Intense selection pressures result in major evolutionary changes. This is best exemplified by pests responding to pesticides or bacteria to antibiotics. While the cause of these evolutionary changes is genetic, the consequence is demographic: the selection of a mutation increasing fitness drives the population dynamics. The most tolerant individuals increase in abundance and the population grows again, relegating the last selection pressure to the annals of past evolution; this is the fundamental paradigm of evolutionary biology.
But the selection arena is spatially heterogeneous, resulting in variation in demography and selection, and modulating the spread of beneficial mutations. This heterogeneity is currently overlooked in most studies as empirical testing often focuses on a single spatial scale for which these factors are assumed constant. We argue that different processes dominate at different scales, having a dramatic impact on population management outcomes. With population genetics quantifying evolutionary change and demography identifying key processes, a unified framework connecting the genetic cause with the demographic consequence is the way to address this outstanding issue over the multiple spatial scales; the time is ripe for a step change towards such a unified framework.
At a local scale of metres, dispersal of mutations in plants are density-limited. Most pollen and seeds remaining close to the source and submitted to patchy selection5. At a landscape scale, dispersal is limited by larger geographic barriers and establishment by climate6, becoming the crucial agents through which mutations can spread from one region to another. How do these parameters vary spatially and at which scale do they need to be measured to capture the effect of environmental heterogeneity? At the population scale, which processes determine the nature and intensity of selection given the species life-history and the management practices? Finally at the genome scale, what is the molecular context in which mutations occur and is there a potential for genomic conflict with other loci to affect population dynamics?
Exploring the potential of gene drives to restore herbicide susceptibility