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[
Cell,
2004]
Heterotrimeric G proteins are well known for their function in signal transduction downstream of seven transmembrane receptors. More recently, however, genetic analysis in C. elegans and in Drosophila has revealed a second, essential function of these molecules in positioning the mitotic spindle and attaching microtubules to the cell cortex. Five new publications in Cell (Afshar et al., 2004; Du and Macara, 2004 [this issue of Cell]; Hess et al., 2004), Developmental Cell (Martin-McCaffrey et al., 2004), and Current Biology (Couwenbergs et al., 2004) show that this function is conserved in vertebrates and-like the classical pathway- involves cycling of G proteins between GDP and GTP bound conformations.
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Journal of Gerontology,
1999]
In recent years, oxidative damage to macromolecules has gained popularity as the basis of the molecular mechanism of aging. Martin proposes oxidative damage to macromolecules as one of the major public mechanisms of aging. Interest in modifications of protein by reactive oxygen species in aging was apparently introduced by Stadtman. Although various types of oxidative modifications can occur in proteins, carbonyl residues believed to be generated by metal catalyzed reaction or otherwise introduced by lysine, arginine and/or proline residues in vivo are often used as a marker of direct or
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[
Journal of Gerontology,
1988]
Genetic approaches have been used to gain insights into many complex biological phenomena, but until recently most attempts to use genetic approaches to understand aging or senescence processes in metazoans have met with little success. The first review in this series (Martin and Tucker, 1988) surveyed model organisms used in the genetic analysis of aging; here I will review the analysis of life span and of the aging process by means of genetics. Problems inherent in the genetic analysis of aging will be reviewed first. Successful applications of genetics to the phenomena of aging will next be highlighted. Finally, I will present examples of ways in which both molecular and classical genetic approaches can be fruitfully and realistically applied to the study of the aging processes. Where applicable, misinterpretations and possible future directions will be noted.
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[
FASEB J,
2011]
In this contribution to the series of reflective essays celebrating the 25th anniversary of The FASEB Journal, our task is to assess the growth of research on the biology of aging during this period and to suggest where we might be heading during the next 25 yr. A review of the literature suggests a healthy acceleration of progress during the past decade, perhaps largely due to progress on the genetics of longevity of model organisms. Progress on the genetics of health span in these model organisms has lagged, however. Research on the genetic basis of the remarkable interspecific variations in life span has only recently begun to be seriously addressed. The spectacular advances in genomics should greatly accelerate progress. Research on environmental effects on life span and health span needs to be accelerated. Stochastic variations in gene expression in aging have only recently been addressed. These can lead to random departures from homeostasis during aging.-Martin, G. M. The biology of aging: 1985-2010 and beyond.
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Le Mentec H, Heindel JJ, Mohajer N, Podechard N, Kassotis CD, Touma C, Babin PJ, Howard S, Shree N, Martin-Chouly C, Lagadic-Gossmann D, Choudhury M, Munic Kos V, Barouki R, Bansal A, Ji Kim M, Legrand A, Vom Saal FS, Audouze K, Langouet S, Blumberg B
[
Biochem Pharmacol,
2022]
There is increasing evidence of a role for environmental contaminants in disrupting metabolic health in both humans and animals. Despite a growing need for well-understood models for evaluating adipogenic and potential obesogenic contaminants, there has been a reliance on decades-old in vitro models that have not been appropriately managed by cell line providers. There has been a quick rise in available in vitro models in the last ten years, including commercial availability of human mesenchymal stem cell and preadipocyte models; these models require more comprehensive validation but demonstrate real promise in improved translation to human metabolic health. There is also progress in developing three-dimensional and co-culture techniques that allow for the interrogation of a more physiologically relevant state. While diverse rodent models exist for evaluating putative obesogenic and/or adipogenic chemicals in a physiologically relevant context, increasing capabilities have been identified for alternative model organisms such as Drosophila, C. elegans, zebrafish, and medaka in metabolic health testing. These models have several appreciable advantages, including most notably their size, rapid development, large brood sizes, and ease of high-resolution lipid accumulation imaging throughout the organisms. They are anticipated to expand the capabilities of metabolic health research, particularly when coupled with emerging obesogen evaluation techniques as described herein.
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J Cell Biochem,
2013]
microRNA (miRNA) is a family of small, non-coding RNA first discovered as an important regulator of development in Caenorhabditis elegans (C. elegans). Numerous miRNAs have been found in C. elegans, and some of them are well conserved in many organisms. Though, the biologic function of miRNAs in C. elegans was largely unknown, more and more studies support the idea that miRNA is an important molecular for C. elegans. In this review, we revisit the research progress of miRNAs in C. elegans related with development, aging, cancer, and neurodegenerative diseases and compared the function of miRNAs between C. elegans and human.
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[
Methods Mol Biol,
2006]
The genome of the nematode Caenorhabditis elegans was the first animal genome sequenced. Subsequent sequencing of the Caenorhabditis briggsae genome enabled a comparison of the genomes of two nematode species. In this chapter, we describe the methods that we used to compare the C. elegans genome to that of C. briggsae. We discuss how these methods could be developed to compare the C. elegans and C. briggsae genomes to those of Caenorhabditis remanei, C. n. sp. represented by strains PB2801 and CB5161, among others (1), and Caenorhabditis japonica, which are currently being sequenced.
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[
Dev Dyn,
2010]
We review recent studies that have advanced our understanding of the molecular mechanisms regulating transcription in the nematode C. elegans. Topics covered include: (i) general properties of C. elegans promoters; (ii) transcription factors and transcription factor combinations involved in cell fate specification and cell differentiation; (iii) new roles for general transcription factors; (iv) nucleosome positioning in C. elegans "chromatin"; and (v) some characteristics of histone variants and histone modifications and their possible roles in controlling C. elegans transcription.
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[
Exp Neurol,
2016]
How axons repair themselves after injury is a fundamental question in neurobiology. With its conserved genome, relatively simple nervous system, and transparent body, C. elegans has recently emerged as a productive model to uncover the cellular mechanisms that regulate and execute axon regeneration. In this review, we discuss the strengths and weaknesses of the C. elegans model of regeneration. We explore the technical advances that enable the use of C. elegans for in vivo regeneration studies, review findings in C. elegans that have contributed to our understanding of the regeneration response across species, discuss the potential of C. elegans research to provide insight into mechanisms that function in the injured mammalian nervous system, and present potential future directions of axon regeneration research using C. elegans.
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[
WormBook,
2005]
C. elegans has emerged as a powerful genetic model organism in which to study synaptic function. Most synaptic proteins in the C. elegans genome are highly conserved and mutants can be readily generated by forward and reverse genetics. Most C. elegans synaptic protein mutants are viable affording an opportunity to study the functional consequences in vivo. Recent advances in electrophysiological approaches permit functional analysis of mutant synapses in situ. This has contributed to an already powerful arsenal of techniques available to study synaptic function in C. elegans. This review highlights C. elegans mutants affecting specific stages of the synaptic vesicle cycle, with emphasis on studies conducted at the neuromuscular junction.