Synthesis and Chemistry of Agrochemicals II - American Chemical

Chapter 3

Plant Biochemistry, Environmental Properties, and Global Impact of the Sulfonylurea Herbicides 1

2

Hugh M. Brown and Philip C. Kearney 1

Agricultural Products Department, Ε. I. du Pont de Nemours and Company, Stine-Haskell Research Center, Newark, DE 19714 Natural Resources Institute, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, MD 20705

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2

The sulfonylurea herbicides are highly active, with use rates ranging from 2 - 75 g a. i./ha. They act by inhibition of acetolactate synthase (E. C. 4.1.3.18), and selectivity, based on rapid metabolic inactivation, has been discovered in wheat, barley, corn, soybeans, rice, oil rapeseed, and other crops. These herbicides are non-toxic to animals, do not accumulate in non-target organisms, are non-volatile, and degrade in soil by chemical and biological processes with half-lives of 1 - 8 weeks. To date, 15 sulfonylurea herbicides for use in diverse crops have been (or soon will be) commercialized, and their favorable agronomic and environmental properties have led to rapid acceptance in the marketplace. This chapter reviews the mode of action, crop selectivity mechanisms, and soil and environmental properties of these compounds, and outlines some aspects of their impact on global agriculture.

The sulfonylurea herbicides, discovered in the mid-1970's by Dr. George Levitt at DuPont ( I - 4 ), signaled a new era in the history of herbicide chemistry. Developments in weed control can be divided into three periods. The first, prior to 1945, was marked by organic and inorganic herbicides having very low activity and no crop selectivity. For example, trichloroacetic acid was used for non selective weed control at rates of 55 - 225 kg/ha. The modern era of chemical weed control began in the mid-1940's with the discovery of the phenoxy herbicides, followed during the next 30 years by the substituted phenylureas, triazines, diphenylethers, glyphosate, and others. These materials offered broad spectrum weed control at 1% to 5% of the application rates of trichloroacetic acid and the inorganic herbicides, with use rates generally ranging from 250 - 4000 g a. i./ha. They also allowed for the first time selective weed control in crops, both pre- and postemergence. The discovery of the sulfonylurea herbicides signaled the start of the present low dose era of herbicide chemistry, which is characterized by crop selective weed control at use rates of 10%/yr from 1989 - 1995 vs growth of 1.9%/yr for the total herbicide market over thistimeperiod (5). This may be an underestimate since some products such as bensulfuron methyl and thifensulfuron methyl (formerly DPX-M6316) have experienced greater market acceptance early after registration than analysts had predicted. To date, sulfonylurea herbicides are registered for major uses in >50 countries. The remainder of this chapter will describe the mode of action, crop selectivity mechanisms and environmental properties of the sulfonylurea herbicides. Other issues including resistant weeds and recropping intervals will also be discussed.


10

MODE OF ACTION Sulfonylureas. The sulfonylurea herbicides were early recognized as potent inhibitors of plant growth. Shoot and root growth is rapidly inhibited (detectable within 2 hours using a variable differential linear transducer) (6), but further visual symptoms develop slowly with vein reddening, chlorosis and terminal bud death appearing over a period of 4 -10 days after treatment (7). Work by Ray (£, 8) and Rost (9) showed that growth inhibition resulted from the arrest of cell division in the G l and/or G2 phases of interphase, with no direct effect on the mitotic apparatus or on cell elongation. Using a 6-hr assay, Ray noted a marked inhibition of DNA synthesis in chlorsulfuron-treated com root tips (as measured by Hthymidine incorporation into DNA), reflecting the arrest of cell division, but he found no direct effect on isolated plant DNA polymerase, thymidine kinase, or on DNA synthesis in isolated plant nuclei (10). This rapid inhibition of cell division was not accompanied by measurable effects on other plant processes including photosynthesis, aerobic respiration, protein synthesis, or RNA synthesis (8, Ï1 13). A breakthrough in sulfonylurea mode of action research resulted from studies with procaryotes by LaRossa and Schloss (14).These workers had found that 3

Baker et al.; Synthesis and Chemistry of Agrochemicals II ACS Symposium Series; American Chemical Society: Washington, DC, 1991.

