Re-winding the tape: experimental evolution of resistance to herbicides.

Lead Research Organisation: University of Exeter
Department Name: Biosciences

Abstract

The evolution of resistance to herbicides in plant (weed) populations is a classic example of rapid,
human-induced evolution. Herbicide resistance is a global phenomenon, causing significant economic
impacts through the loss of weed control in agroecosystems. Two mechanisms of resistance have been
described; target-site resistance (TSR) which is conferred by single nucleotide polymorphisms (SNPs)
in herbicide target genes, and non-target site resistance (NTSR) which involves the upregulation of
metabolic enzymes that underpin detoxification and cellular sequestration of herbicides. A major
remaining challenge is to understand the fitness landscape and evolutionary trajectory of herbicide
resistance in plant populations under contrasting selection regimes to inform best management
practices to slow or mitigate the evolution of resistance.
These studies of 'evolution in action' are hampered in higher plant populations by long generation
times, small experimental population sizes and often, by a lack of molecular genetic resources. In
previous research, we have established Chlamydomonas reinhardtii as a suitable model organism to
study the experimental evolution of herbicide resistance. This work focused on phenotypic
characterisation of evolved Chlamy populations following a series of selection experiments that
explored the impacts of herbicide cycling (Lagator et al., Evolutionary Applications, 2012), mixtures
(Lagator et al., New Phytologist, 2013) and sequences (Lagator et al., Proceedings of the Royal Society
B, 2014) on evolution of resistance. We also explored the impacts of sex and migration on resistance
evolution (Lagator et al., Evolution, 2014).
A full genome sequence is available for C. reinhardtii and we are now in a position to extend these
studies to identify the genomic basis of adaptation to herbicides. These studies will enable us to
identify the mutations that underlie de novo evolution of resistance, establish genotype-phenotype
relationships and quantify co-variation with other life history traits, including fitness costs and crossresistance
between diverse herbicide modes of action. Having established the mutations responsible
for adaptation to herbicides and their phenotypic consequences, we will be able to perform a series
of hypothesis-driven selection experiments to understand interactions between the fitness landscape
for herbicide resistance and the efficacy of different management strategies to slow or prevent the
evolution of resistance.
This exciting inter-disciplinary project will bring the combined power of experimental evolution and
genomics to bear on a pressing issue in global food security, addressing fundamental questions
relating to the evolutionary dynamics of adaptation to novel stresses and applied questions
concerning pesticide resistance management.

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