The longer duration of seasonal influenza virus infection in young children may provide opportunities for within-host evolution as a result of maintenance of genetic diversity through mutation-selection balance.

Whole genome DNA sequence analysis, genome wide gene expression and complex organismal phenotypes in Drosophila mutation accumulation lines provide a robust estimate of the spontaneous mutation rate and mutational effects.

The quiescence-driven mutational landscape reveals replication-independent mutagenesis as a novel evolutionary force.

The Atlantic herring has the lowest mutation rate yet estimated in a vertebrate species and this partially explains its moderate nucleotide diversity given the large population size.

Population mutation rates are highly flexible and evolvable under extreme stress conditions, matching changes in selective pressure to avoid extinction of the entire population.

Cell biological features are subject to stochastic forces of mutation and random genetic drift, which together cause lineages exposed to identical selection pressures to diverge, and mean phenotypes to deviate from expectations under optimizing selection.

Loss-of-function mutations in human genes are an important class of disease causing variation, and estimates of their effects on evolutionary fitness can be used to evaluate their pathogenicity.

Chromosomal instability of cancer can be quantitatively measured by phylogenetic analysis of 200 tumor cells while using evolutionary principles to account for cellular selection.

To maintain genomic integrity during oocyte development, the tumor suppressor BRCA1/BRC-1 and the SMC-5/6 complex both repress intersister crossover recombination events while BRCA1/BRC-1 also specifically inhibits error prone repair of DNA breaks during meiotic prophase I.

A simple mathematical model reveals that antibiotic interactions and collateral effects of evolution are inseparable drivers of multidrug resistance linked by the well-known Price equation from evolutionary theory.