Poole CB et al. (2007) Mol Biochem Parasitol "Subtilisin-like proteases in nematodes."

McReynolds LA, Jin J, Poole CB

[Mol Biochem Parasitol, 2007]

Cleavage by subtilisin-like proteases (subtilases) is an essential step in post-translational processing of proteins found in organisms ranging from yeast to mammals. Our knowledge of the diversity of this protease family in nematodes is aided by the rapid increase in sequence information, especially from the Brugia malayi genome project. Genetic studies of the subtilases in Caenorhabitis elegans give valuable insight into the biological function of these proteases in other nematode species. In this review, we focus on the subtilases in filarial nematodes as well as other parasitic and free-living nematodes in comparison to what is known in C. elegans. Topics to be addressed include expansion and diversity of the subtilase gene family during evolution, enhanced complexity created by alternative RNA splicing, molecular and biochemical characterization of the different subtilases and the challenges of designing subtilase-specific inhibitors for parasitic nematodes.

Felix MA et al. (2002) Hermann, Editeurs des Sciences et des Arts. Paris, France. "Caenorhabditis elegans. Un organisme modele en biologie."

Labouesse M, Segalat L, Felix MA

[Hermann, Editeurs des Sciences et des Arts. Paris, France., 2002]

L'espce Caenorhabditis elegans fut dcrite en 1900 Alger par E. Maupas, qui s'intressait son mode de reproduction hermaphrodite. Plus tard, vers le milieu du vingtime sicle, V. Nigon et ses collaboratuers Lyon tudirent les reorganizations cellulaires accompagnant la fecundation et les premiers clivages. J. Brun isola les preiers mutants morpholgiques.

Hoogeboom D et al. (2009) Biochim Biophys Acta "Should I stay or should I go: beta-catenin decides under stress."

Burgering BM, Hoogeboom D

[Biochim Biophys Acta, 2009]

Reactive oxygen species (ROS) are essential for efficient and proper execution of a large number of cellular processes including signalling induced by exogenous factors. However, ROS are highly reactive in nature and excessive or prolonged ROS formation can result in considerable damage to cellular constituents and is implicated in the onset of a large variety of diseases as well as in the process of ageing [reviewed in [1] T.M. Paravicini, R.M. Touyz, Redox signaling in hypertension, Cardiovasc. Res. 71 (2006) 247-258, [2] P. Chiarugi, From anchorage dependent proliferation to survival: lessons from redox signalling, IUBMB life 60 (2008) 301-307, [3] M. Valko, D. Leibfritz, J. Moncol, M.T. Cronin, M. Mazur, J. Telser, Free radicals and antioxidants in normal physiological functions and human disease, Int. J. Biochem. Cell Biol. 39 (2007) 44-84]. Management of ROS to prevent potential damage, yet enabling its signalling function is achieved through numerous enzyme systems e.g. peroxidases, superoxide dismutases etc. and small molecules e.g. glutathione that collectively form the cellular anti-oxidant system. The O-class of Forkhead box (FOXO) transcription factors regulates amongst others cellular resistance against oxidative stress [[4] Y. Honda, S. Honda, The daf-2 gene network for longevity regulates oxidative stress resistance and Mn-superoxide dismutase gene expression in Caenorhabditis elegans, Faseb J. 13 (1999) 1385-1393]. In turn FOXOs themselves are regulated by ROS and cellular oxidative stress results in the activation of FOXOs [[5] M.A. Essers, S. Weijzen, A.M. de Vries-Smits, I. Saarloos, N.D. de Ruiter, J.L. Bos, B.M. Burgering, FOXO transcription factor activation by oxidative stress mediated by the small GTPase Ral and JNK, EMBO J. 23 (2004) 4802-4812]. A prominent feature of ROS-induced FOXO activation is ROS-induced binding of beta-catenin to FOXO [[6] M.A. Essers, L.M. de Vries-Smits, N. Barker, P.E. Polderman, B.M. Burgering, H.C. Korswagen, Functional interaction between beta-catenin and FOXO in oxidative stress signaling, Science (New York, NY) 308 (2005) 1181-1184, [7] M. Almeida, L. Han, M. Martin-Millan, C.A. O'Brien, S.C. Manolagas, Oxidative stress antagonizes Wnt signaling in osteoblast precursors by diverting beta-catenin from T cell factor- to forkhead box O-mediated transcription, J. Biol. Chem. 282 (2007) 27298-27305, [8] D. Hoogeboom, M.A. Essers, P.E. Polderman, E. Voets, L.M. Smits, B.M. Burgering, Interaction of FOXO with beta-catenin inhibits beta-catenin/T cell factor activity, J. Biol. Chem. 283 (2008) 9224-9230]. However, ROS affect many transcriptional programs besides that of FOXOs. Here, we discuss the recent progress in our understanding as to how ROS may regulate the interplay between some of the ROS-sensitive transcription factors through diverting beta-catenin binding to these transcription factors. We propose that beta-catenin acts as a key switch between the various ROS-sensitive transcription programs.

