EP2148568A1

EP2148568A1 - Method for improving the bud quality of a plant

Info

Publication number: EP2148568A1
Application number: EP08750331A
Authority: EP
Inventors: Dominique Rosati; Luk De Maeyer; Piet Creemers; Hilde Schoofs; Tom Deckers
Original assignee: Bayer CropScience SA
Current assignee: Bayer CropScience AG
Priority date: 2007-05-16
Filing date: 2008-05-16
Publication date: 2010-02-03
Also published as: NZ579268A; BRPI0808254A2; AU2008252991B2; JP2010526855A; AR066612A1; JP5323817B2; CL2008001461A1; CN105265474A; KR101504107B1; US20100311590A1; MX2009012218A; AU2008252991A1; KR20100014485A; CN101720187A; US8404279B2; WO2008142029A1; ZA200905963B

Abstract

The present invention relates to the use of a compound, in particular of a derivative of phosphorous acid, especially of fosetyl-AI, for treating plants for the purpose of improving the bud quality thereof.

Description

METHOD FOR IMPROVING THE QUALITY OF BUDS IN A PLANT

DESCRIPTION

The present invention relates to the use of a compound, in particular a phosphorous acid derivative, in particular fosetyl-Al, for the treatment of plants with a view to improving the quality of the buds.

Fosetyl aluminum or fosetyl-AI is a known fungicidal compound. Its chemical name is aluminum ethylhydrogenphosphonate whose chemical structure is as follows:

Moreover, the bactericidal activity of fosetyl-AI is also known, in particular by the European patent application EP-249566.

The problem of withering flower buds is not new and has long been examined. For many years, the phenomenon of flower buds withered, especially on pear trees, has been observed. Such a phenomenon can in a few years reduce the productivity of fruit trees dramatically. This phenomenon may also lead to the uprooting or destruction of the affected plants in order to prevent the spread of the organisms involved.

The origin or reasons for this phenomenon are not known. It could be related to bacterial infections, for example caused by Pseudomonas syringae pv. syringae or even fungal infections, for example caused by Alternaria alternata. This phenomenon could also be explained by a late availability of nitrogen that stimulates the physiological activation of flower buds that are not visible externally and that may make them more vulnerable to such dieback of flower buds.

In addition, the frequency of decayed flower buds can vary considerably from year to year and the youngest plants may be more sensitive than older plants for the same cultivar, the phenomenon may vary from one variety to another. During the season, climatology can also influence the phenomenon; a period hot weather at the end of the autumn season followed by a period of strong frost has often been considered a decisive factor that can lead to withering of the flower buds. It can also occur that flower buds are not sufficiently dormant at the time of the first frosts. The inner tissue of the flower buds can then be damaged and then infected.

The damage of bud dieback is often visible only several months after initiation, or even the following year at the time of flowering, fruit formation or harvest. It is then impossible to undertake any treatment aimed at restoring the situation. Some anti-biotic or anti-bacterial products, such as streptomycin, have been used to combat this phenomenon. Such phytosanitary uses of products are now limited to the maximum, or even prohibited, especially because of resistance problems in phytopathogenic bacteria that are generated by the massive spreading of such antibiotic or anti-bacterial products. Such resistance problems could be transferred to pathogenic bacteria of animals or even humans.

It has now been found that the use according to the present invention is a solution to all or some of these problems.

Thus, the present invention relates to the use for improving the quality of the buds of a perennial plant by the application of a compound on this plant at the time of the period of initiation of flower buds in the post-floral period.

Preferably, the use according to the present invention implements a compound chosen from pesticidal compounds, in particular fungicidal compounds, bactericidal compounds, herbicides, plant growth regulators, insecticides or nematicides.

More preferably, the use according to the present invention implements a compound chosen from: B1) a compound capable of inhibiting the synthesis of RNA nucleic acids such as benalaxyl, benalaxyl-M, bupirimate, clozylacon, dimethirimol, ethirimol, furalaxyl, hymexazol, mefenoxam, metalaxyl, metalaxyl-M ofurace, oxadixyl, oxolinic acid;

B2) a compound capable of inhibiting mitosis and cell division such as benomyl, carbendazim, diethofencarb, ethaboxam, fuberidazole, pencycuron, thiabendazole, thiophanate-methyl, zoxamide; B3) a compound capable of inhibiting respiration, for example a respiratory inhibitor C1 such as diflumetorim; a respiratory inhibitor CII such as boscalid, carboxin, fenfuram, flutolanil, furametpyr, furmecyclox, mepronil, oxycarboxin, penthiopyrad, thifluzamide;

a CIII inhibitor of respiration such as amisulbrom, azoxystrobin, cyazofamid, dimoxystrobin, enestrobin, famoxadone, fenamidone, fluoxastrobin, kresoxim-methyl, metominostrobin, orysastrobin, picoxystrobin, pyraclostrobin, trifloxystrobin;

B4) a compound acting as a decoupling of respiration such as dinocap, fluazinam, meptyldinocap; B5) a compound capable of inhibiting the production of ATP such as fentin acetate, fentin chloride, fentin hydroxide, silthiofam;

