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[
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.
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[
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.
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[
WormBook,
2006]
There are two sexes in C. elegans, hermaphrodite and male. While there are many sex-specific differences between males and hermaphrodites that affect most tissues, the basic body plan and many of its structures are identical. However, most structures required for mating or reproduction are sexually dimorphic and are generated by sex-specific cell lineages. Thus to understand cell fate specification in hermaphrodites, one must consider how the body plan, which is specified during embryogenesis, influences the fates individual cells. One possible mechanism may involve the asymmetric distribution of POP-1 /Tcf, the sole C. elegans Tcf homolog, to anterior-posterior sister cells. Another mechanism that functions to specify cell fates along the anterior-posterior body axis in both hermaphrodites and males are the Hox genes. Since most of the cell fate specifications that occur in hermaphrodites also occur in males, the focus of this chapter will be on those that only occur in hermaphrodites. This will include the cell fate decisions that affect the HSN neurons, ventral hypodermal P cells, lateral hypodermal cells V5 , V6 , and T ; as well as the mesodermal M, Z1 , and Z4 cells and the intestinal cells. Both cell lineage-based and cell-signaling mechanisms of cell fate specification will be discussed. Only two direct targets of the sex determination pathway that influence cell fate specification to produce hermaphrodite-specific cell fates have been identified. Thus a major challenge will be to learn additional mechanisms by which the sex determination pathway interacts with signaling pathways and other cell fate specification genes to generate hermaphrodite-specific cell fates.
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[
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.
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[
1977]
The workshop on nematodes presented current research from four laboratories on the development and physiology of C. elegans.
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[
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.
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[
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.
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[
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.
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[
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
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[
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.