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Genetic drive represents a fundamental force of evolution that operates by biasing allele transmission by individuals in a population. Genetic engineering now makes the anthropogenic manipulation of genetic drive feasible in a process termed 'genetic welding'. Genetic welding with synthetic gene drives, which is similar to but distinct from artificial selection, is extremely powerful and profoundly capable of promoting the evolution of complex and novel phenotypic changes to both captive and wild populations. Bioethical analysis and biological research into genetic welding of natural populations with synthetic gene drives requires further consideration, including potential application to humans and the long-term evolutionary consequences of synthetic gene drive elements. Genetic drive represents a fundamental evolutionary force that can exact profound change to the genetic composition of populations by biasing allele transmission. Herein I propose that the use of synthetic homing gene drives, the human-mediated analog of endogenous genetic drives, warrants the designation of 'genetic welding' as an anthropogenic evolutionary force. Conceptually, this distinction parallels that of artificial and natural selection. Genetic welding is capable of imposing complex and rapid heritable phenotypic change on entire populations, whether motivated by biodiversity conservation or public health. Unanticipated possible long-term evolutionary outcomes, however, demand further investigation and bioethical consideration. The emerging importance of genetic welding also compels our explicit recognition of genetic drive as an addition to the other four fundamental forces of evolution. [ABSTRACT FROM AUTHOR]

Speciation research has largely assumed that the genetic causes of reproductive isolation are the work of fixed, divergent alleles that interact to cause genetic problems in hybrids: Bateson–Dobzhansky–Muller incompatibilities. However, many recent studies demonstrate substantial heritable polymorphism within species for hybrid incompatibility, herein called variable reproductive isolation (VRI). In this review, I outline the causes and importance of this general phenomenon. I also identify the new challenges of quantifying the relative contributions to reproductive isolation of fixed alleles versus polymorphisms, and the change in these contributions over the course of speciation. Explicit integration of VRI into speciation theory will help to quantify the relative roles of genetic drift and selection in speciation, but this synthesis requires substantial new contributions from both theory and empirical studies. [Copyright &y& Elsevier]

Single nucleotide polymorphisms (SNPs) and short tandem repeats (STRs) differ in mutation rate and mechanism. As a result of these differences, simultaneous consideration of polymorphism patterns at SNPs and STRs can provide insights that are difficult to obtain from analysis of either marker type in isolation. Here, we use coalescent simulations to model the opposing effects of contrasting mutational dynamics and of shared genealogical history on the correlation between polymorphism at linked SNPs and STRs. Results show that polymorphism patterns are correlated only weakly despite the shared underlying genealogy, underscoring the importance of divergent mutational processes. Examples illustrate how knowledge of these relationships could aid population genetic inference, indicating the need for thorough theoretical studies. [Copyright &y& Elsevier]