Tobin DM et al. (2004) J Neurobiol "Invertebrate nociception: behaviors, neurons and molecules."

Tobin DM, Bargmann CI

[J Neurobiol, 2004]

Genetic analysis of nociceptive behaviors in the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster has led to the discovery of conserved sensory transduction channels and signaling molecules. These are embedded in neurons and circuits that generate responses to noxious signals. This article reviews the neurons and molecular mechanisms that underlie invertebrate nociception. We begin with the neurobiology of invertebrate nociception, and then focus on molecules with conserved functions in vertebrate nociception and sensory biology. Copyright 2004 Wiley Periodicals, Inc. J Neurobiol 61: 161-174, 2004

Godfray HCJ et al. (1991) Nature "More fecund but not so fit."

Harvey PH, Godfray HCJ

[Nature, 1991]

Populations of the soil nematode Caenorhabditis elegans normally consist almost exclusively of self-fertilizing hermaphrodites. The animal first matures about 300 sperm and then a much larger number of oocytes (eggs). Nearly every sperm is used to fertilize an egg and so the maximum fecundity is around 300. Why doesn't the nematode mature more sperm and thus increase its fecundity? In a paper in the Proceedings of the Royal Society (B246, 19-24; 1991), J. Hodgkin and T.M. Barnes provide both an elegant answer and a rare insight into the mechanistic basis of an important life-history trade-off.

Labbe JC et al. (2006) Clin Genet "New developmental insights from high-throughput biological analysis in Caenorhabditis elegans."

Labbe JC, Roy R

[Clin Genet, 2006]

Labbe J-C, Roy R. New developmental insights from high-throughput biological analysis in Caenorhabditis elegans.The use of Caenorhabditis elegans as a model system for understanding animal development and human disease has long been recognized as an efficient tool of discovery. Recent developments, particularly in our understanding of RNA-mediated interference and its ability to modify gene activity, have facilitated the use of C. elegans in determining gene function via high-throughput analysis. These new strategies have provided a framework that allows investigators to analyse gene function globally at the genomic level and will likely become a prototypic model for biological analysis in the post-genome era.

Tavernarakis NN et al. (1999) Trends in Biochemical Sciences "The SPFH domain: implicated in regulating targeted protein turnover in stomatins and other membrane-associated proteins."

Driscoll MA, Tavernarakis NN, Kyrpides NC

[Trends in Biochemical Sciences, 1999]

Stromatin, also known as band 7.2b protein, is one of the major integral membrane proteins of human erythrocytes. This protein is apparently absent in the red cell membranes of patients suffering form overhydrated hereditary stomatocytosis, a form of autosomal dominant hemolytic anemia. Although he protein is missing, no mutations have been found within the stomatin gene in patients with this condition. However, an aberrant splice mutation associated with multi-system pathology early in life suggests that the protein is crucial for development (A. Argent, J. Delaunay and G. Stewart, pers. commun.). the genome of the nematode Caenorhabditis elegans encodes nine stomatin-related genes, three of which have been genetically characterized. MEC-2 is a protein expressed predominantly in six touch-receptor neurons and plays an essential role in mechanotransduction, whereas UNC-24 is required for normal locomotion. UNC-1 also affects locomotion and is required for normal responsiveness to volatile anesthetics.

