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Articles

Atrazine, Bromacil, and Diuron Resistance in Chlamydomonas¹

A Single Non-Mendelian Genetic Locus Controls the Structure of the Thylakoid Binding Site

Department of Biology, Washington University, St. Louis, Missouri 63130, Department of Biology, University of Chicago, 1103 East 57th Street, Chicago, Illinois 60637

A series of Chlamydomonas reinhardii mutants were selected for resistance to the herbicides atrazine, bromacil, and diuron. Four of these have reduced herbicide binding to the thylakoid membranes and show the non-Mendelian inheritance pattern characteristic of chloroplast genes. These mutants show a variety of selective alterations in binding of the three herbicides. These changes account for the observed patterns of in vivo cross-resistance. Analyses of chloroplast gene recombination indicate that these four mutations are in the same gene. Overall, the results suggest that this gene codes for a protein component of the herbicide binding site. One of the mutants has slow phototrophic growth and altered electron transport as has been observed in atrazine-resistant higher plant varieties, but the others are normal in these respects. The slow growth characteristic of this mutant seems to be the consequence of the same mutation which confers herbicide resistance.

The mutants isolated also include a large number which achieve resistance by some secondary mechanism. These are all nuclear gene mutations, and represent numerous loci. They also show a variety of patterns of cross-resistance, but the mechanisms behind them have not yet been investigated.

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				J. M. ERICKSON, M. RAHIRE, J.-D. ROCHAIX, and L. METS Herbicide Resistance and Cross-Resistance: Changes at Three Distinct Sites in the Herbicide-Binding Protein Science, April 12, 1985; 228(4696): 204 - 207. [Abstract] [PDF]