B6) a compound capable of inhibiting protein biosynthesis and AA biosynthesis such as andoprim, blasticidin-S, cyprodinil, kasugamycin, kasugamycin hydrochloride hydrate, mepanipyrim, pyrimethanil; B7) a compound capable of inhibiting signal transmission such as Fenpiclonil, Fludioxonil, Quinoxyfen;

B8) a compound capable of inhibiting lipid and membrane synthesis such as biphenyl, chlozolinate, edifenphos, etridiazole, iodocarb, iprobenfos, iprodione, isoprothiolane, procymidone, propamocarb, propamocarb hydrochloride, pyrazophos, tolclofos-methyl, vinclozolin;

B9) a compound capable of inhibiting the biosynthesis of ergosterol such as aldimorph, azaconazole, bitertanol, bromuconazole, cyproconazole, diclobutrazole, difenoconazole, diniconazole, diniconazole-M, dodemorph, dodemorph acetate, epoxiconazole, etaconazole, fenarimol, fenbuconazole, fenhexamid, fenpropidin, fenpropimorph, fluquinconazole, flurprimidol, flusilazole, flutriafol, furconazole, furconazole-cis, hexaconazole, imazalil, imazalil sulfate, imibenconazole, ipconazole, metconazole, myclobutanil, naftifin, nuarimol, oxpoconazole, paclobutrazol, pefurazoate, penconazole, prochloraz, propiconazole, prothioconazole , pyributicarb, pyrifenox, simeconazole, spiroxamine, tebuconazole, terbinafine, tetraconazole, triadimefon, triadimenol, tridemorph, triflumizole, triforine, triticonazole, uniconazole, viniconazole, voriconazole;

B10) a compound capable of inhibiting cell membrane synthesis such as benthiavalicarb, dimethomorph, flumorph, iprovalicarb, mandipropamid, polyoxins, polyoxorim, validamycin A; B11) a compound capable of inhibiting the biosynthesis of melanin such as carpropamid, diclocymet, fenoxanil, phthalide, pyroquilon, tricyclazole;

B12) a compound capable of inducing plant defense reactions such as acibenzolar-S-methyl, probenazole, tiadinil; B13) a compound having a multi-site activity such as Bordeaux mixture, captafol, captan, chlorothalonil, copper naphthenate, copper oxide, copper oxychloride, copper-based preparations such as copper hydroxide, copper sulphate, dichlofluanid , dithianon, dodine, dodine free base, ferbam, fluorofolpet, folpet, guazatine, guazatine acetate, iminoctadine, iminoctadine albesilate, iminoctadine triacetate, mancopper, mancozeb, maneb, metiram, zinc metiram, oxine-copper, propineb, sulfur and sulfur preparations such as polysulphide calcium, thiram, tolylfluanid, zineb, ziram;

B14) a compound selected from the list: (2E) -2- (2 - {[6- (3-chloro-2-methylphenoxy) -5-fluoropyrimidin-4-yl] oxy} phenyl) -2- (methoxyimino) N-methylacetamide, (2E) -2- {2 - [({[(1E) -1 - (3 - {[(E) -1-fluoro-2-phenylvinyl] oxy} phenyl) ethylidene] amino} oxy) methyl] phenyl) -2- (methoxyimino) -N-methylacetamide, 1- (4-chlorophenyl) -2- (1H-1,2,4-triazol-1-yl) cycloheptanol, H (4-methoxyphenoxy) ) methyl] -2,2-dimethylpropyl-1H-imidazole-1-carboxylate, 1-methyl-N- [2-

