Weeds are a major problem for rice production in California, and late water
grass (Echinochloa phyllopogon (Stapf) Koss) is one of the most serious wee
ds in water-seeded rice. Severe infestations can reduce yields by more than
50%. Flooding only partially controls this weed; thus, farmers rely heavil
y on herbicides. Resistance to several herbicides, including bispyribac-sod
ium, an acetolactate synthase (ALS) inhibitor not yet commercially used, ha
s developed in late watergrass populations of California rice. knowing the
mechanisms of bispyribac resistance is relevant to designing herbicide mana
gement strategies for delaying resistance development to enhance the succes
sful introduction of this new herbicide. We examined whether an insensitive
ALS and cvt P-450-dependent detoxification were possible resistance mechan
isms in a bispyribac-sodium-resistant (R) late watergrass population collec
ted in California rice fields. which was previously determined to be resist
ant to molinate, thiobencarb, and fenoxaprop-ethyl. ALS activity was assaye
d on leaf extracts from young R and susceptible (S) plants for a range of b
ispyribac-sodium concentrations, and cross-resistance to another ALS inhibi
tor, bensulfuron-methyl, was evaluated using whole-plant bioassays. Resista
nce was not due to reduced ALS sensitivity to bispyribac-sodium in R plants
, although the R accession was highly cross-resistant to bensulfuron-methyl
. Although S and R plants had similar ALS activity (mg acetoin mg protein(-
1)) without herbicide. more (P < 0.05) leaf protein was extracted from R 15
.35 mg g(-1) leaf fresh weight) than from S (3.19 mg g(-1)) plants, and gen
eral ALS activity (mg acetoin g leaf fresh weight(-1)) for all herbicide co
ncentrations was higher in R than in S plants. The cyt P-450 inhibitors pip
eronyl butoxide and malathion were used for detection of herbicide degradat
ion by cyt P-450 monooxygenation. The addition of these inhibitors strongly
enhanced herbicide phytotoxicity toward R plant, suggesting that metabolic
degradation of bispyribac-sodium contributed significantly to the observed
resistance. (C) 2000 Academic Press.