33


34

SYNTHESIS AND CHEMISTRY OF AGROCHEMICALS Π

growth of Salmonella typhimurium could be inhibited by relatively high concentrations of sulfometuron methyl on minimal medium, and that this inhibition was prevented in enriched medium, specifically media containing the branched chain amino acids valine, isoleucine and leucine. Their work showed that sulfometuron methyl blocked the biosynthesis of these amino acids by inhibiting acetolactate synthase (ALS) (E. C. 4.1.3.18; also known as acetohydroxyacid synthase) in this procaryotic organism. As seen in Fig. 1, the branched chain amino acids are synthesized by a single set of enzymes. Thus, ALS catalyzes the condensation of 2 molecules of pyruvate to form α/ρΛα-acetolactate on the pathway to L-valine and L-leucine. This enzyme also catalyzes the condensation of pyruvate and alphaketobutyrate to form α/ρΛα-aceto-a/p/ia-hydroxybutyrate to ultimately produce L-isoleucine. The enzyme requires Mg2+ and thiamine pyrophosphate (TPP) and exhibits a surprising requirement for FAD even though there is no net or internal redox chemistry involved in this reaction (15). The discovery of this site of action in bacteria was extended to plants by Ray (16) who showed that whole pea plants as well as pea roottipsgrown in liquid culture were effectively protectedfromchlorsulfuron growth inhibition by 100 μΜ valine and isoleucine. As with S. typhimurium, no other amino acids were effective in reversing chlorsulfuron-induced inhibition of plant growth. Further, sulfonylurea herbicides were found to be potent inhibitors of partially purified acetolactate synthase isolatedfromnumerous plant species. Ray found that plant ALS activity could typically be inhibited in vitro by 5 - 20 nM sulfonylurea herbicide, comparable to concentrations required for whole plant activity. Studies with sulfonylurea-resistant tobacco plants (selected usingtissueculture techniques) verified this site of action by showing that the resistant phenotype of these plants resultedfroma sulfonylurea-insensitive form of ALS, which cosegregated with the resistant phenotype (17,18). These studies also indirectly showed that inhibition of ALS is the only site of action for these herbicides. Plants which are made resistant by virtue of a single nuclear mutation mapping to the ALS gene locus are fully resistant to sulfonylurea herbicide doses at least 100X higher than their susceptible progenitors, providing strong evidence that there is no second site of herbicidal action. The discovery of this site of action was quite consistent with the known very low animal toxicity of the sulfonylurea herbicides. Animals do not biosynthesize the branched-chain amino acids and do not possess the target enzyme acetolactate synthase. Other ALS Inhibitors. A remarkable turn of agrichemical history is found in the independent discovery of the imidazolinone herbicides (also in the mid-1970's) at American Cyanamid, and the subsequent finding that these very active compounds also act solely through inhibition of ALS (19,20). Dow has announced that the triazolopyrimidine sulfonanilide herbicides also act through inhibition of ALS (21, 23, Gerwick, B. C ; Loney, V.; Chandler, D. P.; Subramanian, M. Pestic. Sci. 990, in press), and there is good evidence that the heterocyclic aryl ethers invented by Kumiai Chemical also act through inhibition of this formerly obscure enzyme (54, L. L. Saari, DuPont, unpublished). Although these four herbicide classes have only moderate structural similarity, there is good biochemical (22) and genetic evi dence (DuPont unpublished) that they all bind to the same or highly overlapping sites on the ALS enzyme. Schloss has proposed that these herbicides bind to a vestigial quinone binding site on ALS (22). This argument is based on the sequence (24) and functional homology between bacterial ALS and pyruvate oxidase (which also requires TPP, Mg2+, and conducts redox chemistry using FAD and ubiquinone-40), some structural analogy between these herbicides and the oxidized and reduced forms of quinone, and equilibrium dialysis studies using bacterial ALS


3. BROWN AND KEARNEY

Environmental Properties and Global Impact

35

Table I. Commercialized and Advanced Candidate Sulfonylurea Herbicides Common Name

