EVOP Subgroup Contributed Talks

Matthew Edgington

The Pirbright Institute

" Population-level multiplexing: A strategy to manage gene drive resistance"

Gene drives are predicted to increase in frequency within a population even when harmful to individuals carrying them. This allows associated desirable genetic material to also increase in frequency, potentially allowing their use against globally important issues including disease vectors, crop pests and invasive species. The most high-profile - CRISPR-based gene drives - bias inheritance by “cutting” a target DNA sequence and tricking the system into using the gene drive as a repair template – converting drive heterozygotes into homozygotes. Unfortunately, alternate repair mechanisms can create cut-resistant alleles, causing drive failure. A commonly stated solution is multiplexing – targeting multiple DNA sequences – since this requires resistance at all target sites for drive failure. However, simultaneous DNA “cuts” can lead to the deletion of large DNA sequences and thus the removal of multiple (or all) target sequences within a single event. Here we consider novel approaches for overcoming these issues by multiplexing at the population rather than the individual level. Stochastic mathematical models demonstrate that significant performance improvements can be obtained from these approaches. Based on technical feasibility, we further investigate one approach – demonstrating robustness to key performance parameters and the potential for control of biologically relevant population sizes.

Christof Mast

"Heat flows adjust local ion concentrations in favor of prebiotic chemistry"

Abstract to be determined. Please check back later.

Kalle Parvinen

University of Turku, Finland

"Evolution of dispersal in a spatially heterogeneous population with finite patch sizes"

Dispersal is one of the fundamental life-history strategies of organisms, so understanding the selective forces shaping the dispersal traits is important. In the Wright's island model, dispersal evolves due to kin competition even when dispersal is costly, and it has traditionally been assumed that the living conditions are the same everywhere. In order to study the effect of spatial heterogeneity, we extend the model so that patches may receive different amounts of immigrants, foster different number of individuals and give different reproduction efficiency to individuals therein. We obtain an analytical expression for the fitness gradient, which shows that directional selection consists of three components: as in the homogeneous case, direct cost of dispersal selects against dispersal and kin competition promotes dispersal. The new component, spatial heterogeneity, more precisely the variance of so-called relative reproductive potential, tends to select against dispersal. We also obtain an expression for the second derivative of fitness, which can be used to determine whether there is disruptive selection: Unlike the homogeneous case, we found that divergence of traits through evolutionary branching is possible in the heterogeneous case. Existing spatial heterogeneity in the real world is a key determinant in dispersal evolution.

Ewan Flintham

Imperial College London

"Dispersal alters the nature and scope of sexually antagonistic variation"

Intralocus sexual conflict, or sexual antagonism, occurs when alleles have opposing fitness effects in the two sexes. Previous theory suggests that sexual antagonism is a driver of genetic variation by generating balancing selection. However, most of these studies assume that populations are well-mixed, neglecting the effects of spatial subdivision. Here we use mathematical modelling to show that limited dispersal changes evolution at sexually antagonistic autosomal and X-linked loci due to inbreeding and sex-specific kin competition. We find that if the sexes disperse at different rates, kin competition within the philopatric sex biases intralocus conflict in favour of the more dispersive sex. Furthermore, kin competition diminishes the strength of balancing selection relative to genetic drift, reducing genetic variation in small subdivided populations. Meanwhile, by decreasing heterozygosity, inbreeding reduces the scope for sexually antagonistic polymorphism due to non-additive allelic effects, and this occurs to a greater extent on the X-chromosome than autosomes. Overall, our results indicate that spatial structure is a relevant factor in predicting where sexually antagonistic alleles might be observed. We suggest that sex-specific dispersal ecology and demography can contribute to interspecific and intragenomic variation in sexual antagonism.