Abstract
BackgroundFlixweed (Descurainia sophia L.) is a troublesome and widespread broadleaf weed in winter fields in China, and has evolved high level resistance to acetolactate synthase (ALS)-inhibiting sulfonylurea herbicide tribenuron-methyl.ResultsWe identified a resistant flixweed population (N11) exhibiting 116.3-fold resistance to tribenuron-methyl relative to the susceptible population (SD8). Target-site ALS gene mutation Pro-197-Thr was identified in resistant plants. Moreover, the resistance can be reversed to 28.7-fold by the cytochrome P450 inhibitor malathion. The RNA-Sequencing was employed to identify candidate genes involved in non-target-site metabolic resistance in this population. Total 26 differentially expressed contigs were identified and eight of them (four P450s, one ABC transporter, three glycosyltransferase) verified by qRT-PCR. Consistent over-expression of the two contigs homology to CYP96A13 and ABCC1 transporter, respectively, were further qRT-PCR validated using additional plants from the resistant and susceptible populations.ConclusionsTribenuron-methyl resistance in flixweed is controlled by target-site ALS mutation and non-target-site based mechanisms. Two genes, CYP96A13 and ABCC1 transporter, could play an important role in metabolic resistance to tribenuron-methyl in the resistant flixweed population and justify further functional studies.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-2915-8) contains supplementary material, which is available to authorized users.
Highlights
Flixweed (Descurainia sophia L.) is a troublesome and widespread broadleaf weed in winter fields in China, and has evolved high level resistance to acetolactate synthase (ALS)-inhibiting sulfonylurea herbicide tribenuron-methyl
target-site based resistance (TSR) is widely reported in resistant weed species, which is endowed by gene mutations in target enzymes, such as acetolactate synthase (ALS), acetyl-CoA carboxylase (ACCase), protoporphyrinogen IX oxidase (PPO), 4hydroxyphenylpyruvate dioxygenase (HPPD), and 5enolpyruvylshikimate-3-phosphate synthase (EPSPS) [1,2,3,4,5,6]
To disclose the TSR and non-target-site based resistance (NTSR) mechanisms to tribenuron-methyl, an R flixweed population N11 and an S population SD8 were used in this study
Summary
Flixweed (Descurainia sophia L.) is a troublesome and widespread broadleaf weed in winter fields in China, and has evolved high level resistance to acetolactate synthase (ALS)-inhibiting sulfonylurea herbicide tribenuron-methyl. TSR is widely reported in resistant weed species, which is endowed by gene mutations in target enzymes, such as acetolactate synthase (ALS)-, acetyl-CoA carboxylase (ACCase)-, protoporphyrinogen IX oxidase (PPO)-, 4hydroxyphenylpyruvate dioxygenase (HPPD)-, and 5enolpyruvylshikimate-3-phosphate synthase (EPSPS) [1,2,3,4,5,6]. Flixweed (Descurainia sophia L.) is a self-pollinated annual and notorious weed widely distributed in winter wheat cropping regions in China. Effective control of this weed heavily relied on the ALS-inhibiting herbicide (hereafter referred to as ALS herbicide) tribenuronmethyl, which targeted at ALS enzymes. NTSR mechanisms endowing tribenuron-methyl-resistance in flixweed have not previously investigated
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