agricultural land such as fields, paddy fields, lawns, and orchards. Furthermore, the environmental stress tolerance enhancer in this embodiment can be used by any fertilization method, such as foliar application, mixing with water, application to soil, injection into the subsoil using an injection machine, seed treatment including treatment of bulbs and tubers, and direct fertilization of plants.Therefore, the method for improving environmental stress tolerance in this embodiment includes a procedure for fertilizing using the above-described environmental stress tolerance enhancer.

[0121] When applied by mixing with water supply, for example, granular formulations are administered to water supplied to crops or to the surface water of paddy fields. In one example, the concentration of the active ingredient in the water supply is 0.5 to 500 mg / L, preferably 1 to 300 mg / L. When administered to the surface water of paddy fields, the amount of active ingredient used is, for example, 0.5 to 5000 g per 10 ares of paddy field, preferably 3 to 3000 g.

[0122] For application by foliar spraying or soil application, for example, granular formulations can be applied to the planting hole or its surroundings when transplanting seedlings, or granular and wettable powder formulations can be applied to seeds, plants, or the soil surrounding the plants. It is also preferable to mix the formulation with the soil after application. The amount of active ingredient used when applying by foliar spraying or soil surface application is calculated per square meter of agricultural or horticultural land. 2 For example, the amount per unit is 0.5 to 5000 mg, preferably 3 to 3000 mg.

[0123] In seed treatment, the chemical is applied to the seeds by mixing and stirring wettable powders and powders with the seeds, or by immersing the seeds in diluted wettable powders. Seed treatment also includes seed coating. The amount of active ingredient used in seed treatment is, for example, 0.005 to 10000 g per 100 kg of seeds, preferably 0.05 to 1000 g. Seeds treated with agricultural and horticultural chemicals can be used in the same way as ordinary seeds.

[0124] Furthermore, the concentration and amount used may vary depending on the dosage form, timing of application, method of application, location of application, and target crop, so it is possible to increase or decrease them without being bound by the above range. As explained above, compound (I) and its tautomers show excellent environmental stress tolerance-improving effects on a wide range of plants.

[0125] [Use of environmental stress tolerance enhancers] As described above, the environmental stress tolerance enhancer in this embodiment exhibits an excellent effect in improving environmental stress tolerance in treated plants.

[0126] 〔summary〕 As described above, the plant environmental stress tolerance enhancer according to Embodiment 1 of the present invention contains a compound represented by the following formula (I) or a tautomer thereof, or an agriculturally acceptable salt thereof, as an active ingredient. [ka] (In formula (I), R 1 and R 2 R independently represents a hydrogen atom or an alkyl group having 1 to 4 carbon atoms. 3 ~R 5 (This independently represents an alkyl group having 1 to 4 carbon atoms.)

[0127] Furthermore, in the plant environmental stress tolerance improving agent of embodiment 2 according to the present invention, it is preferable that the compound represented by formula (I) in embodiment 1 is ergothioneine.

[0128] Furthermore, in embodiment 3 of the present invention, the plant environmental stress tolerance enhancer preferably improves tolerance to environmental stress, which is at least one selected from high temperature stress, low temperature stress, freezing stress, salt stress, excess nutrient stress, drought stress, excess water stress, ultraviolet stress, weak light stress, and strong light stress, in embodiment 1 or 2.

[0129] Furthermore, in any of the embodiments 1 to 3, the plant environmental stress tolerance enhancer of embodiment 4 of the present invention is a salt stress tolerance enhancer.

[0130] Furthermore, in any of the embodiments 1 to 3, the plant environmental stress tolerance enhancer of embodiment 5 of the present invention is a drought stress tolerance enhancer.

[0131] Furthermore, in any of the embodiments 1 to 3, the plant environmental stress tolerance enhancer of embodiment 6 of the present invention is a high-temperature stress tolerance enhancer.

[0132] Furthermore, in any of the embodiments 1 to 3, the plant environmental stress tolerance enhancer of embodiment 7 of the present invention is an excess nutrient stress tolerance enhancer.

[0133] Furthermore, in any of embodiments 1 to 3, the plant environmental stress tolerance enhancer of embodiment 8 of the present invention is an excess water stress tolerance enhancer.