Chemical Structure

α a a

3


ο Ν—f" SONHCNH-/ Ν 2

Primary Use

Application Rate (g/ha)

Chlorsulfuron (DuPont)

Cereals

4-26

Metsulfuron methyl (Du Pont)

Cereals

2-8

Tribenuron methyl (DuPont)

Cereals

5-30

Triasulfuron (Ciba-Geigy)

Cereals

10-40

OCH

3

:o CH 2

3

C

H

3

ο N— SONHCNH-^ Ν N=/ 2

OCH

3

co CH 2

3 3

ο N—^ SONHCN-/ Ν έ Ν=< 2

Η 3

0CH3

a

)CH CH Cl 2

2

C

H

3

ο N— SONHCNH-/ Ν 2

OCH

3

s ^

N

)y

cc>2CH3

\ _ f

^ P"3

Thifensulfuron Cereals methyl (Du Pont) Po Soybeans

u

ο

N

SONHCNH

\

2

N

{

10 - 35

4-6

OCH13

C0CHCH

O

2

2

3

C 1

ο Ν—< *SONHCNH —β \

a :

Chlorimuron ethyl (DuPont)

2

N = /

Soybeans

8-13

(preemergence)

35-70

Rice

20 - 75

Rice

20

OCH

3

CH

°2 3

OCR o

3

N-4~ Bensulfuron

CHSONH5NH-^ \ N=/ 2

methyl (Du Pont)

2

0CH3

σ

/O CH CH 2

3

^

u

3

3

ο Ν - / * * PyrazosulS0 NHÎNH-/ ^ furon ethyl N=/ (Nissan)

N

I

CH

2

3

2

OCH

Continued on next page


SYNTHESIS AND CHEMISTRY OF AGROCHEMICALS II

36

Table I. Commercialized and Advanced Candidate Sulfonylurea Herbicides (Cont'd.) Common Name

Chemical Structure

cr a

PCH CH OCH 2

2

CGA-142,464

3

~

/

*


.NHUNH-^

N

1000 >1000

Imazapyr

6000 38000 6

5

a

0

10

30-min 150 values using ALS isolated from susceptible (S) and resistant (R) Kochia biotypes. Specific activities of uninhibited ALS were 0.98 (S) and 1.2 (R) nmol acetolactate formed/min/mg protein. Postemergence treatment rate (a. i.) causing 50% growth reduction assessed by visual estimation 21 days after treatment (42). N-(2,6-dichlorophenyl)-5,7-cumethyl-1,2,4-triazolo[ 1,5-a]pyrimidine-2sulfonamide. M. M. Primiani, Du Pont, unpublished.





