Detecting recombination from gene trees

In this article, a method is proposed for detecting recombination in the sequences of a gene from a set of closely related organisms. The method, the Homoplasy Test, is appropriate when the sequences are rather similar, differing by 1%-5% of nucleotides. It is effective in detecting relatively frequent recombination between a set of rather similar strains, in contrast to previous methods which detect rare or unique transfers between more distant strains. It is based on the fact that, if there is no recombination and if no repeated mutations have occurred (homoplasy), then the number of polymorphic sites, v, is equal to the number of steps, t, in a most-parsimonious tree. If the number of "apparent homoplasies" in the most-parsimonious tree, h = t-v, is greater than zero, then either homoplasies have occurred by mutation or there has been recombination. An estimate of the distribution of h expected on the null hypothesis of no recombination depends on Se, the "effective site number," defined as follows: if ps is the probability that two independent substitutions in the gene occur at the same site, then Se = 1/ps. Se can be estimated if a suitable outgroup is available. The Homoplasy Test is applied to three bacterial genes and to simulated gene trees with varying amounts of recombination. Methods of estimating the rate, as opposed to the occurrence, of recombination are discussed.      

The effect of irradiation in air or in hyperbaric oxygen on the Fib/T tumor in WHT mice pretreated with a hypoxic gas mixture

The effect of exposing WHT mice bearing the Fib/T tumor to a low-oxygen environment (8, 10, and 15% oxygen) for 48 h or 72 h before irradiation was compared, using an in vitro colony-forming excision assay, to the effect obtained when mice were pretreated with air. The response of the Fib/T tumor to radiation delivered in air was improved both by a 48-h and by a 72-h exposure of the animals to 8, 10, and 15% oxygen. However, the greatest tumor sensitization was achieved when mice were kept in 8% oxygen for 48 h before irradiation. These results are interpreted and discussed in relation to increases in the 2,3-DPG concentration, which were shown to occur when mice were exposed to a reduced oxygen environment. The relative importance of two models proposed to explain these findings is assessed. If mice pretreated with air were irradiated in hyperbaric oxygen, a similar tumor response was observed compared to that when mice were exposed to 8% oxygen for 48 h and then irradiated in air.     

Investigating the evolution and development of biological complexity under the framework of epigenetics

Biological complexity is a key component of evolvability, yet its study has been hampered by a focus on evolutionary trends of complexification and inconsistent definitions. Here, we demonstrate the utility of bringing complexity into the framework of epigenetics to better investigate its utility as a concept in evolutionary biology. We first analyze the existing metrics of complexity and explore the link between complexity and adaptation. Although recently developed metrics allow for a unified framework, they omit developmental mechanisms. We argue that a better approach to the empirical study of complexity and its evolution includes developmental mechanisms. We then consider epigenetic mechanisms and their role in shaping developmental and evolutionary trajectories, as well as the development and organization of complexity. We argue that epigenetics itself could have emerged from complexity because of a need to self‐regulate. Finally, we explore hybridization complexes and hybrid organisms as potential models for studying the association between epigenetics and complexity. Our goal is not to explain trends in biological complexity but to help develop and elucidate novel questions in the investigation of biological complexity and its evolution.