Abstract

BackgroundHerbicide resistance in agrestal weeds is a global problem threatening food security. Non-target-site resistance (NTSR) endowed by mechanisms neutralising the herbicide or compensating for its action is considered the most agronomically noxious type of resistance. Contrary to target-site resistance, NTSR mechanisms are far from being fully elucidated. A part of weed response to herbicide stress, NTSR is considered to be largely driven by gene regulation. Our purpose was to establish a transcriptome resource allowing investigation of the transcriptomic bases of NTSR in the major grass weed Alopecurus myosuroides L. (Poaceae) for which almost no genomic or transcriptomic data was available.ResultsRNA-Seq was performed from plants in one F2 population that were sensitive or expressing NTSR to herbicides inhibiting acetolactate-synthase. Cloned plants were sampled over seven time-points ranging from before until 73 h after herbicide application. Assembly of over 159M high-quality Illumina reads generated a transcriptomic resource (ALOMYbase) containing 65,558 potentially active contigs (N50 = 1240 nucleotides) predicted to encode 32,138 peptides with 74 % GO annotation, of which 2017 were assigned to protein families presumably involved in NTSR. Comparison with the fully sequenced grass genomes indicated good coverage and correct representation of A. myosuroides transcriptome in ALOMYbase. The part of the herbicide transcriptomic response common to the resistant and the sensitive plants was consistent with the expected effects of acetolactate-synthase inhibition, with striking similarities observed with published Arabidopsis thaliana data. A. myosuroides plants with NTSR were first affected by herbicide action like sensitive plants, but ultimately overcame it. Analysis of differences in transcriptomic herbicide response between resistant and sensitive plants did not allow identification of processes directly explaining NTSR. Five contigs associated to NTSR in the F2 population studied were tentatively identified. They were predicted to encode three cytochromes P450 (CYP71A, CYP71B and CYP81D), one peroxidase and one disease resistance protein.ConclusionsOur data confirmed that gene regulation is at the root of herbicide response and of NTSR. ALOMYbase proved to be a relevant resource to support NTSR transcriptomic studies, and constitutes a valuable tool for future research aiming at elucidating gene regulations involved in NTSR in A. myosuroides.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-015-1804-x) contains supplementary material, which is available to authorized users.

Highlights

  • Herbicide resistance in agrestal weeds is a global problem threatening food security

  • Establishing ALOMYbase: A. myosuroides transcriptome sequencing and data assembly The expected phenotypes of all plants used for RNA-Seq were confirmed by rating the corresponding phenotype control clones 4 weeks after herbicide application

  • Candidate Non-target-site resistance (NTSR) contigs The primary aim of this work was to identify as many as possible of the contigs presents in plants resistant and/ or sensitive to acetolactate synthase (ALS) inhibitors before herbicide application and at the early stages of herbicide response, in order to establish a transcriptomic resource as comprehensive as possible to allow subsequent studies of A. myosuroides response and NTSR to ALS inhibitors

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Summary

Introduction

Herbicide resistance in agrestal weeds is a global problem threatening food security. Most weeds are annual or short-lived wild plant species. They thrive in agricultural ecosystems because they have evolved traits enabling them to withstand crop competition and cultural practices, including herbicide applications, aimed at disrupting their demography [2, 3]. Understanding weed success requires unravelling the genetic basis of these traits, a task far from being achieved today [3]. Prominent among those traits is resistance to herbicides that has evolved in 246 weed species [4] in response to the powerful and recurrent selective pressure exerted by herbicide applications [5]. The evolution of herbicide resistance in weed populations can result in the disruption of herbicide efficacy, leading to crop failure [6]

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