Standing genetic variation fuels rapid evolution of herbicide resistance in blackgrass

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 120; no. 16; p. e2206808120
• Main Authors: Kersten, Sonja, Chang, Jiyang, Huber, Christian D, Voichek, Yoav, Lanz, Christa, Hagmaier, Timo, Lang, Patricia, Lutz, Ulrich, Hirschberg, Insa, Lerchl, Jens, Porri, Aimone, Van de Peer, Yves, Schmid, Karl, Weigel, Detlef, Rabanal, Fernando A
• Format: Journal Article
• Language: English
• Published: United States National Academy of Sciences 18.04.2023
• Subjects: Acetolactate synthase; Acetyl-CoA carboxylase; Acetyl-CoA Carboxylase - genetics; Acetyl-CoA Carboxylase - metabolism; Agricultural land; Agrochemicals; Biological Sciences; Cereal crops; Chromosomes; Europe; Genetic diversity; Genomes; Haplotypes; Herbicide resistance; Herbicide Resistance - genetics; Herbicides; Herbicides - pharmacology; Mutation; Poaceae - genetics; Poaceae - metabolism; Population studies; Populations; Europe; Alopecurus myosuroides; blackgrass; herbicide resistance; rapid adaptation
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.2206808120

Repeated herbicide applications in agricultural fields exert strong selection on weeds such as blackgrass ( ), which is a major threat for temperate climate cereal crops. This inadvertent selection pressure provides an opportunity for investigating the underlying genetic mechanisms and evolutionary processes of rapid adaptation, which can occur both through mutations in the direct targets of herbicides and through changes in other, often metabolic, pathways, known as non-target-site resistance. How much target-site resistance (TSR) relies on de novo mutations vs. standing variation is important for developing strategies to manage herbicide resistance. We first generated a chromosome-level reference genome for for population genomic studies of herbicide resistance and genome-wide diversity across Europe in this species. Next, through empirical data in the form of highly accurate long-read amplicons of alleles encoding acetyl-CoA carboxylase (ACCase) and acetolactate synthase (ALS) variants, we showed that most populations with resistance due to TSR mutations-23 out of 27 and six out of nine populations for and , respectively-contained at least two TSR haplotypes, indicating that soft sweeps are the norm. Finally, through forward-in-time simulations, we inferred that TSR is likely to mainly result from standing genetic variation, with only a minor role for de novo mutations.