Sulfonylurea herbicides resistance

Mallory-Smith, C.A. (1990). Identification and inheritance of sulfonylurea herbicide resistance in prickly lettuce (Lactuca serriola). Ph.D. dissertation. University of Idaho, Moscow, ID, p. 58. 

Mallory-Smith, C.A., D.C. Thill, M.J. Dial, and R.S. Zemetra (1990b). Inheritance of sulfonylurea herbicide resistance in Lactuca spp. 

Saari, L.L., J.C. Cotterman, and M.M. Primiani (1990). Mechanisms of sulfonylurea herbicide resistance in the broadleaf weed Kochia scoparia. Plant Physiol., 93 55-61. 

Many of the characteristics which combine to make ALS an excellent target for engineering beneficial herbicide resistance in crop plants may also lead to the proliferation of herbicide-resistant weeds. These characteristics include the following sulfonylurea herbicide resistance is a semi-dominant trait that is carried on a nuclear gene(s) ALS is the single primary site of action there are multiple positions in ALS that can be mutated to confer herbicide resistance mutant ALS enzymes can possess full catalytic activity. The latter property results in engineered crop plants that are fit, but can equally well result in weed biotypes that are fit. 

Li, Z.J., Hayashimoto, A., and Murai, N. 1992. A sulfonylurea herbicide resistance gene from arabidopsis-thaliana as a new selectable marker for production of fertile transgenic rice plants. Plant Physiol., 100, 662-668. 

Haughn, G., Smith, J., Mazur, B. Sommerville, C. (1988). Transformation with a mutant Arabidopsis acetolactate synthase gene renders tobacco resistant to sulfonylurea herbicides. Molecular and General Genetics 211, 266-71. 

A more recent factor affecting weed management has been the introduction of crops genetically altered for tolerance or resistance to herbicides. The first herbicide-tolerant field com (IMI hybrid corn) was developed as a way to reduce the effects of carryover from imidazolinone and sulfonylurea herbicides applied to soybean in a corn-soybean rotation. These hybrids also soon found use in areas where triazine use was restricted. 

The development of herbicide-resistant weeds has also been an influence on the selection of herbicides used on field corn or soybean. Weed resistance now affects nearly every decision a farmer makes about herbicide selection either a farmer is trying to control resistant weeds or is selecting herbicides that may reduce the possibility of weed populations becoming resistant. The adoption of the imidazolinone- and sulfonylurea-tolerant com hybrids mentioned above was in part a response to the presence of atrazine-tolerant pigweeds or kochia in many fields. However, a recent decrease in die use of imidazolinone and sulfonylurea herbicides can also be attributed to the development of populations of weeds that have become resistant to these herbicides. 

Christopher et al. (1992) reported that a chlorsulfuron-resistant rigid ryegrass in Australia was resistant to most other sulfonylurea and imidazolinone ALS inhibitors. However, a common cocklebur biotype resistant to several imida-zolinone herbicides was not resistant to sulfonylurea herbicides (Saari et al., 1994). It is, therefore, difficult to generalize as to patterns of resistance within the five classes of ALS inhibitors. Weed biotypes resistant to one herbicide will usually show some level of resistance to most herbicides within the same class, and may in addition show some resistance to ALS inhibitors in other classes. 

Devine et al. (1991) and O Donovan et al. (1994) reported that chlorsulfuron-resistant chickweed populations were also resistant to other sulfonylurea herbicides. Primiani et al. (1990) reported cross-resistance to several sulfonylurea and imidazolinone herbicides in chlorsulfuron-resistant kochia. Lovell et al. (1996a) also documented that chlorsulfuron-resistant kochia biotypes from Idaho and Montana were cross-resistant to imazethapyr. 

The evolution of resistance is not necessarily a slow process, as was first believed. Experience has shown, for example with sulfonylurea herbicides, that resistance can develop very quickly, in some cases fully evident after only 3 years of use of a particular herbicide family. That the genetic composition of a weed population can change so quickly is a sobering thought. 

The sulfonylureas, an extremely potent class of herbicides, act by inhibiting acetolactate synthase (ALS), which is the first common enzyme in the biosynthetic pathways leading to the branched chain amino acids. Two other unrelated classes of herbicides also act by interfering with this enzyme. We have cloned and characterized the genes encoding ALS from several higher plants. The ALS genes isolated from herbicide sensitive and herbicide resistant plants have been compared, and several mutations which confer the herbicide resistant phenotype have been identified. 

These cloned Arabidopsis and tobacco ALS genes have been used as hybridization probes to isolate ALS genes from other crop species and to isolate ALS genes from plants selected for resistance to sulfonylurea herbicides. 

Two selection strategies have been used to obtain plants resistant to sulfonylurea herbicides. 

This biotype evolved resistance to diclofop eethyl after several years of use, and was then found to often be cross-resistant to aost sulfonylurea herbicides. 

Lolium biotypes exist which have resistance to the sulfonylurea herbicides chlorsulfuron and metsulfuron methyl (4). The biotype used in the studies presented here is resistant to both these sulfonylurea herbicides. Sulfonylurea herbicides inhibit the chloroplastic enzyme acetolactate synthase (ALS), also known as acetohydroxyacid synthase (AHAS) (16). Inhibition of this enzyme results in disruption of the synthesis of the branched-chain amino acids valine and isoleucine (161. The imidazolinone herbicides also inhibit ALS Q2). In some species auxins can protect against chlorsulfuron inhibition (S. Frear, USDA North Dakota, personal communication) the mechanistic basis for this protection is not known. We have measured the ALS activity in the resistant and susceptible Lolium and have also checked for any induction of ALS activity following treatment with the sulfonylurea herbicide chlorsulfuron. 

It appears that resistance to the aryloxyphenoxypropionate herbicides, the cyclohexanedione herbicides and to the sulfonylurea herbicides is unlikely to be due to reductions in the sensitivity or increases in the amounts of their respective target enzymes (Figures 2 3). Studies have not yet been performed to examine if die resistance to the dinitroaniline herbicide trifluralin is associated with any change at the tubulin polymerization site. 

Acetolactate synthase (ALS) is the target enzyme for three unrelated classes of herbicides, the sulfonylureas, the imidazolinones, and the triazolopyrimidines. We have cloned the genes which specify acetolactate synthase from a variety of wild type plants, as well as from plants which are resistant to these herbicides. The molecular basis of herbicide resistance in these plants has been deduced by comparing the nucleotide sequences of the cloned sensitive and resistant ALS genes. By further comparing these sequences to ALS sequences obtained from herbicide-resistant yeast mutants, two patterns have become clear. First, the ALS sequences that can be mutated to cause resistance are in domains that are conserved between plants, yeast and bacteria. Second, identical molecular substitutions in ALS can confer herbicide resistance in both yeast and plants. 

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