' îï (Ë -=2 o <u ra ci ra resistance have not yet appeared. Oxytetracycline has been injected into palm trees and stone fruit trees for several years to control mycoplasmalike organisms, apparently without the development of resistance. In Xanthomonas campestris pv. vesicatoria (which causes bacterial leaf spot of tomatoes and peppers), resistance to copper is conferred by a plasmid gene that appears to cd u ra || <u regulate the absorption of copper ion by the bacterial cell.

ra e is Plants utilize the same general resistance mechanisms as insects. The ra 2 g efficacious use of herbicides on crops is made possible because many crop

° s 13 plants are capable of rapid metabolic inactivation of the chemicals, thereby

~ % £ avoiding their toxic action. Target weeds are notably deficient in this capacity.

I i It is apparent, though, that the capability to metabolize herbicides to innocuous

^ dj g compounds constitutes a potentially important basis of evolved resistance to

■¡S <S is herbicides in weeds. Documented cases of resistance have been due to other

¡3 ~ s mechanisms, however, such as alteration of the herbicide's target site. For % -I example, newly appearing s-triazine-resistant weeds have plastid-mediated j £ resistance that involves a reduced affinity of the thylakoids for triazine x ® ° herbicides (Gressel, this volume).

$ p The herbicide paraquat disrupts photosynthesis in target weeds by intercepting electrons from photosystem I, part of the metabolic cycle that fixes energy from sunlight into plant constituents via a complicated flow of electrons. " a Transfer of electrons from paraquat to oxygen gives rise to highly reactive ® oxygen radicals that damage plant membranes. Paraquat-resistant plants have ra ^ higher levels of the enzyme superoxide dismutase, which quenches the reactive ra oxygen radicals. 1 E The mechanisms of weed resistance to the dinitroaniline herbicides and to diclofop-methyl have not yet been identified.

A number of herbicides act on the photosynthetic mechanism in the chloroplasts. Although the frequency of resistant plants arising from plastid H c ra mutations would normally be very low, a plastome mutator gene has been o S recognized that increases the rate of plastome mutation in weeds. This factor £ s B could be largely responsible for the plastid-level resistance to herbicides that o o ™ has emerged in some weeds (Gressel, this volume).

o £ Resistance to anticoagulants is the most widespread and thoroughly

~ 2 g investigated heritable resistance in vertebrates. Warfarin resistance in rats has <g S been observed in several European countries, and in 1980 more than 10 percent 8 | of rats were resistant to warfarin in 45 out of 98 cities surveyed in the United « £ States (Jackson and Ashton, this volume).

Warfarin interferes with the synthesis of vitamin K-dependent blood-clotting factors in vertebrates. Resistance in rats (Rattus norvegicus) appears to involve a reduced affinity of a vitamin K-metabolizing enzyme or enzymes for warfarin. The affinity of the target site is controlled by one (of four) allelic ~ forms of a gene in linkage group I. In the mouse, there are indications that E increased resistance to warfarin is due to metabolic detoxication and that o http.//www.naGEftEcf(alBgOCHEMïCAL, AND PHYSIOLOGICAL MECHANISMS OF RESISTANCE 49 TO PESTICIDES

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