(1,1,2,2-tetrafluoroethoxy) phenyl] -3- (trifluoromethyl) -1H-pyrazole-4-carboxamide, 2,3,5,6-tetrachloro-4- (methylsulfonyl) pyridine, 2-butoxy- 6-iodo-3-propyl-4H-chromen-4-one, 2-chloro-N- (1,1,3-trimethyl-2,3-dihydro-1H-inden-4-yl) nicotinamide, 2- phenylphenol and salts, 3- (difluoromethyl) -i-methyl-N- [2- (1,1,2,2-tetrafluoroethoxy) phenyl] -1H-pyrazole-4-carboxamide, 3- (difluoromethyl) -N- [(9R) -9-isopropyl-1,2,3,4-tetrahydro-1,4-methanonaphthalen-5-yl] -1-methyl-1H-pyrazole-4-carboxamide, 3- (difluoromethyl) -N - [(9S) -9-isopropyl-1,2,3,4-tetrahydro-1,4-methanonaphthalen-5-yl] -1-methyl-1H-pyrazole-4-carboxamide, 3- (difluoromethyl) - N- [4 '- (3,3-dimethylbut-1-yn-1-yl) biphenyl-2-yl] -1-methyl-1H-pyrazole-4-carboxamide, 3,4,5-trichloropyridine-2 6-dicarbonitrile, 3- [5- (4-chlorophenyl) -2,3-dimethylisoxazolidin-3-yl] pyridine, 3-chloro-5- (4-chlorophenyl) -4- (2,6-difluorophenyl) - 6-methylpyridazine, 4- (4-chlorophenyl) -5- (2,6-difluorophenyl) -3,6-dimethylpyridazine, 5-chloro-7- (4-me) thylpiperidin-1-yl) -6- (2,4,6-trifluorophenyl) [1,2,4] triazolo [1,5-a] pyrimidine, 8-hydroxyquinoline sulfate, benthiazole, bethoxazin, capsimycin, carvone, chinomethionate, cufraneb, cyflufenamid, cymoxanil, dazomet, debacarb, dichlorophen, diclomezine, dicloran, difenzoquat, difenzoquat methylsulphate, diphenylamine, ecomate, ferimzone, flumetover, fluopicolide, fluoroimide, flusulfamide, fosetyl-aluminum, fosetyl-calcium, fosetyl-sodium, hexachlorobenzene, irumamycin isotianil, methasulfocarb, methyl- (2E) -2- {2 - [({cyclopropyl [(4-methoxyphenyl) imino] methyl} thio) methyl] phenyl} -3-methoxyacrylate, methyl 1 - (2,2-dimethyl) -2,3-dihydro-1H-inden-1-yl) -1H-imidazole-5-carboxylate, methyl isothiocyanate, metrafenone, N- (3 ', 4'-dichloro-5-fluorobiphenyl-2-yl) -3- (difluoromethyl) -1-methyl-1H-pyrazole-4-carboxamide, N- (3-ethyl-3,5) 5-trimethylcyclohexyl) -3- (formylamino) -2-hydroxybenzamide, N- (4-chloro-2-nitrophenyl) -N-ethyl-4-methylbenzenesulfonamide, N- (4-chlorobenzyl) -3- [3-methoxy] -4- (prop-2-yn-1-yloxy) phenyl] propanamide, N - [(4-chlorophenyl) (cyano) methyl] -3- [3-methoxy-4- (prop-2-yn) -1- yloxy) phenyl] propanamide, N - [(5-bromo-3-chloropyridin-2-yl) methyl] -2,4-dichloronicotinamide, N- [1- (5-bromo-3-chloropyridin-2-yl) ethyl] ] -2,4-dichloronicotinamide, N- [1- (5-bromo-3-chloropyridin-2-yl) ethyl] -2-fluoro-4-iodonicotinamide, N- [2- (1,3-dimethylbutyl) phenyl] ] -5-fluoro-1,3-dimethyl-1H-pyrazole-4-carboxamide, N - {(Z) -

[(Cyclopropylmethoxy] quinol) difluoromethoxy] N, D-difluorophenylmethyl] phenylacetamide, N- {2- [1,1'-b (cyclopropyl) -2-yl] phenyl} -3- (difluoromethyl) -1-methyl-1 H- pyrazole-4-carboxamide, N- {2- [3-chloro-5- (trifluoromethyl) pyridin-2-yl] ethyl} -2- (trifluoromethyl) benzamide, natamycin, N-ethyl-N-methyl-N'- {2-methyl-5- (trifluoromethyl) -4- [3-

(trimethylsilyl) propoxy] phenyl} imidoformamide, N-ethyl-N-methyl-N '- {2-methyl-5-

(difluoromethyl) -4- [3- (trimethylsilyl) propoxy] phenyl} imidoformamide, nickel dimethyldithiocarbamate, nitrothal-isopropyl, O- {1 - [(4-methoxyphenoxy) methyl] -2,2-dimethylpropyl} 1H-imidazole- 1-carbothioate, octhilinone, oxamocarb, oxyfenthiin, pentachlorophenol and salts, phosphorous acid and its salts, piperalin, propamocarb fosetylate, propanosine-sodium, proquinazid, pyribencarb, pyrrolnitrin, quintozene, S-allyl-5-amino-2-isopropyl-4 (2-methylphenyl) -3-oxo-2,3-dihydro-1H-pyrazole-1-carbothioate, tecloftalam, tecnazene, triazoxide, trichlamide, valiphenal, zarilamid.

The following compounds may also be suitable for the application according to the invention: bronopol, dichlorophen, nitrapyrin, nickel dimethyldithiocarbamate, kasugamycin, octhilinone, furancarboxylic acid, oxytetracycline, probenazole, streptomycin, tecloftalam.

According to another embodiment of the use according to the invention, several of these compounds can be applied to the perennial plant treated at the time of the post-floral period.

Most preferably, the use according to the present invention uses a compound selected from phosphorous acid and fosetyl-Al.

Advantageously, the use according to the present invention is implemented by beginning application at the time of initiation of the flower bud of the treated plant. Even more advantageously, the use according to the present invention is implemented by application carried out at the time of the initiation of the flower bud and the cell multiplication in the buds. Also advantageously, the use according to the present invention is carried out by application ending about 10 weeks after starting, preferably about 8 weeks after starting.

According to a preferred embodiment of the invention, the compound used in the use according to the invention is applied several times during the post-floral period of the plant, at least three applications give particularly advantageous results.

The use according to the present invention also gives very advantageous results when the compound is applied in quantities making it possible to reach a concentration, in particular of phosphorous acid, within the plant of 15 ppm, preferably of at least 30 ppm. .

According to a particularly advantageous embodiment of the use according to the invention, fosetyl-AI is applied repeatedly, for example three times, in an amount of at least 1.5 kg / ha, preferably at least 2kg / ha, more preferably at least 3kg / ha, for example 3.75kg / ha.

For its use according to the present invention, the compound used is generally applied in a conventional manner as regards its formulation or the type of application. Thus, said compound is generally applied to the aerial parts of the plant, such as the trunk, stems, leaves, fruits or flowers of said plant.