[0134] Furthermore, in any of the embodiments 1 to 3, the plant environmental stress tolerance enhancer of embodiment 9 of the present invention is an ultraviolet stress tolerance enhancer.

[0135] Furthermore, in any of the embodiments 1 to 3, the plant environmental stress tolerance enhancer of embodiment 10 of the present invention is a light stress tolerance enhancer.

[0136] Furthermore, in any of the embodiments 1 to 3, the plant environmental stress tolerance enhancer of embodiment 11 of the present invention is a freeze stress tolerance enhancer.

[0137] Furthermore, in any of embodiments 1 to 3, the plant environmental stress tolerance enhancer of embodiment 12 of the present invention is a low-temperature stress tolerance enhancer.

[0138] Furthermore, the method for improving the environmental stress tolerance of plants according to embodiment 13 of the present invention includes treating plants with any of the environmental stress tolerance improving agents described in embodiments 1 to 12.

[0139] The embodiments of the present invention will be further described in detail below, with reference to the following examples. Of course, the present invention is not limited to the following examples, and it goes without saying that various embodiments are possible in terms of details. Furthermore, the present invention is not limited to the embodiments described above, and various modifications are possible within the scope of the claims, and embodiments obtained by appropriately combining the disclosed technical means are also included in the technical scope of the present invention. In addition, all references cited herein are incorporated by reference. [Examples]

[0140] The effects of the environmental stress tolerance enhancer according to this embodiment will be shown below using L-(+)-ergothioneine. In the following description, glycine betaine, a compound different from the environmental stress tolerance enhancer according to this embodiment, will be used as a comparative compound. In the following description, L-(+)-ergothioneine may be abbreviated as "EGT" and glycine betaine as "GB".

[0141] [Evaluation Example 1] Comparison of tolerance effects to salt stress L-(+)-ergothioneine (Examples 1-2, Comparative Example 3) and glycine betaine (Comparative Examples 1-2, Comparative Example 4) were prepared to the concentrations shown in Table 1 below. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0142] Three Arabidopsis thaliana (Col-0) individuals were seeded per well in a 24-well cell culture plate. A liquid culture medium was prepared by adding 1% by weight sucrose and 0.1% by weight agar powder to Murashige-Skoog medium (Fujifilm Wako Pure Chemical Industries), and 2 mL of this medium was added to each well.

[0143] The plants were placed in an artificial climate chamber set to a room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. The lighting conditions were set so that the light intensity in the center under fluorescent lighting was 5000 lx. Four days after sowing, EGT or GB was added to reach a predetermined concentration, and 24 hours later, a sodium chloride solution was added to achieve a final concentration of 100 mM, thereby inducing salt stress.

[0144] The number of surviving plants was counted 10 days after sowing, and the plant mortality rate was evaluated as an indicator of physiological disorders. The evaluation results are shown in Table 1. The mortality rate and environmental stress suppression rate were calculated using the following formulas. Mortality rate (%) ={1-(number of surviving plants / number of plants tested)}×100 Environmental stress reduction rate (%) ={1-(death rate in the treated area / death rate in the untreated area)}×100 [Table 1]

[0145] As shown in Table 1, salt stress caused physiological disorders such as chlorosis in Arabidopsis thaliana, and 75% of the tested Arabidopsis thaliana died (Comparative Example 5). Treatment with GB did not suppress death due to salt stress (Comparative Examples 1 and 2). In contrast, treatment with EGT suppressed death due to salt stress, reducing the mortality rate to 14% at 1 mM (Example 1) and 39% at 0.1 mM (Example 2).

[0146] [Evaluation Example 2] Comparison of resistance effects to drought stress EGT (Example 3) was prepared to the concentrations shown in Table 2 below. A commercially available EGT was used, and pure water was used as the solvent.

[0147] One Arabidopsis thaliana (Col-0) seed was sown per pot in a plastic pot measuring 60 mm in diameter and 55 mm in height. Six pots were placed in a deep plastic dish measuring 160 mm in diameter and 28 mm in height. As soil, 45 mL of vermiculite, 22.5 mL of granular potting soil (Kumiai Horticultural Potting Soil), and 22.5 mL of vermiculite were added to the pots in that order.

