Structure‐activity relationships of triazinone herbicides on resistant weeds and resistant <i>Chlamydomonas reinhardtii</i>

Abstract

Abstract 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 Ser 264 of the photosystem II D‐1 reaction centre protein) in general show a higher pI 50 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 Ser 264 , Ala 251 , Leu 275 , Phe 255 , and Val 219 ). Inhibitory activity of all triazinones was generally enhanced in the Phe 255 mutant but decreased in the Val 219 mutant. In the other mutants, biological activity was decreased when position 3 of the triazinone was substituted by CH 3 , OCH 3 , SCH 3 , NHCH 3 or N(CH 3 ) 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.