The use according to the invention can be implemented on many plants and in particular on cotton; flax; Vine; fruit or vegetable crops such as Rosaceae sp. (for example, pome fruit crops such as apple trees, pear trees, but also stone fruit crops such as apricot, cherry, plum, rye, almond, peach); Ribesioidae sp., Juglandaceae sp., Betulaceae sp., Anacardiaceae sp., Fagaceae sp., Moraceae sp., Oleaceae sp., Actinidaceae sp., Lauraceae sp., Musaceae sp. (eg banana or plantain crops), Rubiaceae sp., Theaceae sp., Sterculiceae sp., Rutaceae sp. (eg lemon, orange or grapefruit crops); vegetable crops, Umbelliferae sp., Cruciferae sp., Chenopodiaceae sp., Cucurbitaceae sp., Rosaceae sp. (for example strawberries); industrial crops or cereals; Solanaceae sp. (eg potato), Chenopodiaceae sp .; horticultural, shrub and forest crops; Ericaceae sp. (eg rhododendron); Azalea sp; as well as the genetically modified counterparts of these crops. Such genetically engineered plants whose genome comprises a heterologous gene encoding a protein of interest has been stably inserted. A heterologous gene coding for a protein of interest mainly makes it possible to bring new agronomic properties to the modified plant or to improve the agronomic qualities of this modified plant. Preferably, the use according to the invention is implemented on fruit crops for example pome fruit crops such as apple trees, pear trees but also stone fruit crops such as apricots, cherries, plums, the griottiers, the almond trees, the peach trees.

The amount of compound used for the use according to the invention may vary, in particular because of the pathogens targeted, the type of culture, the climatic conditions as well as the type of compound used. This amount can for example be determined by systematic field tests, within the scope of the skilled person.

It is important that the amount used is effective but also that it is not phytotoxic for the treated plant. Thus, such an amount should not cause any significant symptoms of phytotoxicity on said plant. Depending on the compound employed, the amount used for the use according to the invention can generally range from 2 to 8,000 g / ha, preferably from 20 to 4,000 g / ha.

The use according to the invention is now illustrated by a particular example which is not only intended to give a particular embodiment of this use without limiting the scope or extent.

Example 1: Use against flower buds withered on pear trees (Conference variety)

Introduction

During a consecutive period of three years, a study was conducted on young pear trees

(Conference pear cultivar) in a sensitive orchard.

Material and method

For three consecutive years 2004, 2005 and 2006, a trial was conducted on young pear trees of the Quince Adams Root Crop cultivar. The pear trees of this orchard were planted in 1999 in a single row system at a planting distance of 3.5 m between rows and 1.5 m in row with a tree height of 3m. During the 2004 trial, three products were compared in an arbitrary block design with 10 trees per plot in four replicates: observations were made on the 8 trees within the plot. In 2004, the following products were included in this trial: fosetyl-AI (Aliette product) at a dose ranging from 2 to 3.75 kg / ha standard orchard (corresponding to a dose ranging from 1.33 to 2.50 kg / ha of leaf area), benzothiadiazole (Bion product) at a rate of 200g / ha of standard orchard (corresponding to a dose of 133g / ha of leaf area to account for the volume of application) and phosphonate potassium (or phosphorous acid) ) at two doses: one of 11, 25 l / ha of standard orchard (corresponding to a dose of 7.50 l / ha of leaf area) with the intention of applying the same amount of phosphonate per ha as in the fosetyl-AI treated plot applied at 3.75 kg / ha and at a lower rate of 3.00 l / ha standard orchard (corresponding to 2.00 l / ha foliage area). Applications were positioned in the post-flower period at an interval of 10 days. In 2005, the same applications were repeated on the same trees. Due to some phytotoxicity observed after applications in 2004, potassium phosphonate treatments were not repeated.

In 2006, the full test was repeated on new trees in the same orchard. Fosetyl-AI doses ranging from 2 to 3.75 kg / ha standard orchard (corresponding to doses of 1.33 and 2.50 kg / ha leaf area) were applied in the post-flower period during the months May and June at an interval of 5 or 10 days between treatments. Benzothiadiazole applied at a rate of 200g / ha of standard orchard (corresponding to a dose of 133g / ha of leaf area) was included as a reference product to induce plant defense responses by trees.

After one year during flowering, the effect of the treatments on the quality of the flower bud was evaluated. The statistical analysis of the various parameters is performed (continued Unistat Statistical Package, version 5.5). The original or transformed data are analyzed according to the General Linear Model and the averages of treatments are separated in a standard way using Duncan's multiple ranking test (level 5%).

In 2006, the magnitude of residue levels of fosetyl-AI and phosphorous acid in developing flower buds was monitored in three plots: in the untreated control plot, in the fosetyl-AI treated plot according to 3 x 3.75 kg / ha (application on 18/05, 30/05 and 08/06) and in the fosetyl-AI treated plot on 6 x 2.0 kg / ha (application on 18/05, on 30/05, 08/06, 19/06, 29/06 and 10/07).