[0148] The plants were placed in an artificial climate chamber set to a room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. Lighting conditions were set so that the light intensity in the center under fluorescent lighting was 5000 lx. Water was supplied from the bottom, with the water level set to approximately 5 mm. 50 mL of EGT was added 22 days after sowing, and watering was stopped for 18 days starting 2 days later to induce drought stress.

[0149] The number of surviving plants 18 days after water rationing was counted, and the plant mortality rate was evaluated as an indicator of physiological disorder. The evaluation results are shown in Table 2. The mortality rate and environmental stress suppression rate were calculated using the following formulas. Mortality rate (%) ={1-(number of surviving plants / number of plants tested)}×100 Environmental stress reduction rate (%) ={1-(death rate in the treated area / death rate in the untreated area)}×100 [Table 2]

[0150] As shown in Table 2, drought stress caused physiological disorders such as wilting or necrosis in Arabidopsis thaliana, and 50% of the tested Arabidopsis thaliana died (Comparative Example 7). In contrast, all Arabidopsis thaliana survived after treatment with EGT (Example 3).

[0151] [Evaluation Example 3] Comparison of resistance effects to drought stress EGT (Example 4) or GB (Comparative Example 9) were prepared to the concentrations shown in Table 3 below. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0152] 90 mL of granular potting soil (Kumiai Horticultural Potting Soil) was placed in a plastic pot measuring 60 mm in diameter and 55 mm in height, and one cotton plant (Tohoku Co., Ltd.) was sown per pot.

[0153] The plants were managed in a greenhouse set at a room temperature of 25°C. On the 23rd day after sowing, 50 mL of EGT or 50 mL of GB was added, and watering was stopped for 4 days starting 4 days later to induce drought stress.

[0154] Leaves were collected four days after the water supply was cut off and photographed with a digital camera. The photographs of the leaves were analyzed using the image analysis software WinROOF (manufactured by Mitani Corporation) to quantify the total leaf area and green leaf area.

[0155] The leaf necrosis rate four days after water cessation was evaluated using the total leaf area and green leaf area described above. The evaluation results are shown in Table 3. The leaf necrosis rate and environmental stress reduction rate were calculated using the following formulas. Leaf necrosis rate (%) ={1-(green leaf area / total leaf area)}×100 Environmental stress reduction rate (%) ={1-(necrosis rate of leaves in the tested compound treatment group / necrosis rate of leaves in the untreated group)}×100 [Table 3]

[0156] As shown in Table 3, drought stress caused wilting, chlorosis, or necrosis in the cotton plants, and 52% of the cotton leaves tested underwent necrosis (Comparative Example 10). Treatment with GB did not suppress necrosis due to drought stress (Comparative Example 9). In contrast, treatment with EGT suppressed the necrosis rate due to drought stress to 26% (Example 4).

[0157] [Evaluation Example 4] Comparison of resistance effects to high temperature stress EGT (Example 5, Comparative Example 13) or GB (Comparative Example 12, Comparative Example 14) were prepared to the concentrations shown in Table 4 below. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0158] 80 mL of potting soil (made by Hanagokoro Co., Ltd.) was placed in plastic pots measuring 60 mm in diameter and 55 mm in height, and one Arabidopsis thaliana (Col-0) seed was sown per pot. Four pots were placed in a deep plastic dish measuring 160 mm in diameter and 28 mm in height.

[0159] The plants were placed in an artificial climate chamber set to a room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. The lighting conditions were set so that the light intensity in the center under fluorescent lighting was 5000 lx. Water was supplied from the bottom, with the water level set to approximately 5 mm. 41 days after sowing, 50 mL of EGT or 50 mL of GB was added, and one day later, the plants were exposed to a 42°C environment for 3 hours to induce high-temperature stress.

[0160] The number of surviving plants 12 days after being subjected to high-temperature stress was counted, and the plant mortality rate was evaluated as an indicator of physiological disorder. The evaluation results are shown in Table 4. The mortality rate and environmental stress suppression rate were calculated using the following formulas. Mortality rate (%) ={1-(number of surviving plants / number of plants tested)}×100 Environmental stress reduction rate (%) ={1-(death rate in the treated area / death rate in the untreated area)}×100 [Table 4]

[0161] As shown in Table 4, high-temperature stress caused physiological disorders such as wilting or necrosis in Arabidopsis thaliana, and 75% of the tested Arabidopsis thaliana died (Comparative Example 15). Treatment with GB did not suppress the mortality rate due to high-temperature stress (Comparative Example 12). In contrast, treatment with EGT suppressed the mortality rate due to high-temperature stress to 25% (Example 5).

