Atrazine, Bromacil, and Diuron Resistance in Chlamydomonas1: A Single Non-Mendelian Genetic Locus Controls the Structure of the Thylakoid Binding Site

摘要

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.