At each date (with the exception of the first sampling date), 40 flower buds with surrounding leaves were collected. At the first sampling date 40 flower buds were collected without leaves. The flower bud samples were taken before the next treatment on the following dates: 30/05, 08/06, 19/06, 28/06, 10/07 and 28/08. For both fosetyl-AI and phosphorous acid products, residue levels in flower buds were determined using an LC-MS-MS analytical method. The limit of quantification (LOQ) was 0.1 mg / kg for fosetyl-AI, 2 mg / kg for phosphorous acid and 3 mg / kg for the total residue expressed as fosetyl-AI equivalent. The total residue is the sum of the residues resulting from fosetyl-AI and phosphorous acid expressed in fosetyl-AI equivalent.

The results are calculated according to the following formula:

Mfosetyl-Al X Residue Acid Phosphor BIX (mg / kg)

Residue (mg / kg) = Residue ΘSaltyl-Al (mg / kg) + -

3 x Macidephosphoreix

in which :

Mw _{OS and} Yi-Ai represents the molecular weight of fosetyl-AI: 354.1 g / mol M phosphorous _acre represents the molecular weight of phosphorous acid: 82 g / mol; multiplied by 3, since 1 mol of fosetyl-AI corresponds to 3 mol of phosphorous acid.

For pear button samples, residues of fosetyl-AI and phosphorous acid are extracted using a mixture of acetonitrile / water (50:50, v / v). After centrifugation and dilution of the sample material, the residues are quantified by HPLC and detected by tandem mass spectrometry with electrospray ionization. Quantification is performed by external standardization. The statistical analysis is performed by parameter on the complete set of data of the different sampling dates.

Results

Table 1 shows the percentage of good quality flower buds as a result of 2004 treatments. The following year, in 2005, 66% of the flower buds on trees in the untreated control plot are normal, well developed, and with 5 to 7 flowers per bud and with rosette leaves around the flower buds. The data show that the two plots treated with phosphorous acid (having as their origin fosetyl-AI or phosphorous acid itself) show a significantly increased flower bud quality (> 88% good quality buds). . The plot treated with fosetyl-AI at 3.75 kg / ha combines the best results of efficacy and absence of phytotoxicity thus allowing the better optimization of fruit production. The results lead to insufficient activity of the benzothiadiazole used as a reference product

The addition of additional treatment with fosetyl-AI after harvest results in results comparable to those obtained after post-flower treatments alone.

Table 1 also shows the number of incomplete flower buds per tree in the plots receiving phosphorous acid, these data show a significant reduction in the formation of incomplete flower buds. In the untreated plot, 26 incomplete flower buds were counted per tree, which means leafless flower buds or with a limited number of flowers per cluster. For trees that received phosphorous acid, this number was reduced to about 8 incomplete flower buds per tree.

Table 1: Formation of the flower bud 2005 as a result of treatments carried out in 2004 AH: after harvest; Number: number

Table 2 shows the percentage of good quality flower buds as a result of treatments 2004 and 2005. On 13/02/2006, a first observation was made during the dormant season and at this moment, the external qualities of the bud floral were comparable. In 2006, during flowering, a second observation was made showing that 58% of the flower buds on the two year old wood were normal, well-developed buds with 5-7 flowers per bud and leaves around the flower buds. In plots treated with fosetyl-AI at 3 x 3.75 kg / ha in May or 6 x 3.75 kg / ha in May and June, the percentage of good quality flower buds increased to 86% and 92% respectively. % respectively. Earlier During the primary flowering period in 2005, the positioning of fosetyl-AI treatments resulted in a lower percentage of only 75% of good-quality flower buds in 2006. A detailed assessment of flower bud quality across different ages fruiting wood indicates that the reduced quality of the flower bud is more common on two-year-old flower buds. On one-year-old wood in the lateral position and in the terminal position, the quality of the flower bud may be less influenced by fosetyl-AI treatments. In 2006, differences in flower bud quality observed at the beginning of the season resulted in higher fruit per tree at the end of the season in fosetyl-AI treated plots in May or May-June. (Table 3). The results were higher productivity in kg per tree.

Table 2: Floral bud formation 2006 as a result of tree and branch level treatments in 2004 and 2005 with separate assessment of branches on 2-year-old wood (2vw) and 1-year-old wood in lateral position (1vwL) and terminal position (1 vwT)

Table 3: Productivity of pear trees 2006 as a result of treatments carried out in 2004 and 2005 - Nb: number Table 4 shows the percentages of well-developed, decayed or incomplete flower buds in 2007 as a result of treatments performed in 2006. A well-developed flower bud contained 5-7 flowers per cluster in the presence of well-developed leaves around the cluster. An incomplete button contained only 2 to 3 flowers per cluster without the presence of leaves around the cluster. In the untreated plot, 44.7 of flower buds are well developed. Fosetyl-AI treatments, in May at 3 x 3.75 kg / ha with an interval of 10 days or at 6 x 2 kg / ha with an interval of 5 days, increased the percentage of well-developed flower buds to 59%. Fosetyl-AI treatments in June at 3 x 3.75 kg / ha with an interval of 10 days or at 6 x 2 kg / ha with an interval of 5 days increased the percentage of well-developed flower buds to 62.5%, respectively 63.5%. Fosetyl-AI treatments repeated at 6 x 2kg / ha applied during the May-June period with an interval of 10 days led to a percentage of 61.2% well-developed flower buds. Percentages of decayed or incomplete flower buds were significantly reduced in all fosetyl-AI treated objects without distinct differences between the different application patterns. This means that the different applications of fosetyl-AI in the post-flower period in 2006 resulted in a significant increase in the quality of the flower bud in 2007.