[0162] [Evaluation Example 5] Comparison of Tolerance Effects to Excess Nutrient Stress EGT (Example 6) or GB (Comparative Example 17) were prepared to the concentrations shown in Table 5 below. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0163] One Arabidopsis thaliana (Col-0) seed was sown per pot in a plastic pot measuring 60 mm in diameter and 55 mm in height. Four pots were placed in a deep plastic dish measuring 160 mm in diameter and 28 mm in height. As soil, 45 mL of vermiculite, 22.5 mL of granular potting soil (Kumiai Horticultural Potting Soil), and 22.5 mL of vermiculite were added to the pots in that order.

[0164] The plants were placed in an artificial climate chamber set to a room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. Lighting conditions were set so that the light intensity in the center under fluorescent lighting was 5000 lx. Watering was done from the bottom, with the water level set to approximately 5 mm. 61 days after sowing, 50 mL of EGT or 50 mL of GB was added, and one day later, liquid fertilizer (HYPONeX, manufactured by Hyponex Japan) was applied at a 5-fold dilution to induce nutrient stress.

[0165] The number of wilted leaves one day after applying excessive nutrient stress was evaluated. The evaluation results are shown in Table 5. The leaf wilting rate and the environmental stress suppression rate were calculated using the following formulas. Leaf wilting rate (%) = (Number of withered leaves / Total number of leaves on the tested plant) × 100 Environmental stress reduction rate (%) ={1-(Wilting rate in the treated area / Wilting rate in the untreated area)}×100 [Table 5]

[0166] As shown in Table 5, 100% of the Arabidopsis thaliana leaves tested showed wilting due to excessive nutrient stress (Comparative Example 18), and treatment with GB hardly suppressed the wilting rate due to excessive nutrient stress (Comparative Example 17). In contrast, Arabidopsis thaliana leaves treated with EGT (Example 6) showed a lower wilting rate compared to leaves treated with GB, indicating that wilting due to excessive nutrient stress was suppressed.

[0167] [Evaluation Example 6] Comparison of resistance effects to drought stress EGT (Examples 7, 8) or GB (Comparative Examples 20, 21) were prepared to the concentrations shown in Table 6 below. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0168] 150 mL of granular potting soil (Kumiai Horticultural Potting Soil) was placed in a 60 mm square, 66 mm high plastic pot, and one soybean seed was sown per pot.

[0169] The plants were managed in a greenhouse set at a room temperature of 25°C. On the 23rd day after sowing, 50 mL of EGT or 50 mL of GB was added, and then watering was stopped for 7 days to induce drought stress.

[0170] The number of dead leaves was counted seven days after the water supply was cut off, and the leaf mortality rate was evaluated as an indicator of physiological disorder. The evaluation results are shown in Table 6. The leaf mortality rate and the environmental stress suppression rate were calculated using the following formulas. Leaf mortality rate (%) = (Number of dead leaves / Total number of leaves of the tested plant) × 100 Environmental stress reduction rate (%) ={1-(leaf mortality rate in the treatment group with the test compound / leaf mortality rate in the untreated group)}×100 [Table 6]

[0171] As shown in Table 6, drought stress caused physiological disorders in soybeans, such as leaf wilting or necrosis, and 62% of the leaves of the soybeans tested died (Comparative Example 22). Treatment with GB did not suppress the mortality rate due to drought stress (Comparative Examples 20 and 21). In contrast, treatment with EGT suppressed the mortality rate due to drought stress to 55% at 0.1 mM (Example 8) and to 38% at 1.0 mM (Example 7).

[0172] [Evaluation Example 7] Comparison of resistance effects to drought stress EGT (Example 9) or GB (Comparative Example 24) were prepared to the concentrations shown in Table 7 below. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0173] 1 kg of granular potting soil (Kumiai Horticultural Potting Soil) was placed in a plastic pot measuring 135 mm in diameter and 110 mm in height, and 5 radish (Red Round Radish) seeds were sown per pot.