spray tank. However, since pH and pKa control the proportion of neutral to anionic molecular forms, these factors also control soil sorption and mobility of the sulfonylureas. Several studies have shown that sulfonylurea herbicide soil sorption increases with increasing organic matter and decreasing pH (see 43,44). Using the U. S. EPA Soil Mobility Classifications, which are based on soil TLC measurements, chlorsulfuron was classified as having intermediate to high mobility in a series of diverse soils. On the other hand, bensulfuron methyl is less mobile, due to its higher pKa and more lipophilic nature, and was classified as immobile to intermediately mobile in the same soils. Field and modeling studies confirm that chlorsulfuron is mobile in the soil. Despite this mobility, chlorsulfuron and other sulfonylurea herbicides are not likely to threaten groundwater. This conclusion is a result of their extremely low use rates (90 - 99% less chemical applied than conventional herbicides), relatively rapid degradation after application (especially in soils of pH < 7.5), low animal toxicities, and introduction during an era when awareness of correct chemical handling to prevent point source contamination is increasingly widespread. In fact, these and other low use rate herbicides represent a major advance in efforts to reduce the potential for agrichemical groundwater contamination. The most important effect of pH on these molecules derives from the fact that the neutral form is at least 250 -1000 times more susceptible to bridge hydrolysis than the anionic form. As seen in Table IV, hydrolysis proceeds through attack of the neutral bridge carbonyl carbon by water, releasing the herbicidallyinactive phenylsulfonamide and aminoheterocyclic halves of the molecule. This reaction is markedly inhibited in the anionic form since the negative charge is broadly distributed through the bridge (and into the heterocycle), reducing the electrophilic nature of the carbonyl carbon (L. L. Shipman, DuPont, unpublished). The effect of pH is demonstrated by the data in Table 4 showing the hydrolysis half-lives of several sulfonylureas at pH 5 and 7 at 45° C. Comparable effects of pH on hydrolysis rate are also seen at lower temperatures (43). Laboratory and field studies have shown that sulfonylurea bridge hydrolysis is a major degradation pathway in the soil (43,44,46- 48). Fig. 2 illustrates the effect of soil pH on metsulfuron methyl degradation in both sterilized and non-sterilized soils held at 30° C and 1 bar moisture. Note the faster degradation seen in the sterilized acidic vs alkaline soils. In these microbially-inactive soils, degradation is entirely due to bridge hydrolysis, as shown by finding only the arylsulfonamide and aminoheterocyclic degradation products. Comparable results are obtained with other sulfonylureas and numerous studies have shown that bridge hydrolysis, as controlled by soil pH, is a key sulfonylurea degradation process (see 43). It is for this reason that several longer residual sulfonylurea herbicides are restricted to use on soils having pH's below a certain value (often pH 7 - 7.9). Sulfonylurea herbicides are also susceptible to significant microbial degradation in soil. This was first established by Joshi et al. (46) who showed that initial chlorsulfuron degradation was significantly faster infresh,non-sterile soils than in the same soils sterilized by autoclaving, ethylene oxide treatment or gamma ray irradiation. Rapid degradation could be restored by adding back a mixture of soil microorganisms extractedfromnon-sterile soil. Furthermore, the mixture of chlorsulfuron degradation products was more complexfromthe microbially-active soil, and these workers isolated 3 distinct soil microorganisms which could metabolize chlorsulfuron in pure culture (see also 49,£0). A major role for microbial degradation has also been established for chlorimuron ethyl ( 5L Brown, H. M. Pestic. Sci. 1990 (in press)), thifensulfuron methyl (52), metsulfuron methyl (51), and other sulfonylurea herbicides (Dupont, unpublished). The microbial component of metsulfuron methyl degradation is also illustrated in Figure 2. Note the significantly


43

44



Table IV. Ionization and Hydrolysis of Selected Sulfonylurea Herbicides

R

3

Hvdrolvsis Half-Ï.ife (4S°C) pH 5,0 pH 7.0 (days) (days)

Compound

pKa

Metsulfuron methyl

3.3

2.1

33

Chlorsulfuron

3.6

1.7

51

Chlorimuron ethyl

4.2

0.6

14

Sulfometuron methyl

5.2

0.4

6





τ Γ

0

I

0

ι

I

40

ι

I

60

ι

I

80

Days

ι

I

160

1

1—I

200

Figure 2. Degradation of metsulfuron methyl in sterilized and non-sterilized acidic (upper figure) and alkaline (lower figure) soils. Soils were treated with 100 ppb (final concentration, soil dry weight) C-metsulfuron methyl and incubated at 25° C and 1 bar moisture. Subsamples were extracted and analyzed by HPLC and soil sterility was monitored and maintained throughout the experiment (A. T. Van, Du Pont, unpublished; See ref. 4£ for description of comparable experimental methods). 14


