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[
WormBook,
2007]
Because of their free-living life cycle alternatives, Strongyloides and related nematode parasites may represent the best models for translating C. elegans science to the study of nematode parasitism. S. stercoralis, a significant pathogen of humans, can be maintained in laboratory dogs and gerbils. Biosafety precautions necessary for work with S. stercoralis, though unfamiliar to many C. elegans researchers, are straightforward and easily accomplished. Although specialized methods are necessary for large-scale culture of the free-living stages of S. stercoralis, small-scale cultures for experimental purposes may be undertaken using minor modifications of standard C. elegans methods. Similarly, the morphological similarities between C. elegans and the free-living stages of S. stercoralis allow investigational methods such as laser cell ablation and DNA transformation by gonadal microinjection to be easily adapted from C. elegans to S. stercoralis. Comparative studies employing these methods have yielded new insights into the neuronal control of the infective process in parasites and its similarity to regulation of dauer development in C. elegans. Furthermore, we have developed a practical method for transient transformation of S. stercoralis with vector constructs having various tissue- and cell-specific expression patterns and have assembled these into a modular vector kit for distribution to the community.
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[
1981]
A neuron can be characterized by its morphology, transmitter (s?), receptor(s) and the nature of its synaptic contacts (chemical or electrical; excitatory or inhibitory; number and distribution of synapses; identity of the cells to which it is presynaptic or postsynaptic). It is clear that according to such criteria nervous sytems consist of neurons of many distinct types. The origin of neuronal diversity is unknown. Both how such diversity is generated during development and how the relevant developmental programme is encoded in the genome remain to
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[
2020]
Onchocerciasis, also known as the African river blindness, is the second most important cause of infectious blindness worldwide after trachoma. It is caused by the filarial nematode, <i>Onchocerca volvulus</i>, and transmitted by repeated bites of the vector, female black fly of the genus <i>Simulium damnosum</i>. The vector breeds in fast-flowing and oxygen-rich rivers in affected areas with transmission and disease prevalence usually stretching along these river basins and thereby the name river blindness.[1]Aside from blindness, onchocerciasis results in a troubling chronic dermatitis.[1]
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[
WormBook,
2006]
Although several Caenorhabditis species are now studied in laboratories in great detail, the knowledge of the ecology of most Caenorhabditis species is scarce. In this chapter we present data on the habitat, animal associations, and geographical distribution of the eighteen described and five undescribed Caenorhabditis species currently known to science. The habitats of these species are very diverse, ranging from rotting cactus tissue to inflamed auditory canals of zebu cattle. Some species, including C. elegans , have only been isolated from anthropogenic habitats. Consequently, their natural habitat is unknown. All Caenorhabditis species are colonizers of nutrient- and bacteria-rich substrates and none of them is a true soil nematode. Dauer juveniles of many Caenorhabditis species were shown to be associated with terrestrial arthropods or gastropods. An association with invertebrates is also likely for the remaining species. The type of association is either phoresy (for transport to a new habitat) or necromeny (to secure the body of the associated animal as a future food source). There are also some records of Caenorhabditis species associated with vertebrates. The Caenorhabditis stem species was probably a colonizer of nutrient-rich substrates and was phoretic on arthropods. Some evolutionary trends within the taxon are discussed.
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[
Methods Cell Biol,
1995]
Genetic balancers are genetic constructs or chromosomal rearrangements that allow lethal or sterile mutations to be stably maintained in heterozygotes. In this chapter we use the term balancer primarily to refer to chromosomal duplications or rearrangements that suppress crossing over. In addition, we define lethal as any mutation that blocks survival or reproduction. Phenotypes associated with lethal mutations in Caenorhabditis elegans range from egg or larval lethality to adult sterility and maternal effect lethality, and can include conditional effects such as temperature sensitivity. The number of essential genes in C. elegans (those identified by lethal mutations) may range as high as 7000 according to genetic estimates. Thus, lethal mutations constitute a rich source of information about basic biological processes in this nematode.
