Abstract
More than ten weed species resistant to herbicides inhibiting enzyme acetolactate synthase (ALS) or acetohydroxy acid synthase (ALIAS) were recently reported in several countries throughout the world. The evolution of resistant weed populations was generally attributed to continuous application of sulfonylurea or imidazolinone herbicides for more than 3 years. Resistant redroot pigweed (Amaranthus retroflexus; GR1) and prostrate pigweed (A. blitoides; GR11) were first discovered in 1991 at Ganot junction in the coastal plain of Israel, following successive application for 3 years of sulfometuron combined with simazine. Seeds of the GR1 and GRll biotypes were collected from Ganot, and those of the respective sensitive populations ($3 and $24) were collected from untreated fields at Mishmar haShiv'a and Mazkeret Batya. The response of these populations to various sulfonylurea, imidazolinone and triazolopyrimidine herbicides applied postemergence at the three- to four-leaf stage was examined in greenhouse experiments. GRs0 (herbicide rate which inhibits shoot growth by 50%) values were established for each herbicide and population. ALS activity was determined in a crude enzyme preparation isolated from young shoots of the four biotypes, and their response to various sulfometuron concentrations was tested in vivo.
Based on the GRso, it was found that the resistance factor for both species was 35 to 41 for sulfonylureas, 10 to 13 for imidazolinones, and 20 for triazolopyrimidine herbicides. In vitro studies have shown that ALS isolated from the GR1 and GRll biotypes was 105- and 97-fold more resistant to sulfometuron than that isolated from $3 and $24 biotypes, respectively. Furthermore, using a root elongation bioassay, the GR1 biotype was found to be 200-fold more resistant than the $3 biotype. These data indicate clearly that the resistance to ALS inhibitors found in redroot pigweed and prostrate pigweed is due mainly to an altered target site. The fact that this resistance evolved shortly after the introduction of sulfometuron onto the market, suggests that the initial frequency of the resistant mutant in certain weeds is relatively high. Thus, special weed management practices should be employed in order to prevent further spread of the resistant biotypes.
Based on the GRso, it was found that the resistance factor for both species was 35 to 41 for sulfonylureas, 10 to 13 for imidazolinones, and 20 for triazolopyrimidine herbicides. In vitro studies have shown that ALS isolated from the GR1 and GRll biotypes was 105- and 97-fold more resistant to sulfometuron than that isolated from $3 and $24 biotypes, respectively. Furthermore, using a root elongation bioassay, the GR1 biotype was found to be 200-fold more resistant than the $3 biotype. These data indicate clearly that the resistance to ALS inhibitors found in redroot pigweed and prostrate pigweed is due mainly to an altered target site. The fact that this resistance evolved shortly after the introduction of sulfometuron onto the market, suggests that the initial frequency of the resistant mutant in certain weeds is relatively high. Thus, special weed management practices should be employed in order to prevent further spread of the resistant biotypes.
Original language | American English |
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Pages (from-to) | 132 |
Journal | Phytoparasitica |
Volume | 22 |
State | Published - 24 Jan 1994 |