Mutability of mononucleotide repeats, not oxidative stress, explains the discrepancy between laboratory-accumulated mutations and the natural allele-frequency spectrum in .

Important clues about natural selection can be gleaned from discrepancies between the properties of segregating genetic variants and of mutations accumulated experimentally under minimal selection, provided the mutational process is the same in the laboratory as in nature. The base-substitution spectrum differs between laboratory mutation accumulation (MA) experiments and the standing site-frequency spectrum, which has been argued to be in part owing to increased oxidative stress in the laboratory environment. Using genome sequence data from MA lines carrying a mutation (-) that increases the cellular titer of reactive oxygen species (ROS), leading to increased oxidative stress, we find the base-substitution spectrum is similar between -, its wild-type progenitor (N2), and another set of MA lines derived from a different wild strain (PB306).

Development of functional trait biomarkers for trace metal exposure in freshwater clams (Musculium spp.).

Exposure to trace metals typically causes oxidative stress; these consequences are better-characterized in estuarine and marine species than in freshwater species. How cellular-level responses to metal pollution influence whole-organism and population-level traits is poorly understood. We tested whether exposure to single metals (zinc and cadmium) and to metal mixtures (water in equilibrium with sediment from a highly polluted lake) alters two ecologically-relevant traits in freshwater clams, locomotion and reproduction.

Abiotic stress does not magnify the deleterious effects of spontaneous mutations.

Although the effects of deleterious alleles often are predicted to be greater in stressful environments, there is no theoretical basis for this prediction and the empirical evidence is mixed. Here we characterized the effects of three types of abiotic stress (thermal, oxidative and hyperosmotic) on two sets of nematode (Caenorhabditis elegans) mutation accumulation (MA) lines that differ by threefold in fitness. We compared the survival and egg-to-adult viability between environments (benign and stressful) and between fitness categories (high-fitness MA, low-fitness MA).

The red death meets the abdominal bristle: polygenic mutation for susceptibility to a bacterial pathogen in Caenorhabditis elegans.

Understanding the genetic basis of susceptibility to pathogens is an important goal of medicine and of evolutionary biology. A key first step toward understanding the genetics and evolution of any phenotypic trait is characterizing the role of mutation. However, the rate at which mutation introduces genetic variance for pathogen susceptibility in any organism is essentially unknown.

Evolution of a higher intracellular oxidizing environment in Caenorhabditis elegans under relaxed selection.

We explored the relationship between relaxed selection, oxidative stress, and spontaneous mutation in a set of mutation-accumulation (MA) lines of the nematode Caenorhabditis elegans and in their common ancestor. We measured steady-state levels of free radicals and oxidatively damaged guanosine nucleosides in the somatic tissues of five MA lines for which nuclear genome base substitution and GC-TA transversion frequencies are known. The two markers of oxidative stress are highly correlated and are elevated in the MA lines relative to the ancestor; point estimates of the per-generation rate of mutational decay (ΔM) of these measures of oxidative stress are similar to those reported for fitness-related traits.

Persisting in papyrus: size, oxidative stress, and fitness in freshwater organisms adapted to sustained hypoxia.

Aquatic hypoxia is generally viewed as stressful for aerobic organisms. However, hypoxia may also benefit organisms by decreasing cellular stress, particularly that related to free radicals. Thus, an ideal habitat may have the minimum O2 necessary to both sustain aerobic metabolism and reduce the need to scavenge free radicals and repair free radical damage.

No evidence of elevated germline mutation accumulation under oxidative stress in Caenorhabditis elegans.

Variation in rates of molecular evolution has been attributed to numerous, interrelated causes, including metabolic rate, body size, and generation time. Speculation concerning the influence of metabolic rate on rates of evolution often invokes the putative mutagenic effects of oxidative stress. To isolate the effects of oxidative stress on the germline from the effects of metabolic rate, generation time, and other factors, we allowed mutations to accumulate under relaxed selection for 125 generations in two strains of the nematode Caenorhabditis elegans, the canonical wild-type strain (N2) and a mutant strain with elevated steady-state oxidative stress (mev-1).

Rapid decline in fitness of mutation accumulation lines of gonochoristic (outcrossing) Caenorhabditis nematodes.

Evolutionary theory predicts that the strength of natural selection to reduce the mutation rate should be stronger in self-fertilizing than in outcrossing taxa. However, the relative efficacy of selection on mutation rate relative to the many other factors influencing the evolution of any species is poorly understood. To address this question, we allowed mutations to accumulate for ∼100 generations in several sets of "mutation accumulation" (MA) lines in three species of gonochoristic (dieocious) Caenorhabditis (C.

Assessment of cellular and functional biomarkers in bivalves exposed to ecologically relevant abiotic stressors.

An understanding of the complex effects of the environment on biomarkers of bivalve health is essential for aquaculturists to successfully select field culture sites and monitor bivalve health in these sites and in hatcheries. We tested several whole-organism (functional) and cellular-level biomarkers as indicators of health of the cultured, stress-tolerant northern quahog (hard clam) Mercenaria mercenaria. We performed single- and dual-stressor experiments that were consistent with available water quality data from a clam culture area on the Gulf coast of Florida.

Genetic (Co)variation for life span in rhabditid nematodes: role of mutation, selection, and history.

The evolutionary mechanisms maintaining genetic variation in life span, particularly post-reproductive life span, are poorly understood. We characterized the effects of spontaneous mutations on life span in the rhabditid nematodes Caenorhabditis elegans and C. briggsae and standing genetic variance for life span and correlation of life span with fitness in C.

Hydrogen sulfide induces oxidative damage to RNA and DNA in a sulfide-tolerant marine invertebrate.

Hydrogen sulfide acts as an environmental toxin across a range of concentrations and as a cellular signaling molecule at very low concentrations. Despite its toxicity, many animals, including the mudflat polychaete Glycera dibranchiata, are periodically or continuously exposed to sulfide in their environment. We tested the hypothesis that a broad range of ecologically relevant sulfide concentrations induces oxidative stress and oxidative damage to RNA and DNA in G.

Increased expression of stress proteins in the surf clam Donax variabilis following hydrogen sulfide exposure.

Endogenous free radical production and resulting oxidative damage may result from exposure to hypoxia, hyperoxia, or hydrogen sulfide. Previous investigations of sulfide-induced oxidative damage have produced conflicting results, perhaps because these studies utilized species presumably adapted to sulfide. We examined the effects of sulfide, hypoxia and hyperoxia on the surf clam Donax variabilis to test whether these stressors induce a cellular response to oxidative stress.