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Non‐target‐site resistance to PDS‐inhibiting herbicides in a wild radish ( Raphanus raphanistrum ) population
Author(s) -
Lu Huan,
Yu Qin,
Han Heping,
Owen Mechelle J,
Powles Stephen B
Publication year - 2020
Publication title -
pest management science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.296
H-Index - 125
eISSN - 1526-4998
pISSN - 1526-498X
DOI - 10.1002/ps.5733
Subject(s) - fluridone , biology , population , raphanus , genetics , wild type , pesticide resistance , mutant , botany , gene , pesticide , agronomy , abscisic acid , sociology , demography
BACKGROUND Diflufenican resistance has been reported in wild radish populations since 1998, but the resistance mechanisms have not been investigated. Recently, we identified a wild radish population (H2/10) from the Western Australian grain belt that is resistant (R) to the phytoene desaturase (PDS)‐inhibiting herbicide diflufenican. RESULTS Dose–response results showed this R population is 4.9‐fold more resistant than the susceptible (S) population based on the LD 50 R/S ratio. In addition, the R population also exhibits cross‐resistance to the PDS‐inhibiting herbicide fluridone. The cytochrome P450 inhibitor malathion reversed diflufenican resistance and partially reversed fluridone resistance in the R population. The full coding sequences of the PDS gene were cloned from the S and R plants and there are natural variations in the PDS gene transcripts/alleles with no correlation to resistance. In addition, the R plants had a level of PDS gene expression that is not significantly different from the S plants. CONCLUSION These results demonstrated that diflufenican resistance in this R wild radish population is likely due to non‐target‐site based enhanced herbicide metabolism involving cytochrome P450s. © 2019 Society of Chemical Industry