Two populations of Echinochloa crus-galli (R and I) exhibited resistan
ce to quinclorac. Another population (X) exhibited resistance to quinc
lorac and atrazine. The R and I populations were collected from monocu
ltures of rice in southern Spain. The X population was collected from
maize fields subjected to the application of atrazine over several yea
rs. The susceptible (S) population of the same genus was collected fro
m locations which had never been treated with herbicides. The quinclor
ac ED50 value (dose causing 50% reduction in shoot fresh weight) for t
he R and I biotypes were 26- and 6-fold greater than for the S biotype
. The X biotype was 10 times more tolerant to quinclorac than the S bi
otype and also showed cross-resistance to atrazine, being 82-fold more
resistant to atrazine than the R, I and S biotypes. Chlorophyll fluor
escence and Hill reaction analysis supported the view that the mechani
sm of resistance to atrazine in the X biotype was modification of the
target site, the DI protein. Quinclorac at 20 mg litre(-1) did not inh
ibit photosynthetic electron transport in any of the test biotypes. Th
e quinclorac I-50 values (herbicide dose needed for 50% Hill reaction
reduction) of the S population was over 50000-fold higher than the atr
azine I-50 value for the same S population, indicating that quinclorac
is not a PS II inhibiting herbicide. Propanil at doses greater than 0
.5 kg ha(-1) controlled all the biotypes.