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WormBook,
2008]
The role of neuropeptides in modulating behavior is slowly being elucidated. With the sequencing of the C. elegans genome, the extent of the neuropeptide genes in C. elegans can be determined. To date, 113 neuropeptide genes encoding over 250 distinct neuropeptides have been identified. Of these, 40 genes encode insulin-like peptides, 31 genes encode FMRFamide-related peptides, and 42 genes encode non-insulin, non-FMRFamide-related neuropeptides. As in other systems, C. elegans neuropeptides are derived from precursor molecules that must be post-translationally processed to yield the active peptides. These precursor molecules contain a single peptide, multiple copies of a single peptide, multiple distinct peptides, or any combination thereof. The neuropeptide genes are expressed extensively throughout the nervous system, including in sensory, motor, and interneurons. In addition, some of the genes are also expressed in non-neuronal tissues, such as the somatic gonad, intestine, and vulval hypodermis. To address the effects of neuropeptides on C. elegans behavior, animals in which the different neuropeptide genes are inactivated or overexpressed are being isolated. In a complementary approach the receptors to which the neuropeptides bind are also being identified and examined. Among the knockout animals analyzed thus far, defects in locomotion, dauer formation, egg laying, ethanol response, and social behavior have been reported. These data suggest that neuropeptides have a modulatory role in many, if not all, behaviors in C. elegans.
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Adv Exp Med Biol,
2010]
Neuropeptides are short sequences ofamino acids that function in all multicellular organisms to communicate information between cells. The first sequence ofa neuropeptide was reported in 1970' and the number of identified neuropeptides remained relatively small until the 1990s when the DNA sequence of multiple genomes revealed treasure troves ofinformation. Byblasting away at the genome, gene families, the sizes ofwhich were previously unknown, could now be determined. This information has led to an exponential increase in the number of putative neuropeptides and their respective gene families. The molecular biology age greatly benefited the neuropeptide field in the nematode Caenorhabditis elegans. Its genome was among the first to be sequenced and this allowed us the opportunity to screen the genome for neuropeptide genes. Initially, the screeningwas slow, as the Genefinder and BLAST programs had difficulty identifying small genes and peptides. However, as the bioinformatics programs improved, the extent of the neuropeptide gene families in C. elegans gradually emerged.
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Methods Mol Biol,
2013]
The nematode Caenorhabditis elegans is an excellent model organism for studying the mechanisms -controlling cell death, including apoptosis, a cell suicide event, and necrosis, pathological cell deaths caused by environmental insults or genetic alterations. C. elegans has also been established as a model for understanding how dying cells are cleared from animal bodies. In particular, the transparent nature of worm bodies and eggshells make C. elegans particularly amenable for live-cell microscopy. Here we describe methods for identifying apoptotic and necrotic cells in living C. elegans embryos, larvae, and adults and for monitoring their clearance during development. We further discuss specific methods to distinguish engulfed from unengulfed apoptotic cells, and methods to monitor cellular and molecular events occurring during phagosome maturation. These methods are based on Differential Interference Contrast (DIC) microscopy or fluorescence microscopy using GFP-based reporters.
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[
WormBook,
2005]
Genetic suppression has provided a very powerful tool for analyzing C. elegans. Suppression experiments are facilitated by the ability to handle very large numbers of individuals and to apply powerful selections. Because the animal grows as a self-fertilizing diploid, both dominant and recessive suppressors can be recovered. Many different kinds of suppression have been reported. These are discussed by category, with examples, together with discussion of how suppressors can be used to interpret the underlying biology, and to enable further experimentation. Suppression phenomena can be divided into intragenic and extragenic classes, depending on whether the suppressor lies in the same gene as the starting mutation, or in a different gene. Intragenic types include same-site replacement, compensatory mutation, alteration in splicing, and reversion of dominant mutations by cis- knockout. Extragenic suppression can occur by a variety of informational mechanisms, such as alterations in splicing, translation or nonsense-mediated decay. In addition, extragenic suppression can occur by bypass, dosage effects, product interaction, or removal of toxic products. Within signaling pathways, suppression can occur by modulating the strength of signal transmission, or by epistatic interactions that can reveal the underlying regulatory hierarchies. In C. elegans biology, the processes of muscle development, vulva formation and sex determination have provided remarkably rich arenas for the investigation and exploitation of suppression.