Abstract
A uniparentally inherited 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU)-resistant mutant of C. reinhardii, Dr2, which has a resistance mechanism of the type defined as primary, was isolated. In vitro Hill reactions catalyzed by isolated thylakoid membranes reveal a reduced apparent affinity of the thylakoids for DCMU. These changes in membrane properties quantitatively account for the resistance of mutant Dr2 to herbicide inhibition of growth. The properties of this mutant show that all of the Hill reaction-inhibiting DCMU binding sites are under identical genetic control. Mutant Dr2 is a useful new uniparental genetic marker, since it has a novel phenotype and it may be possible to identify its altered gene product. The low cross-resistance of Dr2 to atrazine suggests that there may be considerable flexibility in exploiting induced herbicide resistance of crop plants for improving herbicide specificity. Four Mendelian mutants in at least 3 loci all have resistance mechanisms in the class defined as secondary. They are as sensitive as wild type to in vitro inhibition of the Hill reaction and must acquire resistance in vivo by preventing the active form of the herbicide from reaching the sensitive site.

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