Combining Microbial Culturing With Mathematical Modeling in an Introductory Course-Based Undergraduate Research Experience.

Quantitative techniques are a critical part of contemporary biology research, but students interested in biology enter college with widely varying quantitative skills and attitudes toward mathematics. Course-based undergraduate research experiences (CUREs) may be an early way to build student competency and positive attitudes. Here we describe the design, implementation, and assessment of an introductory quantitative CURE focused on halophilic microbes. In this CURE, students culture and isolate halophilic microbes from environmental and food samples, perform growth assays, then use mathematical modeling to quantify the growth rate of strains in different salinities. To assess how the course may impact students' future academic plans and attitudes toward the use of math in biology, we used pre- and post-quarter surveys. Students who completed the course showed more positive attitudes toward science learning and an increased interest in pursuing additional quantitative biology experiences. We argue that the classroom application of microbiology methods, combined with mathematical modeling using student-generated data, provides a degree of student ownership, collaboration, iteration, and discovery that makes quantitative learning both relevant and exciting to students.

Draft Genome Sequences of 16 Halophilic Prokaryotes Isolated from Diverse Environments.

Halophile-specific enzymes have wide-ranging industrial and commercial applications. Despite their importance, there is a paucity of available halophile whole-genome sequences. Here, we report the draft genome sequences of 16 diverse salt-tolerant strains of bacteria and archaea isolated from a variety of high-salt environments.

The role of migration in the evolution of phenotypic switching.

Stochastic switching is an example of phenotypic bet hedging, where an individual can switch between different phenotypic states in a fluctuating environment. Although the evolution of stochastic switching has been studied when the environment varies temporally, there has been little theoretical work on the evolution of phenotypic switching under both spatially and temporally fluctuating selection pressures. Here, we explore the interaction of temporal and spatial change in determining the evolutionary dynamics of phenotypic switching. We find that spatial variation in selection is important; when selection pressures are similar across space, migration can decrease the rate of switching, but when selection pressures differ spatially, increasing migration between demes can facilitate the evolution of higher rates of switching. These results may help explain the diverse array of non-genetic contributions to phenotypic variability and phenotypic inheritance observed in both wild and experimental populations.

Epigenetic inheritance, epimutation, and the response to selection.

There has been minimal theoretical exploration of the role of epigenetic variation in the response to natural selection. Using a population genetic model, I derive formulae that characterize the response of epigenetic variation to selection over multiple generations. Unlike genetic models in which mutation rates are assumed to be low relative to the strength of selection, the response to selection decays quickly due to a rapid lowering of parent-offspring epiallelic correlation. This effect is separate from the slowing response caused by a reduction in epigenetic variation. These results suggest that epigenetic variation may be less responsive to natural selection than is genetic variation, even in cases where levels of heritability appear similar.

Genetic variation and the evolution of epigenetic regulation.

Epigenetic variation has been observed in a range of organisms, leading to questions of the adaptive significance of this variation. In this study, we present a model to explore the ecological and genetic conditions that select for epigenetic regulation. We find that the rate of temporal environmental change is a key factor controlling the features of this evolution. When the environment fluctuates rapidly between states with different phenotypic optima, epigenetic regulation may evolve but we expect to observe low transgenerational inheritance of epigenetic states, whereas when this fluctuation occurs over longer time scales, regulation may evolve to generate epigenetic states that are inherited faithfully for many generations. In all cases, the underlying genetic variation at the epigenetically regulated locus is a crucial factor determining the range of conditions that allow for evolution of epigenetic mechanisms.

Environment-sensitive epigenetics and the heritability of complex diseases.

Genome-wide association studies have thus far failed to explain the observed heritability of complex human diseases. This is referred to as the "missing heritability" problem. However, these analyses have usually neglected to consider a role for epigenetic variation, which has been associated with many human diseases. We extend models of epigenetic inheritance to investigate whether environment-sensitive epigenetic modifications of DNA might explain observed patterns of familial aggregation. We find that variation in epigenetic state and environmental state can result in highly heritable phenotypes through a combination of epigenetic and environmental inheritance. These two inheritance processes together can produce familial covariances significantly higher than those predicted by models of purely epigenetic inheritance and similar to those expected from genetic effects. The results suggest that epigenetic variation, inherited both directly and through shared environmental effects, may make a key contribution to the missing heritability.