[0174] The plants were managed in a greenhouse set at a room temperature of 25°C. On the 22nd day after sowing, 50 mL of EGT or 50 mL of GB was added, followed by 7 days of withholding water. After that, the plants were grown under water for 7 days, and then drought stress was induced by withholding water again for 7 days.

[0175] The number of dead leaves in radishes subjected to drought stress was counted, and the leaf mortality rate was evaluated as an indicator of physiological disorder. The evaluation results are shown in Table 7. The leaf mortality rate and the environmental stress suppression rate were calculated using the following formulas. Leaf mortality rate (%) = (Number of dead leaves / Total number of leaves of the tested plant) × 100 Environmental stress reduction rate (%) ={1-(leaf mortality rate in the treatment group with the test compound / leaf mortality rate in the untreated group)}×100 [Table 7]

[0176] As shown in Table 7, drought stress caused physiological disorders such as leaf wilting or necrosis in radishes, and 59% of the leaves of the tested radishes died (Comparative Example 25). Treatment with GB did not suppress the mortality rate due to drought stress (Comparative Example 24). In contrast, treatment with EGT suppressed the mortality rate due to drought stress to 17% (Example 9).

[0177] [Evaluation Example 8] Comparison of resistance effects to drought stress EGT (Example 10) or GB (Comparative Example 27) were prepared to the concentrations shown in Table 8 below. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0178] I placed 1 liter of seedling growing medium (manufactured by Takii Seed Co., Ltd.) into plastic pots measuring 135 mm in diameter and 110 mm in height, and then laid 100 mm square pieces of Korean grass (Zoysia japonica) in each pot.

[0179] The plants were managed in a greenhouse set at a room temperature of 25°C. Approximately one month after laying the turf, 12.5 mL of EGT or 12.5 mL of GB was added, and then watering was stopped for 7 days. After cultivating under watering for another 7 days, drought stress was induced by stopping watering again for 7 days.

[0180] The number of dead leaves in grasses subjected to drought stress was counted, and the leaf mortality rate was evaluated as an indicator of physiological disorder. The evaluation results are shown in Table 8. The leaf mortality rate and the environmental stress suppression rate were calculated using the following formulas. Leaf mortality rate (%) = (Number of dead leaves / Total number of leaves of the tested plant) × 100 Environmental stress reduction rate (%) ={1-(leaf mortality rate in the treatment group with the test compound / leaf mortality rate in the untreated group)}×100 [Table 8]

[0181] As shown in Table 8, drought stress caused physiological disorders such as necrosis in the grass, and 100% of the grass leaves tested died (Comparative Example 28). Treatment with GB did not suppress the mortality rate due to drought stress (Comparative Example 27). In contrast, treatment with EGT suppressed the mortality rate due to drought stress to 35% (Example 10).

[0182] [Evaluation Example 9] Comparison of Tolerance Effects to Excess Water Stress EGT (Example 11, Comparative Example 31) or GB (Comparative Examples 30, 32) were prepared to the concentrations shown in Table 9 below. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0183] 5 mL of pure water was added to a 9 cm petri dish lined with filter paper, and 12 rapeseed seeds were sown per dish. The plants were kept in an artificial climate chamber set to room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. The lighting conditions were set so that the light intensity in the center under fluorescent lighting was 5000 lx.

[0184] Six days after sowing, the pure water in the petri dish was removed, and then 5 mL of EGT or 5 mL of GB was added to the petri dish. One day later, 50 mL of pure water was added to the petri dish to induce excess water stress.

[0185] The number of surviving plants 19 days after being subjected to excessive water stress was counted, and the plant mortality rate was evaluated as an indicator of physiological disorder. The evaluation results are shown in Table 9. The mortality rate and environmental stress suppression rate were calculated using the following formulas. Mortality rate (%) ={1-(number of surviving plants / number of plants tested)}×100 Environmental stress reduction rate (%) ={1-(death rate in the treated area / death rate in the untreated area)}×100 [Table 9]

[0186] As shown in Table 9, excessive water stress caused physiological disorders such as chlorosis in rapeseed, and 60% of the tested rapeseed died (Comparative Example 33). Treatment with GB did not suppress the mortality rate due to excessive water stress (Comparative Example 30). In contrast, treatment with EGT suppressed the mortality rate due to excessive water stress to 25% (Example 11).

