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Neuroscience,
1980]
Genetics in the study of less complicated organisms like bacteria has been a tremendously powerful way of recognizing individual elements hidden within a process, mutationally tagging them in ways easier to recognize by the biochemist. Identifying the elements used in the construction and function of nervous systems might be easier if genetics were readily applicable. The problem has been that the larger organisms with cells most suitable for impaling with microelectrodes and for obtaining isolated tissue for biochemical studies are the organisms most cumbersome genetically. Smaller, simpler organisms which can be raised rapidly and in the myriad quantity required for genetics usually lack the favorable attributes for study of the nervous system that come with size. One notable exception to this rule is the lowly, single-celled paramecium, which combines physiological accessibility with reasonably good genetics. But otherwise, for those interested in the genetics of multicellular nervous systems, it has been a matter of catch-as-catch-can. The attention of a few scientists has come to rest on the nematode, a worm not too many steps up the evolutionary
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J Dev Biol,
2019]
Comparative developmental biology and comparative genomics are the cornerstones of evolutionary developmental biology. Decades of fruitful research using nematodes have produced detailed accounts of the developmental and genomic variation in the nematode phylum. Evolutionary developmental biologists are now utilising these data as a tool with which to interrogate the evolutionary basis for the similarities and differences observed in Nematoda. Nematodes have often seemed atypical compared to the rest of the animal kingdom-from their totally lineage-dependent mode of embryogenesis to their abandonment of key toolkit genes usually deployed by bilaterians for proper development-worms are notorious rule breakers of the bilaterian handbook. However, exploring the nature of these deviations is providing answers to some of the biggest questions about the evolution of animal development. For example, why is the evolvability of each embryonic stage not the same? Why can evolution sometimes tolerate the loss of genes involved in key developmental events? Lastly, why does natural selection act to radically diverge toolkit genes in number and sequence in certain taxa? In answering these questions, insight is not only being provided about the evolution of nematodes, but of all metazoans.
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Ageing Res Rev,
2024]
This paper addresses how long lifespan can be extended via multiple interventions, such as dietary supplements [e.g., curcumin, resveratrol, sulforaphane, complex phytochemical mixtures (e.g., Moringa, Rhodiola)], pharmaceutical agents (e.g., metformin), caloric restriction, intermittent fasting, exercise and other activities. This evaluation was framed within the context of hormesis, a biphasic dose response with specific quantitative features describing the limits of biological/phenotypic plasticity for integrative biological endpoints (e.g., cell proliferation, memory, fecundity, growth, tissue repair, stem cell population expansion/differentiation, longevity). Evaluation of several hundred lifespan extending agents using yeast, nematode (Caenorhabditis elegans), multiple insect and other invertebrate and vertebrate models (e.g., fish, rodents), revealed they responded in a manner [average (mean/median) and maximum lifespans] consistent with the quantitative features [i.e., 30-60% greater at maximum (Hormesis Rule)] of the hormetic dose response. These lifespan extension features were independent of biological model, inducing agent, endpoints measured and mechanism. These findings indicate that hormesis describes the capacity to extend life via numerous agents and activities and that the magnitude of lifespan extension is modest, in the percentage, not fold, range. These findings have important implications for human aging, genetic diseases/environmental stresses and lifespan extension, as well as public health practices and long-term societal resource planning.
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Curr Opin Neurobiol,
2012]
The simplicity and genetic tractability of the nervous system of the nematode Caenorhabditis elegans make it an attractive system in which to seek biological mechanisms of decision making. Although work in this area remains at an early stage, four basic types paradigms of behavioral choice, a simple form of decision making, have now been demonstrated in C. elegans. A recent series of pioneering studies, combining genetics and molecular biology with new techniques such as microfluidics and calcium imaging in freely moving animals, has begun to elucidate the neuronal mechanisms underlying behavioral choice. The new research has focussed on choice behaviors in the context of habitat and resource localization, for which the neuronal circuit has been identified. Three main circuit motifs for behavioral choice have been identified. One motif is based mainly on changes in the strength of synaptic connections whereas the other two motifs are based on changes in the basal activity of an interneuron and the sensory neuron to which it is electrically coupled. Peptide signaling seems to play a prominent role in all three motifs, and it may be a general rule that concentrations of various peptides encode the internal states that influence behavioral decisions in C. elegans.
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[
Annual Review of Genetics,
1991]
Cell interactions are vital to the regulation of cell division, differentiation, and pattern formation during the development of most multicellular creatures. The nematode Caenorhabditis elegans is no exception to this rule. Like other metazoans, this small worm relies heavily on cell interactions during development. With the powerful genetics of C. elegans and its relatively simple anatomy, researchers have been able to delineate the genetic mechanisms regulating cell interactions with an unparralleled degree of precision. In addition, as the analysis of cell fate regulation in C. elegans has advanced to the molecular level, it has merged to a remarkable degree with the rapidly expanding field of signal transduction biochemistry, which has been intensively studied in vertebrate cells. The conjunction of these two areas of research is certain to enhance our understanding of the mechanisms, regulation, and evolution of cell interactions during development. In this review, we emphasize those interactions in C. elegans that have been best characterized genetically. These include examples of both induction and lateral signaling. Induction occurs between separate tissues, with one tissue regulating the fate of another, whereas lateral signaling occurs within a single tissue and results in the adoption of distinct fates by cells with equivalent developmental potential. In addition to our discussion of the genetics of these better characterized interactions, we briefly mention other cell interactions and other genetic controls that promise to provide special insight into how cell interactions
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Int J Parasitol,
2000]
Onchocerca volvulus, the filarial parasite that causes onchocerciasis or river blindness, contains three distinct genomes. These include the nuclear genome, the mitochondrial genome and the genome of an intracellular endosymbiont of the genus Wolbachia. The nuclear genome is roughly 1.5x10(8) bp in size, and is arranged on four chromosome pairs. Analysis of expressed sequence tags from different life-cycle stages has resulted in the identification of transcripts from roughly 4000 O. volvulus genes. Several of these transcripts are highly abundant, including those encoding collagen and cuticular proteins. Analysis of several gene sequences from O. volvulus suggests that the nuclear genes of O. volvulus are relatively compact and are interrupted relatively frequently by small introns. The intron-exon boundaries of these genes generally follow the GU-AG rule characteristic of the splice donor and acceptors of other vertebrate organisms. The nuclear genome also contains at least one repeated sequence family of a 150 bp repeat which is arranged in tandem arrays and appears subject to concerted evolution. The mitochondrial genome of O. volvulus is remarkably compact, only 13747 bp in size. Consistent with the small size of the genome, four gene pairs overlap, eight contain no intergenic regions and the remaining gene pairs are separated by small intergenic domains ranging from 1 to 46 bp. The protein-coding genes of the O. volvulus mitochondrial genome exhibit a striking codon bias, with 15/20 amino acids having a single codon preference greater than 70%. Intraspecific variation in both the nuclear and mitochondrial genomes appears to be quite limited, consistent with the hypothesis that O. volvulus has suffered a genetic bottleneck in the recent past.