45


46


faster degradation of this herbicide in the non-sterilized soils relative to their sterilized counterparts. The relationship between concurrent sulfonylurea hydrolysis and microbial degradation in the soil has been investigated at Dupont (see 45). The sulfonylureas exhibit biexponential degradation kinetics both in diefieldand under conditions of constant temperature and moisture in the laboratory. The initial, relatively rapid degradation rate begins to decrease within several days or weeks to approach the (slower) chemical hydrolysis rate expected for that soil pH and temperature. These biexponential kinetics have been interpreted through an adaptation of an earlier model (53) as resulting from degradation within two slowly exchanging compartments. Upon application, the herbicide is available for both chemical hydrolysis and microbial degradation, and this degradation rate depends on the pH, temperature, and current microbial activity of the soil (as affected by fertility, moisture, etc.). At the sametime,a portion of the applied chemical diffuses into "protected" compartments where it is unavailable for microbial degradation (envisioned as molecular-sized pores in organic matter polymers and/or clay lattices). Since degradation is faster in the "available" compartment, with time this compartment becomes depleted of compound and degradation proceeds only through pH-controlled hydrolysis in the "protected" compartment plus very slow diffusion back into the "available" compartment. These kinetics and their interpretation thus account for the overriding role that soil pH plays in the long-term degradation of sulfonylureas. Even though the microbial degradation component is 5-10timesthe hydrolysis rate, especially in alkaline soils, it doesn't act on the compound found in the "protected" compartment, and the long term dissipation of this "protected" fraction is determined by pH. These degradation kinetics are not unique to the sulfonylureas (53,56,57) and are probably applicable to most or all small molecules in the soil. However, the sulfonylureas (and some other agrichemicals) differfromthose that are subject solely to microbial degradation in that they are still degradable by chemical hydrolysis in the protected compartment rather than relying solely on slow movement back into the available compartment. The Relationship Between Soil Degradation and Rotational Cropping. These degradation processes combine in the field to give sulfonylurea herbicides average degradation half-lives of 1 - 8 weeks, depending on the specific compound, soil pH, temperature, spring vs fall application, etc. (see 43,44). By this measure, sulfonylurea herbicides are not chemically persistent relative to other agrichemicals, where degradation half-lives can range from 1-40 weeks. However, sulfonylureas differfrommost other herbicides in that some rotational crops are so sensitive to these herbicides that 99.5% or more of the applied compound must degrade before these crops can be safely replanted. For example, chlorimuron ethyl applied preemergence at 35 g/ha to a 3% Ο. M. soil must degradefroman initial concentration of ca. 35 ppb (soil weight basis, distributed 10 cm deep) to about 0.1 ppb before sorghum orricecan be replanted withoutrisk.Thus, some sulfonylurea herbicides are subject to use and/or recrop restrictions primarily based on soil pH guidelines insuring that the chemical hydrolysis degradation component is adequate to provide sufficient degradation within a single growing season. Another solution to avoiding rotational crop carryover derivesfromthe diversity of this herbicidal chemistry. Two short residual sulfonylureas for use in cereals have been developed which offer full recropping freedom without soil pH restrictions (42,44,32). Tribenuron methyl (formerly DPX-L5300) and thifensulfuron methyl degrade 10 - 50timesfaster than chlorsulfuron or metsulfuron methyl in all agricultural soils. The methylated bridge of tribenuron methyl makes this compound much more susceptible to hydrolysis than sulfonylureas with a normal bridge, markedly increasing its degradation rate at all




soil pH's. Thifensulfuron methyl is distinctly more susceptible to microbial degradation than other sulfonylureas (56). Thus, each of the primary degradation processes has been exploited through manipulation of sulfonylurea herbicide chemistry to produce analogs which degrade very rapidly in soil. Conclusion. In this chapter, we have attempted a broad overview of the biochemical and environmental properties of the sulfonylurea herbicides. The history of these herbicides is distinguished by the apparently endless variation in structure leading to new weed control spectra, crop selectivities and soil degradation properties. They have already achieved significant use in practice, and it is likely that Dr. Levitt's discovery will continue to yield new herbicide tools offering viable solutions to the needs of world agriculture and of society. Downloaded by AUBURN UNIV on November 15, 2016 | http://pubs.acs.org Publication Date: December 7, 1991 | doi: 10.1021/bk-1991-0443.ch003

Acknowledgments We are pleased to acknowledge the valuable technical and editorial comments of Drs. L. L. Saari, J. C. Cotterman, M. J. Duffy, B. L. Finkelstein, and J. V. Hay. We also thank Lois D. Philhower and the Dupont Agricultural Products Word Processing Center for their expert assistance. Literature Cited 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.

