Confirmation of Flixweed (Descurainia sophia) Resistance to Tribenuron in China

Abstract

Reports arose from major Chinese wheat production regions that flixweed was not controlled by tribenuron after the herbicide was continuously used for several years. Flixweed seeds were collected from wheat fields that had been treated with tribenuron repeatedly over 3 to 15 yr or from road sides and remote hills that had never received tribenuron in Jiangsu, Hebei, Shanxi, Sichuan, Shandong, Shaanxi, and Henan provinces, and Tianjin and Beijing metropolises in China. The response of various biotypes to tribenuron was determined by whole plant experiments in the greenhouse. The experiments demonstrated that 11 of 32 flixweed biotypes were susceptible to tribenuron. The remaining 21 biotypes expressed moderate to high levels of tribenuron resistance with resistance indices ranging from 4 to > 1,500. DNA sequence analysis of acetolactate synthase (ALS) genes of selected biotypes 6, 7, 27, and 29 revealed a point mutation at position 197 of the ALS gene, as numbered relative to the protein sequence of Arabidopsis, where proline was substituted by leucine in biotype 7 and by threonine in biotype 29. These mutations are known to confer resistance to ALS-inhibiting herbicides and are responsible for the high resistance of these biotypes to tribenuron. The results also indicate that tribenuron resistance in flixweed is widespread in China and management programs to control these resistant populations are warranted.

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.…”

Mutation at residue 376 of ALS confers tribenuron-methyl resistance in flixweed (Descurainia sophia) populations from Hebei Province, China

“…4). These results showed that the mutation of ALS at Asp376 can confer flixweed with resistance to tribenuron, in addition to mutation at the Pro197 site as previously reported [17][18][19][20][21].…”

“…However, until now, only mutation at Pro197 had been reported in tribenuronresistant flixweed populations [17][18][19][20][21]. It was unknown whether there were any other mutations affording tribenuron resistance in populations of this weed.…”