[0187] [Evaluation Example 10] Comparison of resistance effects to UV stress EGT (Examples 12, 13, Comparative Examples 37, 38) or GB (Comparative Examples 35, 36, 39, 40) were prepared to the concentrations shown in Table 10 below. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0188] 5 mL of pure water was added to a 9 cm petri dish lined with filter paper, and 10 wheat seeds were sown per dish. The plants were kept in an artificial climate chamber set to room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. The lighting conditions were set so that the light intensity in the center under fluorescent lighting was 5000 lx.

[0189] On the 7th day after sowing, after removing the pure water from the petri dish, 5 mL of EGT or 5 mL of GB was added to the petri dish. One day later, under irradiation with a UV lamp (Toshiba, GL-15), the UV radiation intensity at a wavelength of 254 nm was measured to 550 μW / cm². -2 The device was set to perform this action, and UV stress was inflicted by exposing it to the light for one hour.

[0190] The number of dead leaves six days after exposure to ultraviolet stress was counted, and the leaf mortality rate was evaluated as an indicator of physiological disorder. The evaluation results are shown in Table 10. The leaf mortality rate and the environmental stress suppression rate were calculated using the following formulas. Leaf mortality rate (%) = (Number of dead leaves / Total number of leaves of the tested plant) × 100 Environmental stress reduction rate (%) ={1-(leaf mortality rate in the treatment group with the test compound / leaf mortality rate in the untreated group)}×100 [Table 10]

[0191] As shown in Table 10, UV stress caused physiological disorders such as chlorosis in wheat, and 53% of the wheat leaves tested died (Comparative Example 41). Treatment with GB did not suppress the mortality rate due to UV stress to any significant extent (Comparative Examples 35, 36). In contrast, wheat treated with EGT had a lower mortality rate compared to wheat treated with GB, and the mortality rate due to UV stress was suppressed to 34% at 0.1 mM (Example 13) and 23% at 1.0 mM (Example 12).

[0192] [Evaluation Example 11] Comparison of resistance effects to UV stress EGT (Examples 14, 15, Comparative Examples 45, 46) or GB (Comparative Examples 43, 44, 47, 48) were prepared to the concentrations shown in Table 11 below. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0193] Zoysia grass (Korean grass) cut into 50mm squares was placed in petri dishes and managed in a greenhouse set to a room temperature of 25°C. The grass was trimmed to a length of 10mm. 10mL of EGT or 10mL of GB was added to each petri dish, and one day later, under irradiation with a UV lamp (Toshiba, GL-15), the UV radiation intensity at a wavelength of 254nm was 525μW / cm². -2 The device was set to perform this action, and UV stress was inflicted by exposing it to the light for one hour.

[0194] The number of dead leaves was counted 7 days after exposure to ultraviolet stress, and the leaf mortality rate was evaluated as an indicator of physiological disorder. The evaluation results are shown in Table 11. The leaf mortality rate and the environmental stress suppression rate were calculated using the following formulas. Leaf mortality rate (%) = (Number of dead leaves / Total number of leaves of the tested plant) × 100 Environmental stress reduction rate (%) ={1-(leaf mortality rate in the treatment group with the test compound / leaf mortality rate in the untreated group)}×100 [Table 11]

[0195] As shown in Table 11, UV stress caused physiological disorders such as chlorosis in the grass, and 63% of the leaves of the tested grass died (Comparative Example 49). Treatment with GB did not suppress the mortality rate due to UV stress to any significant extent (Comparative Examples 43, 44). In contrast, grass treated with EGT had a lower mortality rate compared to grass treated with GB, and the mortality rate due to UV stress was suppressed to 13% at 0.1 mM (Example 15) and 6% at 1.0 mM (Example 14).

