A Two-in-One Strategy: Target and Nontarget Site Mechanisms Both Play Important Role in IMI-Resistant Weedy Rice.

Ru-Ann Yean,Beng-Kah Song,Sadequr Rahman,Masilamany Dilipkumar

doi:10.3390/ijms22030982

Abstract

The introduction of Clearfield technology allows the use of imidazolinone (IMI) herbicides to control weedy rice. Imidazolinone herbicides stop the acetolactate synthase (ALS) enzyme from synthesizing branched-chain amino acids, resulting in the death of the plant. Since the launch of Clearfield technology in Malaysia in 2010, many farmers have replaced traditional cultivars with Clearfield (CL) rice lines (MR220-CL1 and MR220-CL2). This technology was initially effective; however, in recent years, local farmers have reported the reduced efficacy of IMI herbicides in controlling the spread of weedy rice. Under IMI herbicide treatment, in previous weedy rice studies, the target-site resistance (TSR) mechanism of the ALS gene has been suggested as a key factor conferring herbicide resistance. In our study, a combination of ALS gene sequencing, enzyme colorimetric assay, and a genome-wide association study (GWAS) highlighted that a non-target-site resistance (NTSR) can be an alternative molecular mechanism in IMI-resistant weedy rice. This is supported by a series of evidence, including a weak correlation between single nucleotide polymorphisms (SNPs) within the ALS exonic region and ALS enzyme activity. Our findings suggest that the adaptability of weedy rice in Clearfield rice fields can be more complicated than previously found in other rice strains.

Highlights

Resistance toward herbicides is a specific process enabling plants to survive the application of herbicide treatments
Direct Sanger sequencing generated a total of 2086 bp of the aligned acetolactate synthase (ALS) sequence, which spanned the 1935 bp single exon of the ALS gene
Forty-three single nucleotide polymorphisms (SNPs) were identified along the exon of the ALS gene (Supplementary Table S1)

Summary

Introduction

Resistance toward herbicides is a specific process enabling plants to survive the application of herbicide treatments. This can be achieved through either “target-site” or “‘non-target-site” resistance. Target-site resistance (TSR) occurs when there is an alteration at the target site, resulting in the structural or biochemical change of the targeted enzyme in the plant. The herbicide is no longer be able to bind to its site of action, allowing the plant to survive the herbicide treatments. Is a mechanism that does not involve changes at the target site but still enables a plant to survive herbicide application. The potential NTSR mechanisms include reduced herbicide uptake, reduced translocation, reduced herbicide activation, enhanced herbicide detoxification, changes in intra- or intercellular compartmentalization, and enhanced repair of herbicide-induced damage [1]

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