Here is a made-to-order topic of gene-environment interactions: the environmental signal is an “herbicide”, and genetic networks must quickly “adapt” [i.e. find a means of combatting this toxicant (the “response”)] — or else the plant will not survive. Pesticide resistance in plants is a great example of rapid evolution in response to strong, human-mediated selection. Due to widespread use of insecticides and herbicides in agriculture, multiple resistant pest populations often arise. These repeated examples of resistance allow for questions about the level at which parallel adaptation occurs (e.g. are parallel resistant phenotypes in separate lineages due to parallel changes at the developmental, physiological, or genetic level?).
Herbicide-resistant weeds represent fantastic examples of evolutionary parallelism — because the same nucleotide change can lead to resistance among separate lineages — and even separate species; this is an example of genomic constraint (i.e. parallel evolution of a trait occurs because of a finite number of genetic solutions to the same, but often novel, environmental pressure). Among herbicide-resistant weeds, data that support the genomic constraint hypothesis stem from sequence analysis of genes that are theoretically known to produce the protein targeted by the herbicide (i.e. cases of target-site resistance; TSR) — rather than genome-wide sequence surveys — (e.g. population genomics scans or gene-mapping studies). As a result, very little is understood about the potential for parallel genetic responses (that may occur, across the genome), beyond the potential for changes within the (most often) single genes responsible for TSR.
This can become a problem, because many weed species exhibit non-target-site resistance (NTSR; caused by any mechanism not due to TSR). NTSR can include a range of mechanisms — (from herbicide detoxication, to transport alterations to vacuole sequestration). Currently, it is unclear if cases of herbicide resistance via NTSR support the idea of extreme genetic parallelism. Previous research on the genetic basis of resistance to the herbicide glyphosate (active ingredient in the widely-used herbicide RoundUp) has focused largely on changes at the target-site (the enzyme 5-enolpyruvylshikimate-3-phosphate synthase; EPSPS). Conformational changes in EPSPS (due to mutations at the EPSPS locus) result in TSR.
Authors [see attached article] performed a population genomics screen, plus targeted exome re-sequencing, to uncover potential genetic mechanisms of glyphosate resistance in the common morning glory; they wished to determine if genetic parallelism underlies the (repeated) evolution of resistance across numerous resistant populations. Authors found no evidence for changes in the EPSPS gene, but instead identified five genomic regions that showed evidence of selection. Within these regions, genes involved in herbicide detoxication — (cyt. P450s, ABC transporters, and glycosyltransferases) —were enriched and exhibited signs of selective sweeps. One region under selection showed parallel changes across all resistant populations studied; other regions exhibited signs of divergence. Therefore, whereas it appears that the mechanism of resistance in this species is likely the same among resistant populations, authors found patterns of both similar, and divergent, selection — across separate resistant populations at particular loci. 😊
PLoS Genet Feb 2020; 16: e1008593