-
[
1987]
Since the last review in this series [Johnson, 1985], many papers have appeared dealing directly with the aging process in both Caenorhabditis elegans and Turbatrix aceti. We will review this work and also briefly review other areas of C. elegans research that may impact on the study of aging. C. elegans has become a major biological model; four "News" articles in Science [Lewin, 1984a,b; Marx, 1984a,b] and inclusion as one of three developmental genetics models in a recent text [Wilkins, 1986] indicate its importance. Recent work has verified earlier results and has advanced progress toward new goals, such as routine molecular cloning. The aging studies reviewed here, together with new findings from other areas of C. elegans research, lay the groundwork for rapid advances in our understanding of aging in nematodes. Several areas of research in C. elegans have been reviewed recently: the genetic approach to understanding the cell lineage [Sternberg and Horvitz, 1984] and a brief summary of cell lineage mutants [Hedgecock, 1985]. The specification of neuronal development and neural connectivity has been a continuing theme in C. elegans research and reviews of these areas have also appeared [Chalfie, 1984; White, 1985]. A major genetic advance is the development of reliable, if not routine, mosaic analysis [Herman, 1984; Herman and Kari, 1985], which is useful for the genetic analysis of tissue-limited gene expression. Hodgkin [1985] reviews studies on a series of mutants involved in the specification of sex. These include her mutations that cause XO worms (normally males) to develop as hermaphrodites and tra mutations that change XX hermaphrodites into phenotypic males. The work on the structure and development of nematode muscle has been summarized by Waterston and Francis [1985]. A comprehensive review of aging research, containing useful reference material on potential biomarkers, has appeared [Johnson and Simpson, 1985], as well as a review including
-
[
WormBook,
2005]
C. elegans has emerged as a powerful genetic model organism in which to study synaptic function. Most synaptic proteins in the C. elegans genome are highly conserved and mutants can be readily generated by forward and reverse genetics. Most C. elegans synaptic protein mutants are viable affording an opportunity to study the functional consequences in vivo. Recent advances in electrophysiological approaches permit functional analysis of mutant synapses in situ. This has contributed to an already powerful arsenal of techniques available to study synaptic function in C. elegans. This review highlights C. elegans mutants affecting specific stages of the synaptic vesicle cycle, with emphasis on studies conducted at the neuromuscular junction.
-
[
WormBook,
2005]
C. elegans presents a low level of molecular diversity, which may be explained by its selfing mode of reproduction. Recent work on the genetic structure of natural populations of C. elegans indeed suggests a low level of outcrossing, and little geographic differentiation because of migration. The level and pattern of molecular diversity among wild isolates of C. elegans are compared with those found after accumulation of spontaneous mutations in the laboratory. The last part of the chapter reviews phenotypic differences among wild isolates of C. elegans.
-
[
WormBook,
2005]
This chapter reviews analytical tools currently in use for protein classification, and gives an overview of the C. elegans proteome. Computational analysis of proteins relies heavily on hidden Markov models of protein families. Proteins can also be classified by predicted secondary or tertiary structures, hydrophobic profiles, compositional biases, or size ranges. Strictly orthologous protein families remain difficult to identify, except by skilled human labor. The InterPro and NCBI KOG classifications encompass 79% of C. elegans protein-coding genes; in both classifications, a small number of protein families account for a disproportionately large number of genes. C. elegans protein-coding genes include at least ~12,000 orthologs of C. briggsae genes, and at least ~4,400 orthologs of non-nematode eukaryotic genes. Some metazoan proteins conserved in other nematodes are absent from C. elegans. Conversely, 9% of C. elegans protein-coding genes are conserved among all metazoa or eukaryotes, yet have no known functions.
-
[
1977]
The workshop on nematodes presented current research from four laboratories on the development and physiology of C. elegans.
