Abstract

Over 200 distinct herbicide resistant weed biotypes have evolved worldwide. In most of these, resistance is conferred by an altered target site, i.e. a modified target protein with reduced affinity for the herbicide(s) in question. This has been documented for herbicides that target most major known sites of action, including those that inhibit photosynthetic electron transfer at photosystem II, acetyl-CoA carboxylase, acetolactate synthase, and tubulin polymerization. Patterns of cross-resistance to structurally similar herbicides and those from other chemical classes that target the same site vary, depending on the mutation and its effect on protein steric and electronic properties. Mechanisms of target site-based herbicide resistance are reviewed, with emphasis on the biochemical and molecular basis for resistance.

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