Occurrence of low sensitive biotype of some herbicides of water foxtail (alopecurus aequalis) in wheat fields in Fukuoka prefecture, and effects of some herbicides to its biotype

Uchikawa, Osamu; Miyazaki, Masahiro; Tanaka, Katsuo; Ohdan, Hideki

doi:10.3719/weed.50.supplement_68

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“…Since the early 1990s, management has relied on postemergence application of thifensulfuron-methyl, a SU herbicide. However, resistance to thifensulfuron-methyl was confirmed in 2004, after seven consecutive years of herbicide treatment ( Uchikawa et al, 2005 ). Resistance of A. aequalis to ALS inhibitors was also recently reported in China ( Guo et al, 2015b , 2016 ; Xia et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Copy Number Variation in Acetolactate Synthase Genes of Thifensulfuron-Methyl Resistant Alopecurus aequalis (Shortawn Foxtail) Accessions in Japan

et al. 2017

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Severe infestations of Alopecurus aequalis (shortawn foxtail), a noxious weed in wheat and barley cropping systems in Japan, can occur even after application of thifensulfuron-methyl, a sulfonylurea (SU) herbicide. In the present study, nine accessions of A. aequalis growing in a single wheat field were tested for sensitivity to thifensulfuron-methyl. Seven of the nine accessions survived application of standard field rates of thifensulfuron-methyl, indicating that severe infestations likely result from herbicide resistance. Acetolactate synthase (ALS) is the target enzyme of SU herbicides. Full-length genes encoding ALS were therefore isolated to determine the mechanism of SU resistance. As a result, differences in ALS gene copy numbers among accessions were revealed. Two copies, ALS1 and ALS2, were conserved in all accessions, while some carried two additional copies, ALS3 and ALS4. A single-base deletion in ALS3 and ALS4 further indicated that they represent pseudogenes. No differences in ploidy level were observed between accessions with two or four copies of the ALS gene, suggesting that copy number varies. Resistant plants were found to carry a mutation in either the ALS1 or ALS2 gene, with all mutations causing an amino acid substitution at the Pro197 residue, which is known to confer SU resistance. Transcription of each ALS gene copy was confirmed by reverse transcription PCR, supporting involvement of these mutations in SU resistance. The information on the copy number and full-length sequences of ALS genes in A. aequalis will aid future analysis of the mechanism of resistance.

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