Abstract
The continuous and sole dependence on imidazolinone (IMI) herbicides for weedy rice control has led to the evolution of herbicide resistance in weedy rice populations across various countries growing IMI herbicide-resistant rice (IMI-rice), including Malaysia. A comprehensive study was conducted to elucidate occurrence, level, and mechanisms endowing resistance to IMI herbicides in putative resistant (R) weedy rice populations collected from three local Malaysian IMI-rice fields. Seed bioassay and whole-plant dose-response experiments were conducted using commercial IMI herbicides. Based on the resistance index (RI) quantification in both experiments, the cross-resistance pattern of R and susceptible (S) weedy rice populations and control rice varieties (IMI-rice variety MR220CL2 and non-IMI-rice variety MR219) to imazapic and imazapyr was determined. A molecular investigation was carried out by comparing the acetohydroxyacid synthase (AHAS) gene sequences of the R and S populations and the MR220CL2 and MR219 varieties. The AHAS gene sequences of R weedy rice were identical to those of MR220CL2, exhibiting a Ser-653-Asn substitution, which was absent in MR219 and S plants. In vitro assays were conducted using analytical grade IMI herbicides of imazapic (99.3%) and imazapyr (99.6%) at seven different concentrations. The results demonstrated that the AHAS enzyme extracted from the R populations and MR220CL2 was less sensitive to IMI herbicides than that from S and MR219, further supporting that IMI herbicide resistance was conferred by target-site mutation. In conclusion, IMI resistance in the selected populations of Malaysian weedy rice could be attributed to a Ser-653-Asn mutation that reduced the sensitivity of the target site to IMI herbicides. To our knowledge, this study is the first to show the resistance mechanism in weedy rice from Malaysian rice fields.
Highlights
Herbicide resistance is the ability of plants to inheritably survive and reproduce following herbicide application at a rate that would normally kill the wild/susceptible type plants [1,2,3]
The IMI herbicide resistance level in the weedy rice populations was quantified based on the resistance index (RI) value of the herbicide rate resulting in 50% mortality (LD50)
Results from the seed bioassay in the present study indicated that continuous exposure of pre-germinated seeds to IMI herbicides can significantly affect seed growth
Summary
Herbicide resistance is the ability of plants to inheritably survive and reproduce following herbicide application at a rate that would normally kill the wild/susceptible type plants [1,2,3]. Resistance may develop naturally in plants owing to herbicide selection pressure or may be induced by genetic engineering or mutagenesis [1,2,3], and it is commonly associated with herbicide rates higher than the recommended dose. Several plant species are naturally able to tolerate certain herbicides; this tolerance is limited to a normal/recommended herbicide dose [1, 2]. Herbicide resistance mechanisms have been broadly categorized into two types, namely, target site resistance (TSR) and non-target site resistance (NTSR) [4]. In TSR, the target enzymes show reduced sensitivity to the herbicide owing to mutation(s) at the site of action that prevents the herbicide from binding to the enzyme, which may lead to altered epigenetic regulation in some cases, such as overexpression of the enzyme or gene amplification [4,5,6,7]. Of the 512 herbicide resistance cases reported worldwide, resistance to acetohydroxyacid synthase (AHAS) inhibitors is the most frequent (165 cases) [9], and amino acid substitutions within the AHAS gene represent the most common mechanism endowing resistance to AHAS inhibitors in weed species [10, 11]
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