Table 4: Formation of the 2007 floral bud as a result of treatments performed in 2006

Tables 5a, 5b, 5c show the levels of phosphorous acid and fosetyl-AI residues as well as the total residue measured in flower buds during the 2006 season for the untreated control plot in comparison with the parcel. fosetyl-AI treated at 3 x 3.75 kg / ha with an interval of 10 days in May and the fosetyl-AI treated plot at 6 x 2 kg / ha with an interval of 10 days in May and June. Sampling was done on dates following: 30/05, 08/06, 19/06, 28/06, 10/07 and 28/08/2006. Pear bud samples were taken before treatment.

Table 5a: Residue of phosphorous acid in mq / kq by sampling date

Table 5b: Residue of fosetyl-AI in mq / kq by sampling date

Table 5c: Total residue (fosetyl-AI + phosphorous acid) in mq / kq by sampling date

Discussion

The results of the flower bud quality assessment indicate that there is a clear increase in flower bud quality in phosphonate (fosetyl-AI or phosphorous acid) treated objects.

A set of factors can occur during this phenomenon: for example bacterial infections caused by Pseudomonas syringae pv syringae or by Pantoaea sp (not systematically isolated in pear pimples); fungal infections caused by Alternaria alternates; climatological influences.

In these trials, the best period of application of fosetyl-AI treatments to resolve the problem of flower buds withered on pear is the post-flower period. This is the period during which the flower buds on the two-year-old wood are formed. It is important to improve plant resistance during the early stage of flower bud development. The systemic feature of the fosetyl-AI product may also be an important aspect for penetration of the product into the leaves around the developing meristems within the two-year-old flower buds.

In the 2006 trial, residual levels of phosphorous acid and fosetyl-AI in developing flower buds were monitored. The samples of the flower buds were taken before the next treatment. The data indicate that after the treatments, there is a substantial increase in phosphorous acid content in flower buds. There is a distinct difference between the object with a higher dose after fosetyl-AI treatment at 3 x 3.75kg / ha and the object with fosetyl-AI treatments at a lower repeated dose of 2kg / ha . In the first object, the phosphonate residue increases after the last treatment and it takes about 4 weeks before the residue falls below the value of 30 mg / kg. In the object with repeated lower doses of 2kg / ha, it takes about 2 weeks after the last treatment for the residue to fall below 30mg / kg. In addition, the fosetyl-AI residue level was maintained for about 4 weeks after the last fosetyl-AI treatment at a dose of 3.75 kg / ha. The residual rate of phosphorous acid during the flower bud formation period on the two-year-old wood is maintained in the plant.

Conclusion

Repeated fosetyl-AI treatments on pear trees in the post-flowering period significantly improved the quality of flower buds for the following year. A repeated dose of 3 x 3.75 kg / ha, applied in the post-flower period with an interval of 10 days is the most advantageous.

The residual effect of fosetyl-AI treatments on the phosphorous acid content within the flower buds up to four weeks after the last treatment is also particularly advantageous.

Claims

1. Use to improve the quality of buds of a perennial plant by applying a compound on this plant at the time of the period of initiation of flower buds in the post-floral period.

2. Use according to claim 1 of a pesticide compound selected from fungicidal compounds, bactericidal, herbicidal, plant growth regulators, insecticides or nematocides.

3. Use according to either of claims 1 or 2 of a compound chosen from:

B1) a compound capable of inhibiting the synthesis of RNA-type nucleic acids such as benalaxyl, benalaxyl-M, bupirimate, clozylacon, dimethirimol, ethirimol, furalaxyl, hymexazol, mefenoxam, metalaxyl, metalaxyl-M ofurace, oxadixyl, oxolinic acid;

B2) a compound capable of inhibiting mitosis and cell division such as benomyl, carbendazim, diethofencarb, ethaboxam, fuberidazole, pencycuron, thiabendazole, thiophanate-methyl, zoxamide;

B3) a compound capable of inhibiting respiration, for example a respiratory inhibitor C1 such as diflumetorim; a respiratory inhibitor CII such as boscalid, carboxin, fenfuram, flutolanil, furametpyr, furmecyclox, mepronil, oxycarboxin, penthiopyrad, thifluzamide;

B4) a compound acting as a decoupling of respiration such as dinocap, fluazinam, meptyldinocap;

B5) a compound capable of inhibiting the production of ATP such as fentin acetate, fentin chloride, fentin hydroxide, silthiofam; B6) a compound capable of inhibiting protein biosynthesis and AA biosynthesis such as andoprim, blasticidin-S, cyprodinil, kasugamycin, kasugamycin hydrochloride hydrate, mepanipyrim, pyrimethanil;

