In many weeds, the emergence of drug-resistant biotypes is the result of genetic modification of herbicide action sites, which has been confirmed in the resistance research of most sulfonylureas, imidazolinones, triazenes and dinitroanilines.
The site of action of sulfonylurea and imidazolinone herbicides is acetolactate synthase (ALS). The study on this kind of herbicide-resistant weed biotype showed that compared with the sensitive biotype ALS, amino acids at several different sites were substituted, and the sensitivity of the changed ALS to the above herbicides decreased.
The resistance of triazine herbicides is related to the mutation of chlorophyll PsbA gene locus. The herbicide binding site encoded by PsbA gene is the D- 1(32KD) protein of photosystem II. In the higher plants studied, all the drug resistance mutations involve the substitution of the 264th amino acid of the D- 1 protein, which leads to the decrease of the affinity of this kind of herbicides with the protein. A new type of β -tubulin was found in the target site of Oxfordia indica, which was resistant to dinitroaniline herbicide, and it was considered that the stability of microtubules composed of this new type of tubulin was enhanced, which was one of the important reasons for Oxfordia indica's resistance to this kind of herbicide.
2. Improve the detoxification ability of herbicides.
The metabolic difference between sensitive biotype and drug-resistant biotype explains the mechanism of drug-resistant biotype. Many drug-resistant weeds can make herbicides metabolize rapidly, thus losing their activity. The main metabolic reactions are as follows:
(1) oxidative metabolism. Oxidation of herbicides is very common in plants, which is often the main metabolic reaction leading to detoxification or activation of herbicides. The main oxidative metabolism is aryl hydroxylation and N- dealkylation. For example, 2,4- D is hydroxylated in grasses and broadleaf plants to form 4-hydroxy-2,4-D, and N- dealkylation in monuron is another example.
(2) Coupling effect. Herbicide and its primary metabolites are coupled with lipophilic compounds such as sugar, amino acids, glutathione, fatty acids and glycerol in plants through valence bonds, thus losing their activity. Generally speaking, coupling enhances the polarity of herbicides and their metabolites, which is a major mechanism of detoxification of herbicides. The resistance of gramineous weeds such as Setaria viridis, Crabgrass, Millet and Millet to atrazine is due to the enhanced coupling with glutathione, which improves the detoxification ability of herbicides.
(3) Other detoxification metabolism. In the herbicide-resistant biotype chloroplast of Artemisia scoparia, it was found that the enzyme activity that can detoxify the oxygen free radicals produced by herbicides increased, and the activities of peroxidase, ascorbate peroxidase and glutathione reductase in the herbicide-resistant biotype chloroplast increased by 1.6, 2.5 and 2.9 times respectively. The increase of detoxification enzyme activity was also observed in the biotype of erigeron breviscapus against paraquat.
3. Shielding or isolation
Previous studies have shown that the chelation and separation of herbicides and their toxic metabolites are considered to be an important mechanism of weed resistance to herbicides. For example, in the drug-resistant biotypes of Gramineae, such as Artemisia capillaris, Erigeron breviflora and barley, it was found that the movement of paraquat was restricted, and the functions of chloroplast CO2 fixation and chlorophyll fluorescence quenching could be quickly restored. All these indicate that the combination of herbicides at their action sites can be prevented.
The influence or mechanism of weed absorption and conduction of herbicides on the biotype of drug-resistant weeds is not completely clear, but there have been some reports on the difference of absorption and conduction between resistant and sensitive biotypes.