Clarke ND et al. (1998) Science "Zinc fingers in Caenorhabditis elegans: finding families and probing pathways."

Berg JM, Clarke ND

[Science, 1998]

More than 3 percent of the protein sequences inferred from the Caenorhabditis elegans genome contain sequence motifs characteristic of zinc-binding structural domains, and of these more than half are believed to be sequence-specific DNA-binding proteins. The distribution of these zinc-binding domains among the genomes of various organisms offers insights into the role of zinc-binding proteins in evolution. In addition, the complete genome sequence of C. elegans provides an opportunity to analyze, and perhaps predict, pathways of transcriptional regulation.AD - Department of Biophysics and Biophysical Chemistry, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.FAU - Clarke, N DAU - Clarke NDFAU - Berg, J MAU - Berg JMLA - engPT - Journal ArticlePT - ReviewPT - Review, TutorialCY - UNITED STATESTA - ScienceJID - 0404511RN - 0 (DNA-Binding Proteins)RN - 0 (Helminth Proteins)RN - 0 (Membrane Proteins)RN - 0 (Receptors, Cell Surface)RN - 0 (Trans-Activators)RN - 0 (Transcription Factors)RN - 0 (erythroid-like transcription factor 1)RN - 0 (tra-1 protein, Caenorhabditis elegans)SB - IM

Davidson EH et al. (1999) J Exp Zool "Themes from a NASA workshop on gene regulatory processes in development and evolution."

Davidson EH, Ruvkun GB

[J Exp Zool, 1999]

A memorable workshop, focused on causal mechanisms in metazoan evolution and sponsored by NASA, was held in early June 1998, at MBL. The workshop was organized by Mike Levine and Eric H. Davidson, and it included the PI and associates from 12 different laboratories, a total of about 30 people. Each laboratory had about two and one half hours in which to represent its recent research and cast up its current ideas for an often intense discussion. In the following we have tried to enunciate some of the major themes that emerged, and to reflect on their implications. The opinions voiced are our own. We would like to tender apologies over those contributions we have not been able to include, but this is not, strictly speaking, a meeting review. Rather we have focused on those topics that bear more directly on evolutionary mechanisms, and have therefore slighted some presentations (including some of our own), that were oriented mainly toward developmental processes. J. Exp. Zool. (Mol. Dev. Evol. ) 285:104-115, 1999.

Eckert A (2012) Int Psychogeriatr "Mitochondrial effects of Ginkgo biloba extract."

Eckert A

[Int Psychogeriatr, 2012]

Oxidative stress and mitochondrial failure promote altered protein degradation, reduced neurotransmission, synapse loss and tau/hyperphosphorylation, which are early stages in the development of Alzheimer's disease (AD). A growing volume of data confirms that Ginkgo biloba extract (GBE) reduces oxidative stress and improves mitochondrial respiration and thus may be useful in preventing or slowing down the progression of AD. Treatment of Caenorhabditis elegans with GBE- extract reduces oxidative stress and extends median lifespan compared with controls. Levels of reactive oxygen species, including the superoxide anion radical, were reduced in brains from GBE-treated mice compared with controls. In older mice, GBE resulted in a protective effect by increasing production of adenosine triphosphate in neurons. A respiratory experiment indicated that GBE was able to rescue A-induced defects in energy metabolism, with results suggesting long-term regulatory effects on mitochondria. GBE also had a selective effect on the activities of mitochondrial enzymes that assemble the electron transport system. The flavonoids, bilobalide and some of the ginkgolides (B and J) had a high protective capacity, indicating that a combination of several compounds within standardized Gingko biloba extracts contribute disproportionately for these protective effects.