B7) a compound capable of inhibiting signal transmission such as Fenpiclonil, Fludioxonil, Quinoxyfen; B8) a compound capable of inhibiting lipid and membrane synthesis such as biphenyl, chlozolinate, edifenphos, etridiazole, iodocarb, iprobenfos, iprodione, isoprothiolane, procymidone, propamocarb, propamocarb hydrochloride, pyrazophos, tolclofos-methyl, vinclozolin; B9) a compound capable of inhibiting the biosynthesis of ergosterol such as aldimorph, azaconazole, bitertanol, bromuconazole, cyproconazole, diclobutrazole, difenoconazole, diniconazole, diniconazole-M, dodemorph, dodemorph acetate, epoxiconazole, etaconazole, fenarimol, fenbuconazole, fenhexamid, fenpropidin, fenpropimorph, fluquinconazole, flurprimidol, flusilazole, flutriafol, furconazole, furconazole-cis, hexaconazole, imazalil, imazalil sulfate, imibenconazole, ipconazole, metconazole, myclobutanil, naftifin, nuarimol, oxpoconazole, paclobutrazol, pefurazoate, penconazole, prochloraz, propiconazole, prothioconazole , pyributicarb, pyrifenox, simeconazole, spiroxamine, tebuconazole, terbinafine, tetraconazole, triadimefon, triadimenol, tridemorph, triflumizole, triforine, triticonazole, uniconazole, viniconazole, voriconazole; B10) a compound capable of inhibiting cell membrane synthesis such as benthiavalicarb, dimethomorph, flumorph, iprovalicarb, mandipropamid, polyoxins, polyoxorim, validamycin A;

B11) a compound capable of inhibiting the biosynthesis of melanin such as carpropamid, diclocymet, fenoxanil, phthalide, pyroquilon, tricyclazole; B12) a compound capable of inducing plant defense reactions such as acibenzolar-S-methyl, probenazole, tiadinil;

B13) a compound having a multi-site activity such as Bordeaux mixture, captafol, captan, chlorothalonil, copper naphthenate, copper oxide, copper oxychloride, copper-based preparations such as copper hydroxide, copper sulphate, dichlofluanid , dithianon, dodine, dodine free base, ferbam, fluorofolpet, folpet, guazatine, guazatine acetate, iminoctadine, iminoctadine albesilate, iminoctadine triacetate, mancopper, mancozeb, maneb, metiram, zinc metiram, oxine-copper, propineb, sulfur and sulfur preparations such as polysulphide calcium, thiram, tolylfluanid, zineb, ziram;

B14) a compound selected from the list: (2E) -2- (2 - {[6- (3-chloro-2-methylphenoxy) -5-fluoropyrimidin-4-yl] oxy} phenyl) -2- (methoxyimino) N-methylacetamide, (2E) -2- {2 - [({[(1E) -1 - (3 - {[(E) -1-fluoro-2-phenylvinyl] oxy} phenyl) ethylidene] amino} oxy) methyl] phenyl) -2- (methoxyimino) -N-methylacetamide, 1- (4-chlorophenyl) -2- (1H-1,2,4-triazol-1-yl) cycloheptanol, 1 - [(4 methoxyphenoxy) methyl] -2,2-dimethylpropyl-1H-imidazole-1-carboxylate, 1-methyl-N- [2-

(1,1,2,2-tetrafluoroethoxy) phenyl] -3- (trifluoromethyl) -1H-pyrazole-4-carboxamide, 2,3,5,6-tetrachloro-4- (methylsulfonyl) pyridine, 2-butoxy- 6-iodo-3-propyl-4H-chromen-4-one, 2-chloro-N- (1,1,3-trimethyl-2,3-dihydro-1H-inden-4-yl) nicotinamide, 2-phenylphenol and salts, 3- (difluoromethyl) -i-methyl-N- [2- (1, 1, 2,2-tetrafluoroethoxy) phenyl] -1H-pyrazole-4-carboxamide, 3- (difluoromethyl) -N - [(9R) -9-isopropyl-1,2,3,4-tetrahydro-1,4 -methanonaphthalen-5-yl] -1-methyl-1H-pyrazole-4-carboxamide, 3- (difluoromethyl) -N - [(9S) -9-isopropyl-1,2,3,4-tetrahydro-1, 4-methanonaphthalen-5-yl] -1-methyl-1H-pyrazole-4-carboxamide, 3- (difluoromethyl) -N- [4 '- (3,3-dimethylbut-1-yn-1-yl) biphenyl) -2-yl] -1-methyl-1H-pyrazole-4-carboxamide, 3,4,5-trichloropyridine-2,6-dicarbonitrile, 3- [5- (4-chlorophenyl) -2,3-dimethylisoxazolidinol) 3-yl] pyridine, 3-chloro-5- (4-chlorophenyl) -4- (2,6-difluorophenyl) -6-methylpyridazine, 4- (4-chlorophenyl) -5- (2,6-difluorophenyl) - 3,6-dimethylpyridazine, 5-chloro-7- (4-methylpiperidin-1-yl) -6- (2,4,6-trifluorophenyl) [1,2,4] triazolo [1,5-a] pyrimidine, 8-hydroxyquinoline sulfate, benthiazole, bethoxazin, capsimycin, carvone, chinomethionat, cufraneb, cyfluf enamid, cymoxanil, dazomet, debacarb, dichlorophen, diclomezine, dicloran, difenzoquat, difenzoquat methylsulphate, diphenylamine, ecomate, ferimzone, flumetover, fluopicolide, fluoroimide, flusulfamide, fosetyl-aluminum, fosetyl-calcium, fosetyl-sodium, hexachlorobenzene, irumamycin, isotianil methasulfocarb, methyl- (2E) -2- {2 - [({cyclopropyl [(4-methoxyphenyl) imino] methyl} thio) methyl] phenyl} -3-methoxyacrylate, methyl 1 - (2,2-dimethyl-2) , 3-dihydro-1H-inden-1-yl) -1H-imidazole-5-carboxylate, methyl isothiocyanate, metrafenone, mildewcin N- (3 ', 4'-dichloro-5-fluorobiphenyl-2-yl) 3- (difluoromethyl) -1-methyl-1H-pyrazole-4-carboxamide, N- (3-ethyl-3,5,5-trimethylcyclohexyl) -3- (formylamino) -2-hydroxybenzamide, N- (4- chloro-2-nitrophenyl) -N-ethyl-4-methylbenzenesulfonamide, N- (4-chlorobenzyl) -3- [3-methoxy-4- (prop-2-yn-1-yloxy) phenyl] propanamide, N- [ (4-Chlorophenyl) (cyano) methyl] -3- [3-methoxy-4- (prop-2-yn-1-yloxy) phenyl] propanamide, N - [(5-bromo-3-chloropyridin-2-yl) ) methyl] -2,4-dich loronicotinamide, N- [1- (5-bromo-3-chloropyridin-2-yl) ethyl] -2,4-dichloronicotinamide, N- [1 - (5-bromo-3-chloropyridin-2-yl) ethyl] 2-fluoro-4-iodonicotinamide, N- [2- (1,3-dimethylbutyl) phenyl] -5-fluoro-1,3-dimethyl-1H-pyrazole-4-carboxamide, N - {(Z) -

