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 modi"ed target protein with reduced a$nity 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 e!ect 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