-
[
WormBook,
2007]
The soil nematode Caenorhabditis briggsae is an attractive model system for studying evolution of both animal development and behavior. Being a close relative of C. elegans, C. briggsae is frequently used in comparative studies to infer species-specific function of the orthologous genes and also for studying the dynamics of chromosome evolution. The genome sequence of C. briggsae is valuable in reverse genetics and genome-wide comparative studies. This review discusses resources and tools, which are currently available, to facilitate study of C. briggsae in order to unravel mechanisms of gene function that confer morphological and behavioral diversity.
-
[
WormBook,
2005]
A wide variety of bacterial pathogens, as well as several fungi, kill C. elegans or produce non-lethal disease symptoms. This allows the nematode to be used as a simple, tractable model host for infectious disease. Human pathogens that affect C. elegans include Gram-negative bacteria of genera Burkholderia, Pseudomonas, Salmonella, Serratia and Yersinia; Gram-positive bacteria Enterococcus, Staphylococcus and Streptococcus; and the fungus Cryptococcus neoformans. Microbes that are not pathogenic to mammals, such as the insect pathogen Bacillus thuringiensis and the nematode-specific Microbacterium nematophilum, are also studied with C. elegans. Many of the pathogens investigated colonize the C. elegans intestine, and pathology is usually quantified as decreased lifespan of the nematode. A few microbes adhere to the nematode cuticle, while others produce toxins that kill C. elegans without a requirement for whole, live pathogen cells to contact the worm. The rapid growth and short generation time of C. elegans permit extensive screens for mutant pathogens with diminished killing, and some of the factors identified in these screens have been shown to play roles in mammalian infections. Genetic screens for toxin-resistant C. elegans mutants have identified host pathways exploited by bacterial toxins.
-
[
WormBook,
2007]
As in all living organisms, survival in C. elegans requires adequate management of energy supplies. Genetic screens have revealed that C. elegans fat regulation involves a complex network of genes with known or likely functions in food sensation, neuroendocrine signaling, uptake, transport, storage and utilization of fats. Core fat and sugar metabolic pathways are conserved in C. elegans. Flux through these pathways is modulated by cellular energy sensors that operate via transcriptional and translational regulatory mechanisms. In turn, neuroendocrine mechanisms couple sensory and metabolic pathways while neuromodulatory pathways influence both metabolic and food seeking/consumption pathways. The shared ancestry of C. elegans and mammalian fat regulatory pathways extends to developmental programs that underlie fat storage capacity, despite lack of dedicated adipocytes, and genes whose human homologs are implicated in obesity. This suggests that many of the newly identified C. elegans fat regulatory pathways play similar roles in mammals. C. elegans is ideally suited for the integrated study of mechanisms that operate in multiple tissues and elicit feedback responses that affect processes as diverse as metabolism and behavior.
-
[
1987]
Current knowledge of sterol biochemistry and physiology in nematodes is reviewed. Nematodes possess a nutritional requirement for sterol because they lack the capacity for de novo sterol biosynthesis. The free-living nematode Caenorhabditis elegans has recently been used as a model organism for investigation of nematode sterol metabolism. C. elegans is capable of removal of the C-24 alkyl substituent of plant sterols such as sitosterol and also possesses the remarkable ability to attach a methyl group at C-4 on the sterol nucleus. An azasteroid and several long-chain alkyl amines disrupt the phytosterol dealkylation pathway in C. elegans by inhibiting its *24-sterol reductase. These compounds inhibit growth and reproduction in certain parasitic nematodes and provide model compounds for development of novel nematode control
-
[
WormBook,
2005]
Gastrulation is the process by which the germ layers become positioned in an embryo. C. elegans gastrulation serves as a model for studying the molecular mechanisms of diverse cellular and developmental phenomena, including morphogenesis, cell polarization, cell-cell signaling, actomyosin contraction and cell-cell adhesion. One distinct advantage of studying these phenomena in C. elegans is that genetic tools can be combined with high resolution live cell imaging and direct manipulations of the cells involved. Here we review what is known to date about the cellular and molecular mechanisms that function in C. elegans gastrulation.