[(cyclopropylmethoxy) imino] [6- (difluoromethoxy) -2,3-difluorophenyl] methyl] -2-phenylacetamide, N- {2- [1,1 '-bi (cyclopropyl) -2-yl] phenyl} -3 - (difluoromethyl) -1-methyl-1H-pyrazole-4-carboxamide, N- {2- [3-chloro-5- (trifluoromethyl) pyridin-2-yl] ethyl} -2- (trifluoromethyl) benzamide, natamycin N-ethyl-N-methyl-N '- {2-methyl-5- (trifluoromethyl) -4- [3- (trimethylsilyl) propoxy] phenyl} imidoformamide, N-ethyl-N-methyl-N' - {2} -methyl-5-

(difluoromethyl) -4- [3- (trimethylsilyl) propoxy] phenyl} imidoformamide, nickel dimethyldithiocarbamate, nitrothal-isopropyl, O- {1 - [(4-methoxyphenoxy) methyl] -2,2-dimethylpropyl} 1H-imidazole- 1-carbothioate, octhilinone, oxamocarb, oxyfenthiin, pentachlorophenol and salts, phosphorous acid and its salts, piperalin, propamocarb fosetylate, propanosine-sodium, proquinazid, pyribencarb, pyrrolnitrin, quintozene, S-allyl-5-amino-2- isopropyl-4- (2-methylphenyl) -3-oxo-2,3-dihydro-1H-pyrazole-1-carbothioate, tecloftalam, tecnazene, triazoxide, trichlamide, valiphenal, zarilamid; bronopol, dichlorophen, nitrapyrin, nickel dimethyldithiocarbamate, kasugamycin, octhilinone, furancarboxylic acid, oxytetracycline, probenazole, streptomycin, tecloftalam.

4. Use according to any one of claims 1 to 3 of a compound selected from phosphorous acid and fosetyl-AI.

5. Use according to any one of claims 1 to 4 by application beginning at the time of initiation of the flower bud of the treated plant.

6. Use according to any one of claims 1 to 5 by application made at the time of initiation of the flower bud and cell multiplication in the buds of the treated plant.

7. Use according to any one of claims 1 to 6 by application ending about 10 weeks after starting.

8. Use according to any one of claims 1 to 7 by application ending approximately 8 weeks after starting.

9. Use according to any one of claims 1 to 8 by application several times during the post-floral period of the plant.

10. Use according to any one of claims 1 to 9 by repeated application at least three times.

11. Use according to any one of claims 1 to 10 by application of the compound in amounts to achieve a concentration in the plant of at least 15ppm.

12. Use according to any one of claims 1 to 11 by application of the compound in amounts to achieve a concentration within the plant of at least 30ppm.

13. Use according to any one of claims 1 to 12 by application of the compound in amounts ranging from 2 to 8000g / ha.

Use according to any one of claims 1 to 13 by applying the compound in amounts ranging from 20 to 4000 g / ha.

15. Use according to any one of claims 1 to 14 by application of fosetyl-AI or phosphorous acid repeatedly.

16. Use according to any one of claims 1 to 15 by application of fosetyl-AI or phosphorous acid repeated at least three times.

17. Use according to any one of claims 1 to 16 by application of fosetyl-AI or phosphorous acid in an amount of at least 1.5 kg / ha.

18. Use according to any one of claims 1 to 17 by fosetyl-AI or phosphorous acid in an amount of at least 3kg / ha.

19. Use according to any one of claims 1 to 18 on fruit crops, pome fruit crops, stone fruit crops, horticultural, shrub and forest crops.

20. Use according to any one of claims 1 to 19 on apple, pear, apricot, cherry, plum, raspberry, almond, peach.