Structure-activity relationships of triazinone herbicides on resistant weeds and resistant Chlamydomonas reinhardtii

Weeds resistant to the s‐triazine herbicide atrazine also show resistance to the triazinone herbicide metribuzin. However, with highly lipophilic triazinones, thylakoids isolated from atrazine‐resistant Amaranthus retroflexus (mutation at position Ser264 of the photosystem II D‐1 reaction centre protein) in general show a higher pI50 value in photosystem II electron transport than those from the wild type (i.e. negative cross‐resistance; ‘supersensitivity’). A quantitative structure–activity relationship (QSAR) can be established, wherein the lipophilicity of the compound plays a major role. In in‐vivo experiments, it was found that the triazinone DRW2698 killed resistant Amaranthus retroflexus and Chenopodium album whereas the wild type was almost unaffected. Triazinones were further investigated in five different mutants of Chlamydomonas rheinhardtii (mutations in the D‐1 protein at positions Ser264, Ala251, Leu275, Phe255, and Val219). Inhibitory activity of all triazinones was generally enhanced in the Phe255 mutant but decreased in the Val219 mutant. In the other mutants, biological activity was decreased when position 3 of the triazinone was substituted by CH3, OCH3, SCH3, NHCH3 or N(CH3)2. However, negative cross‐resistance was again observed when this position was occupied by free thiol. It is therefore suggested that these two groups of triazinones orient themselves differently within the herbicide binding niche of the photosystem II D‐1 protein.