Induced mutants in the nematode Caenorhabditis elegans are used to study genetic pathways of processes ranging from aging to behavior. The effects of such mutations are usually analyzed in a single wildtype background: N2. However, studies in other species demonstrate that the phenotype(s) of induced mutations can vary widely depending on the genetic background. Moreover, induced mutations in one genetic background do not reveal the allelic effects that segregate in natural populations and contribute to phenotypic variation. Because other wildtype Caenorhabditis spp., including C. elegans, are now available, we review how current mapping resources and methodologies within and between species support the use of Caenorhabditis spp. for studying genetic variation, with a focus on pathways associated with human disease.
Journal of Gerontology,
Vanfleteren and colleagues present an interesting example of environmental conditions altering the kinetics of survival. Most previous studies of survival in C. elegans have used abundant bacteria as a food source. Such studies have found that the Gompertz function (exponential growth in mortality rate with age) gives a relatively good fit to survival curves, but that there is some deceleration in the rate of growth of mortality later in the life span. Yulong Yang and I have completed dozens of studies of small populations of the wild-type strain, N2, as well as strains TJ401, TJ411, TJ412,and BA713 in the presence of abundant bacteria in liquid or on agar. Survival curves were better fit by Gompertz more often than by Weibull or logistic functions (unpublished observations).
Rev Environ Contam Toxicol,
Caenorhabditis elegans is a nematode of microscopic size which, due to its biological characteristics, has been used since the 1970s as a model for research in molecular biology, medicine, pharmacology, and toxicology. It was the first animal whose genome was completely sequenced and has played a key role in the understanding of apoptosis and RNA interference. The transparency of its body, short lifespan, ability to self-fertilize and ease of culture are advantages that make it ideal as a model in toxicology. Due to the fact that some of its biochemical pathways are similar to those of humans, it has been employed in research in several fields. C. elegans' use as a biological model in environmental toxicological assessments allows the determination of multiple endpoints. Some of these utilize the effects on the biological functions of the nematode and others use molecular markers. Endpoints such as lethality, growth, reproduction, and locomotion are the most studied, and usually employ the wild type Bristol N2 strain. Other endpoints use reporter genes, such as green fluorescence protein, driven by regulatory sequences from other genes related to different mechanisms of toxicity, such as heat shock, oxidative stress, CYP system, and metallothioneins among others, allowing the study of gene expression in a manner both rapid and easy. These transgenic strains of C. elegans represent a powerful tool to assess toxicity pathways for mixtures and environmental samples, and their numbers are growing in diversity and selectivity. However, other molecular biology techniques, including DNA microarrays and MicroRNAs have been explored to assess the effects of different toxicants and samples. C. elegans has allowed the assessment of neurotoxic effects for heavy metals and pesticides, among those more frequently studied, as the nematode has a very well defined nervous system. More recently, nanoparticles are emergent pollutants whose toxicity can be explored using this nematode. Overall, almost every type of known toxicant has been tested with this animal model. In the near future, the available knowledge on the life cycle of C. elegans should allow more studies on reproduction and transgenerational toxicity for newly developed chemicals and materials, facilitating their introduction in the market. The great diversity of endpoints and possibilities of this animal makes it an easy first-choice for rapid toxicity screening or to detail signaling pathways involved in mechanisms of toxicity.