[0196] [Evaluation Example 12] Comparison of resistance effects to high light stress EGT (Example 16) or GB (Comparative Example 51) were prepared to the concentrations shown in Table 12 below. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0197] 90 mL of potting soil (manufactured by Hanagokoro Co., Ltd.) was placed in a plastic pot measuring 60 mm in diameter and 55 mm in height, and four Arabidopsis thaliana (Col-0) seeds were sown per pot.

[0198] The plants were managed in an artificial climate chamber set to room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. The lighting conditions were set so that the light intensity in the center under fluorescent lighting was 5000 lx. 43 days after sowing, 12.5 mL of EGT or 12.5 mL of GB was added, and one day later, under LED light (Esbaybulbs), the light intensity was set to 2000 μmol / m². -2 The device was exposed to intense light stress by setting the timer to / sec and exposing it for 24 hours.

[0199] The number of whitened leaves in Arabidopsis thaliana subjected to strong light stress was counted, and the leaf whitening rate was evaluated as an indicator of physiological disorder. The evaluation results are shown in Table 12. The leaf whitening rate and the environmental stress suppression rate were calculated using the following formulas. Leaf whitening rate (%) = (Number of bleached leaves / Total number of leaves of the tested plants) × 100 Environmental stress reduction rate (%) ={1-(leaf whitening rate in the tested compound treatment group / leaf whitening rate in the untreated group)}×100 [Table 12]

[0200] As shown in Table 12, strong light stress caused physiological disorders such as chlorosis in Arabidopsis thaliana, and 37% of the leaves of the tested Arabidopsis thaliana turned white (Comparative Example 52). Treatment with GB did not suppress leaf whitening due to strong light stress (Comparative Example 51). In contrast, treatment with EGT suppressed the rate of leaf whitening due to strong light stress to 8% (Example 16).

[0201] [Evaluation Example 13] Comparison of resistance effects to freezing stress EGT (Example 17, Comparative Example 55) or GB (Comparative Examples 54, 56) were prepared to the concentrations shown in Table 13 below. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0202] 5 mL of pure water was added to a 9 cm petri dish lined with filter paper, and 10 broccoli (green stalk) seeds were sown per dish. The plants were kept in an artificial climate chamber set to room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. The lighting conditions were set so that the light intensity in the center under fluorescent lighting was 5000 lx.

[0203] Six days after sowing, the pure water in the petri dish was removed, and then 5 mL of EGT or 5 mL of GB was added to the petri dish. Fourteen days later, the dish was exposed to a -20°C environment for 20 minutes, and then one day later, it was exposed to a -20°C environment for another 20 minutes to induce freezing stress.

[0204] The number of surviving plants 24 hours after being subjected to freezing stress was counted, and the plant mortality rate was evaluated as an indicator of physiological disorder. The evaluation results are shown in Table 13. The mortality rate and environmental stress suppression rate were calculated using the following formulas. Mortality rate (%) ={1-(number of surviving plants / number of plants tested)}×100 Environmental stress reduction rate (%) ={1-(death rate in the treated area / death rate in the untreated area)}×100 [Table 13]

[0205] As shown in Table 13, broccoli exhibited physiological disorders such as stem breakage or necrosis due to freezing stress, and 86% of the tested broccoli died (Comparative Example 57). Treatment with GB did not suppress the rate of death due to freezing stress (Comparative Example 54). In contrast, treatment with EGT suppressed the rate of death due to freezing stress to 38% (Example 17).

[0206] [Evaluation Example 14] Comparison of resistance effects to freezing stress EGT (Example 18, Comparative Example 60) or GB (Comparative Examples 59, 61) were prepared to the concentrations shown in Table 14 below. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0207] 5 mL of pure water was added to a 9 cm petri dish lined with filter paper, and 10 strawberry (wild strawberry) seeds were sown per dish. The plants were kept in an artificial climate chamber set to room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. The lighting conditions were set so that the light intensity in the center under fluorescent lighting was 5000 lx.

[0208] Fifteen days after sowing, the pure water in the petri dish was removed, then 5 mL of EGT or 5 mL of GB was added to the petri dish. Nine days later, the plants were subjected to freezing stress by being exposed to a -20°C environment for 20 minutes.