Levitt, G. Belgian Patent 853,374 (1977). Levitt, G. "The Discovery of the Sulfonylurea Herbicides", this volume. Levitt, G. In Pesticide Chemistry: Human Welfare and the Environment; Miyamato, J.; Kearney, P. C., Eds.Pergamon Press, New York, Vol. 1, 1983, 243. Sauers, R. F., Levitt, G. In Pesticide Synthesis Through Rational Approaches; Magee, P. S.; Kohn, G. K.; Mean, J. J., Eds. American Chemical Society, Washington, D. C. 1984; 21. County NatWest (Wood MacKenzie), The NatWest Investment Bank Group, London, Aug. 1988. Ray, T. B. Proc. Br. Crop Prot. Conf. Weeds 1980, 15, 7. Palm, H. L., Riggleman, J. D., Allison, D. A. Proc. Br. Crop Prot. Conf. Weeds 1980,1,1. Ray, T. B. Pestic. Biochem. Physiol. 1982, 17, 10. Rost, T. L. J. Plant Growth Regul. 1984, 3, 51. Ray, T. B. Pestic. Biochem. Physiol. 1982, 18, 262. Hatzios, Κ Κ., Howe, C. M. Pestic. Biochem. Physiol. 1982, 17, 207. de Villiers, O. T., Vandenplas, M. L., Koch, H. M. Proc. Br. Crop Prot. Conf. Weeds 1980, 15, 237. Suttle, J. C.; Schreiner, D. R. Can. J. Bot. 1982, 60, 741. LaRossa, R. Α., Schloss, J. V. J. Biol. Chem. 1984, 259, 8753. Schloss, J. V.; Van Dyk, D. E.; Vasta, J. E.; Kutny, R. M. Biochemistry 1985, 24, 4952. Rav. T. B. Plant Physiol. 1984, 75, 827. Chaleff, R. S., Ray, T. B. Science 1984, 223, 1148. Chaleff, R. S., Mauvais, C. J. Science 1984, 224, 1443. Shaner, D. L.; Anderson, P. C.; Stidham, M. A. Plant Physiol. 1987, 86, 545. Mutitch, M. J.; Shaner, D. L.; Stidham, M. A. Plant Physiol. 1987, 86, 451.


47

48

SYNTHESIS AND CHEMISTRY OF AGROCHEMICALS Π 21. 22. 23.

24. 25.


26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. 42. 43.

44. 45. 46. 47.

