Abstract
The emergence of herbicide-resistant weeds is a major threat facing modern agriculture. Over 470 weedy-plant populations have developed resistance to herbicides. Traditional evolutionary mechanisms are not always sufficient to explain the rapidity with which certain weed populations adapt in response to herbicide exposure. Stress-induced epigenetic changes, such as alterations in DNA methylation, are potential additional adaptive mechanisms for herbicide resistance. We performed methylC sequencing of Arabidopsis thaliana leaves that developed after either mock treatment or two different sub-lethal doses of the herbicide glyphosate, the most-used herbicide in the history of agriculture. The herbicide injury resulted in 9,205 differentially methylated regions (DMRs) across the genome. In total, 5,914 of these DMRs were induced in a dose-dependent manner, wherein the methylation levels were positively correlated to the severity of the herbicide injury, suggesting that plants can modulate the magnitude of methylation changes based on the severity of the stress. Of the 3,680 genes associated with glyphosate-induced DMRs, only 7% were also implicated in methylation changes following biotic or salinity stress. These results demonstrate that plants respond to herbicide stress through changes in methylation patterns that are, in general, dose-sensitive and, at least partially, stress-specific.
Highlights
The development of herbicide-resistant weed populations is a major crisis facing modern agriculture (Bonny, 2016)
Four-week-old A. thaliana rosettes were exposed to 0%, 5%, 10%, or 15% of a typical field rate of 0.9 kg acid equivalency ha-1 glyphosate, with the 5% and 10% rates causing visible herbicide injury, but allowing for plant survival and reproduction (Fig. 1A). gDNA was collected from newly formed cauline leaves at silique maturation of four individuals from each treatment (Figs. 1B–1D)
An average of 0.2% Methylated cytosines (mCs) was identified on the chloroplast genome, which is not methylated in A. thaliana (Cokus et al, 2008), demonstrating the fidelity of the methylC-seq protocol and data filtering. mCs were distributed across all five nuclear chromosomes
Summary
The development of herbicide-resistant weed populations is a major crisis facing modern agriculture (Bonny, 2016). Other cases, termed non-target site resistance, are poorly understood, but have been attributed to quantitative accumulation of minor resistance alleles selected from standing genetic variation at multiple gene loci (Busi, Neve & Powles, 2013; Delye, 2013). Non-target site resistance may involve various mechanisms that affect herbicide metabolism or translocation (Gonzalez-Torralva et al, 2012). Resistance to glyphosate is interesting in that it often appears to involve non-target site mechanisms, which can emerge and dominate a population after as few as three generations of sub-lethal exposure to the herbicide (Busi & Powles, 2009), and can spread through a population faster than predicted by gene flow or propagule dispersal (Escorial et al, 2011; Espeby, Fogelfors & Milberg, 2011; Okada et al, 2013). Given that herbicides induce a strong abiotic stress, it is likely that weeds respond by activating stress-signaling networks that reprogram gene expression (Busi, Neve & Powles, 2013), and we hypothesize that this involves epigenetic regulation of gene function that could contribute to herbicide resistance as implicated in weed adaptation to other stresses (Verhoeven et al, 2010) and in the response of rice to the pesticide atrazine (Lu et al, 2016)
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