[0209] The number of surviving plants three days after being subjected to freezing stress was counted, and the plant mortality rate was evaluated as an indicator of physiological disorder. The evaluation results are shown in Table 14. The mortality rate and environmental stress suppression rate were calculated using the following formulas. Mortality rate (%) ={1-(number of surviving plants / number of plants tested)}×100 Environmental stress reduction rate (%) ={1-(death rate in the treated area / death rate in the untreated area)}×100 [Table 14]

[0210] As shown in Table 14, frost stress caused physiological disorders such as necrosis in strawberries, and 63% of the tested strawberries died (Comparative Example 62). Treatment with GB did not suppress the rate of death due to frost stress (Comparative Example 59). In contrast, treatment with EGT suppressed the rate of death due to frost stress to 29% (Example 18).

[0211] [Evaluation Example 15] Comparison of Tolerance Effects to Low Temperature Stress EGT (Examples 19, 20, Comparative Examples 66, 67) or GB (Comparative Examples 64, 65, 68, 69) were prepared to the concentrations shown in Table 15 below. Commercially available EGT and GB were used, and pure water was used as the solvent.

[0212] 1 mL of pure water was added to a 3.5 cm petri dish lined with filter paper, and 5 arugula seeds were sown per dish. The plants were kept in an artificial climate chamber set to room temperature of 22°C, with a 16-hour light period and an 8-hour dark period. The lighting conditions were set so that the light intensity in the center under fluorescent lighting was 5000 lx.

[0213] Four days after sowing, the pure water in the petri dish was removed, then 1 mL of EGT or 1 mL of GB was added to the petri dish. Twenty-four hours later, the plants were exposed to a 4°C environment for 48 hours to induce cold stress.

[0214] The number of wilted leaves in arugula plants was evaluated three days after exposure to low-temperature stress. The evaluation results are shown in Table 15. The leaf wilting rate and environmental stress suppression rate were calculated using the following formulas. Leaf wilting rate (%) = (Number of withered leaves / Total number of leaves on the tested plant) × 100 Environmental stress reduction rate (%) ={1-(Leaf wilting rate in the tested compound treatment group / Leaf wilting rate in the untreated group)}×100 [Table 15]

[0215] As shown in Table 15, 67% of the arugula leaves tested showed physiological damage (wilting) due to low-temperature stress (Comparative Example 70), and treatment with GB hardly suppressed the rate of leaf wilting due to low-temperature stress (Comparative Examples 64, 65). In contrast, treatment with EGT suppressed the rate of leaf wilting due to low-temperature stress to 0% (Examples 19, 20).

Claims

1. A plant environmental stress tolerance enhancer for application to germinated plants or the soil surrounding plants, comprising as an active ingredient a compound represented by the following formula (I) or its tautomer, or an agrochemically acceptable salt thereof, 【Chemistry 1】 (In formula (I), R １ and R ２ R independently represents a hydrogen atom or an alkyl group having 1 to 4 carbon atoms. ３ ~R ５ (This independently represents an alkyl group having 1 to 4 carbon atoms.) An environmental stress tolerance enhancer for plants, wherein the aforementioned environmental stress tolerance enhancer improves tolerance to salt stress.

2. The environmental stress tolerance enhancer according to claim 1, wherein the compound represented by formula (I) is ergothioneine.

3. The environmental stress tolerance improving agent according to claim 1 or 2, wherein the environmental stress tolerance improving agent is an inhibitor of the death, chlorosis, necrosis, or wilting of the plant caused by salt stress.

4. The environmental stress tolerance improving agent according to claim 1 or 2, wherein the treatment concentration of the active ingredient in the environmental stress tolerance improving agent is 0.1 mM or more and 1 mM or less.

5. A method for improving the environmental stress tolerance of plants, comprising treating plants after germination with the environmental stress tolerance improving agent described in claim 1 or 2.

6. The method for improving the environmental stress tolerance of plants according to Claim 5, which is a method for suppressing the death, chlorosis, necrosis, or wilting of the plants due to salt stress.

7. The method for improving the environmental stress tolerance of plants according to claim 6, wherein the treatment of the plants with the environmental stress tolerance improving agent is performed before the salt stress occurs in the plants.

8. The method for improving the environmental stress tolerance of plants according to claim 6, wherein the treatment concentration of the active ingredient is 0.1 mM or more and 1 mM or less.

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