Interpreting the Dependence of Mutation Rates on Age and Time.

Mutations can originate from the chance misincorporation of nucleotides during DNA replication or from DNA lesions that arise between replication cycles and are not repaired correctly. We introduce a model that relates the source of mutations to their accumulation with cell divisions, providing a framework for understanding how mutation rates depend on sex, age, and cell division rate. We show that the accrual of mutations should track cell divisions not only when mutations are replicative in origin but also when they are non-replicative and repaired efficiently.

Male bias in distributions of additive genetic, residual, and phenotypic variances of shared traits.

Despite a shared genetic architecture between males and females, sexual differences are widespread. The extent of this shared genetic architecture, reflected in the intersexual genetic correlation, has previously been correlated with the extent of phenotypic sexual dimorphism in shared traits. However, the magnitude of the difference in sex-specific additive genetic variances may also fuel sexual dimorphism.

Determinants of mutation rate variation in the human germline.

Because germline mutations are the source of all evolutionary adaptations and heritable diseases, characterizing their properties and the rate at which they arise across individuals is of fundamental importance for human genetics. After decades during which estimates were based on indirect approaches, notably on inferences from evolutionary patterns, it is now feasible to count de novo mutations in transmissions from parents to offspring. Surprisingly, this direct approach yields a mutation rate that is twofold lower than previous estimates, calling into question our understanding of the chronology of human evolution and raising the possibility that mutation rates have evolved relatively rapidly.

Gene duplication in the evolution of sexual dimorphism.

Males and females share most of the same genes, so selection in one sex will typically produce a correlated response in the other sex. Yet, the sexes have evolved to differ in a multitude of behavioral, morphological, and physiological traits. How did this sexual dimorphism evolve despite the presence of a common underlying genome? We investigated the potential role of gene duplication in the evolution of sexual dimorphism.

Condition-dependence of the sexually dimorphic transcriptome in Drosophila melanogaster.

Sexually dimorphic traits are by definition exaggerated in one sex, which may arise from a history of sex-specific selection-in males, females, or both. If this exaggeration comes at a cost, exaggeration is expected to be greater in higher condition individuals (condition-dependent). Although studies using small numbers of morphological traits are generally supportive, this prediction has not been examined at a larger scale.