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[
Methods Cell Biol,
1995]
Behavioral plasticity is the ability of organisms to modify their behavior over time, based on their experience, and is thus critical to the survival of any organism in a changing environment. It allows organisms to adapt to new surroundings and to take better advantage of novel situational variables they may encounter. It is therefore an extremely important ability, and it has attracted much research attention in innumberable organisms and across several disciplines. Much of the research on plasticity has been characterized by an attempt to integrate information and expertise from a number of these different disciplines within selected invertebrate organisms. Researchers from a variety of fields, including psychology, physiology, biochemistry, genetics, neurobiology, and molecular biology, have been uniting in an effort to investigate "simple system" in which these approaches are being combined and focused on the general goal of elucidating the cellular, molecular, and genetic basis of behavioral plasticity. These simple system approaches have led to considerable progress in our understanding of the mechanisms underlying adaptive behaviors. The general strategy of such approaches is to try to identify the genes, molecules, channels, ion currents, cells, and neural circuits underlying some form of plasticity and then determine the precise nature of their respective roles in producing behavior...
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[
1999]
Caenorhabditis elegans is a free-living soil nematode that is commonly used as a biological model. Recently, much work has been done using the nematode as a toxicological model as well. Much of the work involving C. elegans has been performed in aquatic media, since it lives in the interstitial water of soil. However, testing in soil would be expected to more accurately reproduce the organism's normal environment and may take into consideration other factors not available in an aquatic test, i.e., toxicant availability effects due to sorption, various chemical interactions, etc. This study used a modification of a previous experimental protocol to determine 24h LC50 values for Cu in a Cecil series soil mixture, and examined the use of CuCl2 as a reference toxicant for soil toxicity testing with C. elegans. Three different methods of determining percent lethality were used, each dependent on how the number of worms missing after the recovery process was used in the lethality calculations. Only tests having >/= 80% worm recovery and >/= 90% control survival were used in determining the LC50S, by Probit analysis. The replicate LC50 values generated a control chart for each method of calculating percent lethality. The coefficient of variation (CV) for each of the three methods was </= 14%. The control charts and the protocol outlined in this study are intended to be used to assess test organism health and to monitor precision of future soil toxicity tests with C.
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[
WormBook,
2006]
Transposons are discrete segments of DNA capable of moving through the genome of their host via an RNA intermediate in the case of class I retrotransposon or via a "cut-and-paste" mechanism for class II DNA transposons. Since transposons take advantage of their host''s cellular machinery to proliferate in the genome and enter new hosts, transposable elements can be viewed as parasitic or "selfish DNA". However, transposons may have been beneficial for their hosts as genome evolution drivers, thus providing an example of molecular mutualism. Interactions between transposon and C. elegans research were undoubtedly mutualistic, leading to the advent of needed genomic tools to drive C. elegans research while providing insights into the transposition field. Tc1, the first C. elegans transposon to be identified, turned out to be the founding member of a widespread family of mobile elements: the Tc1/ mariner superfamily. The investigation into transposition regulation in C. elegans has uncovered an unforeseen link between transposition, genome surveillance and RNA interference. Conversely, transposons were utilized soon after their identification to inactivate and clone genes, providing some of the first molecular identities of C. elegans genes. Recent results suggest that transposons might provide a means to engineer site-directed mutations into the C. elegans genome. This article describes the different transposons present in the C. elegans genome with a specific emphasis on the ones that proved to be mobile under laboratory conditions. Mechanisms and control of transposition are discussed briefly. Some tools based on the use of transposons for C. elegans research are presented at the end of this review.
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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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Genetic analysis of C. elegans development has focused on developmental events that take place after hatching, during postembryonic development. After hatching with 558 cells, about 10% of these are blast cells that undergo further cell divisions (Fig. 1) to generate a total of 959 neurons, muscles, intestinal and hypodermal cells in the hermaphrodite and 1031 cells in the male. Like embryonic development (se Edgar, Chap. 19 this Vol.), the pattern of cell division and differentiation during C. elegans postembryonic development is nearly invariant and has been completely described. The cell lineage of wild-type, mutant, or laser-ablated animals can be determined by direct observation of development using Normarski optics. Because most cells during C. elegans postembryonic development generate unique patterns of descendents (though symmetries in the lineage exist), the cell lineage produced by a particular blast cell during development is a signature of that cell's identity. Any changes in cell identity, induce, for example, by laser ablation or neighboring cells or by mutation, can be recognized by a change in the lineage produced by that cell. By laser ablation, it has been shown that in many cases, that patterns of cell lineage executed by particular cells do not depend on their neighbors and instead reflect some intrinsic developmental program. On the other hand, the lineages of particular blast cells, for example, those that generate the hermaphrodite vulva, have been shown by laser ablation experiments to depend on interactions with their neighbors. Thus the pattern of cell divisions and differentiations that normally occur during C. elegans development depends on the ancestry of cells in some cases on their neighbors or positional signals in other cases. Two major goals of developmental genetic analysis in C. elegans have been to explain how genes couple cell lineage information to cell identity and to explain how genes control and mediate cell-cell interactions. As described below, this analysis has revealed molecular mechanisms for the generation of lineage asymmetry and for intercellular signaling that are general to perhaps all metazoans.
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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.