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[
Cell,
1996]
The process of aging influences our poetry, our art, our lifestyle, and our happiness, yet we know surprisingly little about it. Genetics has taught us a great deal about gene regulation, development, and the cell cycle. Can it teach us how we age?
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[
Trends in Genetics,
1998]
On 1 August 1997, US Vice President Gore officially announced the creation of a new World Wide Web database which aims to provide powerful new resources to researchers investigating the molecular basis of cancer...
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[
Nature,
2003]
Studies of worms have revealed hundreds of proteins that, when mutated, extend lifespan. Can this work tell us anything about mammalian ageing? A look at the effects of one such protein on lab mice suggests that it can.
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[
Curr Opin Genet Dev,
1999]
In the past year, several new components involved in cell migration and axon guidance have been identified by genetic analysis in Caenorhabditis elegans, taking us a step closer to being able to trace the pathways which mediate these processes. The completion of the C. elegans genome sequencing project has provided us with the knowledge of the full spectrum of genes that might be involved in cell migration and axon guidance, and can facilitate the analysis of components that have been shown to be important for these processes in other systems.
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Mol Cell,
2005]
An Aurora A regulatory module has been identified in two different proteins: TPX2 in Xenopus laevis and TPXL-1 in C. elegans. The diverse roles of these two proteins in spindle assembly leave us to beckon the true C. elegans TPX2 ortholog to center stage.
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Curr Opin Cell Biol,
2001]
Both Drosophila neuroblasts and Caenorhabditis elegans zygotes use a conserved protein complex to establish cell polarity and regulate spindle orientation. Mammalian epithelia also use this complex to regulate apical/basal polarity. Recent results have allowed us to compare the mechanisms regulating asymmetric cell division in Drosophila neuroblasts and the C. elegans zygote.
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Biol Chem,
2015]
Sphingolipid signaling in Caenorhabditis elegans is vital for sensing environmental change and effecting appropriate cellular response. Many molecular components in sphingolipid intermediary metabolism are conserved throughout evolution. Here we review use of C. elegans as a model system for conducting sphingolipid-based scientific investigation, which has helped us better understand vital roles these remarkable lipids play in human metabolism and disease.
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Mech Ageing Dev,
2002]
It strikes me that among our relatively small community of gerontologists concerned with genetic approaches to our science, there is somewhat of a dichotomization. On the one hand, there are those of us, like myself, who tend to be dour ''complificationists''. Journalists talk to us, but are usually disappointed by the encounter. We are perhaps too impressed with the enormous diversity of genetic modulations of human senescence and with our interpretations of the implications of the evolutionary biological theory of senescence, namely that senescent phenotypes per se are non-adaptive, non-determinative, subject to stochastic events as well as highly polygenic modulations, with resulting wide variability in mechanisms of senescence among and within species. Quite happily, however, there are wonderful optimists among us. They seem to be convinced that there are likely to be a rather small number of major gene effects for a few major mechanisms. They include most Saccharomyces cerevisiae and Caenorhabditis elegans geneticists, some Drosophila melanogaster geneticists, and some mouse geneticists. They also include caloric restriction enthusiasts. Let''s call these colleagues ''simplificationists''. Journalists and friends generally find them to be delightful companions. Where does the truth lie? Perhaps the truth lies somewhere between these two extremes and is largely dependent upon the organisms and the range of environments being investigated.
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Nat Rev Genet,
2003]
Invaluable insights into how animals, humans included, defend themselves against infection have been provided by more than a decade of genetic studies that have used fruitflies. In the past few years, attention has also turned to another simple animal model, the nematode worm Caenorhabditis elegans. What exactly have we learned from the work in Drosophila? And will research with C. elegans teach us anything new about our response to pathogen attack?.
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Cell Res,
2012]
The amyloid precursor protein (APP) has been under intensive study in recent years, mainly due to its critical role in the pathogenesis of Alzheimer's disease (AD). -Amyloid (A) peptides generated from APP proteolytic cleavage can aggregate, leading to plaque formation in human AD brains. Point mutations of APP affecting A production are found to be causal for hereditary early onset familial AD. It is very likely that elucidating the physiological properties of APP will greatly facilitate the understanding of its role in AD pathogenesis. A number of APP loss- and gain-of-function models have been established in model organisms including Caenorhabditis elegans, Drosophila, zebrafish and mouse. These in vivo models provide us valuable insights into APP physiological functions. In addition, several knock-in mouse models expressing mutant APP at a physiological level are available to allow us to study AD pathogenesis without APP overexpression. This article will review the current physiological and pathophysiological animal models of APP.