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[
WormBook,
2005]
In C. elegans, the germ line is set apart from the soma early in embryogenesis. Several important themes have emerged in specifying and guiding the development of the nascent germ line. At early stages, the germline blastomeres are maintained in a transcriptionally silent state by the transcriptional repressor PIE-1 . When this silencing is lifted, it is postulated that correct patterns of germline gene expression are controlled, at least in part, by MES-mediated regulation of chromatin state. Accompanying transcriptional regulation by PIE-1 and the MES proteins, RNA metabolism in germ cells is likely to be regulated by perinuclear RNA-rich cytoplasmic granules, termed P granules. This chapter discusses the molecular nature and possible roles of these various germline regulators, and describes a recently discovered mechanism to protect somatic cells from following a germline fate.
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[
WormBook,
2005]
Cell-division control affects many aspects of development. Caenorhabditis elegans cell-cycle genes have been identified over the past decade, including at least two distinct Cyclin-Dependent Kinases (CDKs), their cyclin partners, positive and negative regulators, and downstream targets. The balance between CDK activation and inactivation determines whether cells proceed through G 1 into S phase, and from G 2 to M, through regulatory mechanisms that are conserved in more complex eukaryotes. The challenge is to expand our understanding of the basic cell cycle into a comprehensive regulatory network that incorporates environmental factors and coordinates cell division with growth, differentiation and tissue formation during development. Results from several studies indicate a critical role for CKI-1 , a CDK inhibitor of the Cip/Kip family, in the temporal control of cell division, potentially acting downstream of heterochronic genes and dauer regulatory pathways.
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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.
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[
Methods Cell Biol,
1995]
The genetics of Caenorhabditis elegans provides a convenient experimental entry point into many developmental processes and a powerful tool that can be exploited to characterize interactions among a set of genes regulating a particular pathway. Eventually, though, the study of developmental processes becomes a molecular study of gene regulation. At this level, the determination of the on/off state of a gene requires an understanding of not only its transcriptional state, but also post-transcriptional, translational, and post-translational control mechanisms. Although the vertebrate literature is rich in details of factors that influence these regulatory processes, relatively few of the factors responsible for gene expression in the nematode C. elegans have been characterized. This lag in knowledge reflects both the relatively recent arrival of C. elegans on the list of experimental systems, as well as its general unsuitability for biochemistry. There are no tissue culture cell lines established from C. elegans, and it is difficult to isolate, in large amounts, any homogeneous cell type. Moreover, the impermeable eggshell encasing the embryo and the cuticle encasing the worm make pharmacological studies in intact animals difficult and tedious. Grim as this sounds, progress has been made in C. elegans in the field of gene expression. The sensitivity of techniques has improved and the available molecular tool kit has expanded. The study of individual genes has provided descriptions of several regulatory processes, some general and some gene specific. Our current level of understanding of gene regulation is sufficient to say that C. elegans appears, in general, to be a typical eukaryote. As such, C. elegans is amenable to many of the standard analytical approaches used in other developmental systems. The purpose of this chapter is to review our current state of knowledge of transcription and translation in C. elegans (for a review
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[
WormBook,
2006]
The C. elegans genome encodes many RNA-binding proteins (RBPs) with diverse functions in development, indicative of extensive layers of post-transcriptional control of RNA metabolism. A number of C. elegans RBPs have been identified by forward or reverse genetics. They tend to display tissue-specific mutant phenotypes, which underscore their functional importance. In addition, several RBPs that bind regulatory sequences in the 3'' untranslated regions of mRNAs have been identified molecularly. Most C. elegans RBPs are conserved throughout evolution, suggesting that their study in C. elegans may uncover new conserved biological functions. In this review, we primarily discuss RBPs that are associated with well-characterized mutant phenotypes in the germ line, the early embryo, or in somatic tissues. We also discuss the identification of RNA targets of RBPs, which is an important first step to understand how an RBP controls C. elegans development. It is likely that most RBPs regulate multiple RNA targets. Once multiple RNA targets are identified, specific features that distinguish target from non-target RNAs and the type(s) of RNA metabolism that each RBP controls can be determined. Furthermore, one can determine whether the RBP regulates all targets by the same mechanism or different targets by distinct mechanisms. Such studies will provide insights into how RBPs exert coordinate control of their RNA targets, thereby affecting development in a concerted fashion.