Acetolactate Synthase Gene Proline (197) Mutations Confer Tribenuron-Methyl Resistance in Flixweed (Descurainia sophia) Populations from China

Abstract

The molecular basis of resistance to tribenuron-methyl, an acetolactate synthase (ALS)–inhibiting herbicide was investigated in four resistant (R) and three susceptible (S) flixweed populations. The resistance level in the R populations was assessed in whole-plant pot experiments in a greenhouse, and resistance indices ranged from 723 to 1422. The ALS genes of the three S populations and four R populations were cloned and sequenced, and the full coding sequence of the ALS gene of flixweed was 2,004 bp. The sequences of the ALS genes of the three S populations collected from Shaanxi, Gansu, and Tianjin were identical. Comparison of the ALS gene sequences of the S and R populations withArabidopsisrevealed that proline at position 197 of the ALS gene was substituted by leucine in R population SSX-2, by alanine in R population SSX-3, and by serine in R populations TJ-2 and GS-2. In another study of two R flixweed populations from Hebei and Shaanxi, resistance was also related to mutation at position 197 of the ALS gene. Both studies confirmed tribenuron-methyl resistance in flixweed in China, with the resistance mechanism being conferred by specific ALS point mutations at amino acid position 197.

Tribenuron-methyl resistance and mutation diversity of Pro197 in flixweed (Descurainia Sophia L.) accessions from China

“…The results of the AHAS mutation tests are highly correlated with those of resistance bioassays, confirming that the Pro197 mutations play an important role in flixweed resistance to tribenuron-methyl. These findings are also consistent with previous reports [9,10,16,17]. Interestingly, we have found that two flixweed accessions (HB01 and HB14) exhibit significant resistance to tribenuron-methyl but have no resistance-endowing mutations in AHAS gene.…”

“…In recent years, farmers found it difficult to control flixweed by tribenuron-methyl. Indeed, the sustained reliance on tribenuron-methyl to control this specie has led to the evolution of resistant accession in winter wheat fields in Shandong, Jiangsu, Hebei, Shaanxi and Tianjin provinces of China [10,[15][16][17]. The tribenuron-methyl resistance in flixweed was mainly due to the target-site mutations.…”

“…The tribenuron-methyl resistance in flixweed was mainly due to the target-site mutations. Various amino acid mutations including Ala, Leu, Thr, Ser, or Pro/Ser have been reported [10,[15][16][17]. The objectives of this study were to (1) test the susceptibility of various flixweed accessions to tribenuron-methyl; (2) identify the potential mutations at site of Pro197; (3) develop a cleaved amplified polymorphic sequence (CAPS) marker to enable rapid identification of flixweed plants with Pro197 mutation.…”

Evaluation of resistance to acetolactate synthase inhibiting herbicide in wild mustard (Sinapis arvensis L.)

“…For herbicide dose-response assay, the dose required to kill 50% of the population (LD50) or cause 50% dry weight reduction (GR50) was calculated by non-linear regression using a threeparameter log-logistic model which fitted better than the other models (Xu et al,2010;Cui et al, 2011).…”

“…ALS enzyme has catalytic effect on the branched chain amino acids, such as valine, leucine and isoleucine (Xu et al, 2010;Cui et al, 2011). ALS enzyme is the target-site of different chemical families such as sulfonylureas, imidazolinones, triazolopyrimidines, pyrimidinylthiobenzoates and sulfonylaminocarbonyl-triazolinones (Cruz-Hipolito et al, 2013).…”