Hawkes, T. R.; Howard, J. L.; Poutin, S. E. In Herbicides and Plant Metabolism (SEB Seminar Series); Dodge, A. D., Ed.; Cambridge University Press: Cambridge, 1987, p. 113. Schloss, J. V.; Ciskanik, L. M.; Van Dyk, D. E. Nature 1988. 331, 360. Subramian, M. V., Loney, V., Pao, L. In Prospects for Amino Acid Biosynthesis Inhibitors in Crop Protection and Pharmaceutical Chemistry: Copping, L. G., Dalziel, J., Dodge, A. D., Eds.; Brit. Crop Prot. Council: Surrey, 1989, p. 97. Grabau, C.; Cronan, J. E. Nucleic Acid Res. 1986, 14, 5449. LaRossa, R. Α.; Van Dyk, T. K.; Smulski, D. R. J. Bacteriol. 1987, 169, 1372. Tramontano, W. Α.; DeCostanza, D. C.; DeLillo, A. R. Plant Physiol.(Supp) 1989, 89, 42. Sweetser, P. B., Schow, G. S., Hutchison, J. M. Pestic. Biochem. Physiol. 1982, 17 ,18. Brown, H. M., Wittenbach, V. Α., Brattsten, L. B. Weed Sci. Soc. Amer. Abstracts 1989, 29, 74. Lichtner, F. T. In Proc. Internat. Phloem Conf. (Asilomar, CA). Lucas,W. J.; Cronshaw, J. Eds.; Alan R. Liss Inc.: New York, 1986, p. 601. Rendina, A. R.; Felts, J. M. Plant Physiol. 1988, 86, 983. Walker, Κ. Α.; Ridley, S.M.; Lewis, T. Harwood, J. L. Biochem. J. 1988, 254, 307. Ray, T. B. Trends Biol. Sci. 1986, 11, 180. Cotterman, J. C. Weed Sci. Soc. Amer. Abstracts 1989, 29, 73. Hutchison, J. M., Shapiro, R., Sweetser, P. B. Pestic. Biochem. Physiol. 1984, 22, 243. Takeda, S., Erbes, D. L., Sweetser, P. B., Hay, J. V., Yuyama, T. Weed Research (Japan) 1986, 31, 157. Brown, H. M., Neighbors, S. M. Pestic. Biochem. Physiol. 1987, 22, 112. Anderson, J. Α., Priester, T. M., Shalaby, L. M. J. Ag. Food Chem. 1989, 37, 1429. Sebastian, S. Α.; Fader, G. M.; Ulrich, J. F.; Forney, D. R.; Chaleff, R. S. Crop Sci. 1989, 29, 1403. Knowlton, S.; Mazur, B. J.; Arntzen, C. J. In Current Communications in Molecular Biology; Fraley, N. M.; Frey, J.; Schell, J.; Eds.; Cold Spring Harbor Laboratory, 1988, p. 55. Mazur, B. J.; Falco, S. C. Annu. Rev. Plant Physiol. Plant Mol. Biol. 1989, 40, 441. Mallory, C. Α.; Thill, D. C.; Dial, M. J. Weed Tech. 1990, 4, 163. Primiani, M. M.; Cotterman, J. C.; Saari, L. L. Weed Tech. 1990, 4, 169. Beyer, Ε. M., Duffy, M. J., Hay, J. V., Schlueter, D. D. In Herbicides: Chemistry, Degradaton and Mode of Action; Kearney, P. C.; Kaufman, D. D. Eds.; Dekker, New York, 1987, Vol. 3, p. 117. Beyer, Ε. M., Brown, Η. M., Duffy, M. J. Proc. Br. Crop Prot. Conf. Weeds 1987, 531. Duffy, M. J., Hanafey, M. K., Linn, D. M., Russell, M. H., Peter, C. J. Proc. Br. Crop Prot. Conf. Weeds 1987, 541. Joshi, M. M., Brown, Η. M., Romesser, J. A. Weed Sci. 1985, 33, 888. Peterson, Μ. Α.; Arnold, W. E. Weed Sci. 1985, 34, 131.


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48. 49. 50. 51. 52.


53.

54.

55. 56. 57.


O'Sullivan. P. A. Can. J. Plant Sci. 1982, 62, 715. Romesser, J. Α., O'Keefe, D. P. Biochem. Biophys. Res. Comm. 1986, 140, 650. O'Keefe, D. P., Romesser, J. Α., Leto, K. L., Arch. Microbiol. 1988, 149, 406. Joshi, M. M.; Brown, Η. M. Weed Sci. Soc. Amer. Abstracts 1985, 25, 147. Brown, H. M.; Joshi, M. M.; Van. A. T. Weed Sci. Soc. Amer. Abstracts 1987, 27, 62. Hamaker, J. W.; Goring, C. A. I. In Bound and Conjugated Pesticide Residues: Kaufman, D. D.; Still, G. G.; Paulson, G. D.; Bandai, S. Κ., Eds.; American Chemical Society, Wash. D. C. 1976, 29, p. 219. Hawkes, T. R. In Prospects for Amino Acid Biosynthesis Inhibitors in Crop Protection and Pharmaceutical Chemistry; Copping, L. G.; Dalziel, J.; Dodge, A. D., Eds.; Brit. Crop Prot. Council: Surrey; 1989, p. 131. Herbicide Resistance Technical Bulletin, Ε. I. du Pont de Nemours and Co. Bulletin No. H-05804, 1989. Lafleur, K. S., McCaskell, W. R., Gale, G. T., Jr. Soil Science 1978, 126, 285. Lafleur, K. S. Soil Science 1980, 130, 83.

Note Added in Proof H . M. Brown, Pesticide Science, 1990, i n press, has been published i n Pesticide Science, 1990, 29, 263-281. RECEIVED

June 5, 1990


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Synthesis and Chemistry of Agrochemicals II - American Chemical

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