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eLS.,
2013]
In the past few years, an increasing number of draft genome sequences of multiple free-living and parasitic nematodes have been published. Although nematode genomes vary in size within an order of magnitude, compared with mammalian genomes, they are all very small. Nevertheless, nematodes possess only marginally fewer genes than mammals do. Nematode genomes are very compact and therefore form a highly attractive system for comparative studies of genome structure and evolution. Strikingly, approximately one-third of the genes in every sequenced nematode genome has no recognisable homologues outside their genus. One observes high rates of gene losses and gains, among them numerous examples of gene acquisition by horizontal gene transfer. Not only does the gene for parasitism not exist, but also there appear to be no common genomic characteristics of parasitic nematode genomes which would distinguish them from genomes of free-living nematodes.
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Trends Glycosci Glycotechnol,
2009]
At the initial stage of cellular degradation of chondroitin sulfate/dermatan sulfate, an endo-type hydrolase is thought to degrade the long chain polysaccharides. Thus far, no endoglycosidases that are specific for chondroitin sulfate/dermatan sulfate have been reported; however, hyaluronan-degrading enzymes, hyaluronidases, are considered responsible. The nematode, Caenorhabditis elegans, is an ideal model for studies in a wide range of fundamental biological disciplines. Studies using the nematode have elucidated the biosynthetic mechanisms and functions of glycosaminoglycans. However, the catabolic pathways for glycosaminoglycans in C. elegans have not been investigated. Since C. elegans contains nonsulfated chondroitin but no hyaluronan, it is an ideal system for studying the hyaluronidase-independent catabolic mechanism of chondroitin/chondroitin sulfate. We have identified a chondroitin-specific endo-type hydrolase in C. elegans for the first time. The discovery of this enzyme suggests the presence of chondroitin sulfate/dermatan sulfate-specific endoglycosidases in mammalian systems.
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J Am Soc Nephrol,
2005]
The nematode Caenorhabditis elegans has no kidney per se, yet "the worm" has proved to be an excellent model to study renal-related issues, including tubulogenesis of the excretory canal, membrane transport and ion channel function, and human genetic diseases including autosomal dominant polycystic kidney disease (ADPKD). The goal of this review is to explain how C. elegans has provided insight into cilia development, cilia function, and human cystic kidney diseases.
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Acta Leiden,
1990]
Ivermectin, a recently developed macrocyclic lactone with broad antiparasitic activity, has been shown by a series of clinical trials to be safe and effective in the treatment of human infection with Onchocerca volvulus. Although it is rapidly microfilaricidal, it does not cause a severe reaction as is seen with diethylcarbamazine treatment. In patients with onchocerciasis, a single oral dose of ivermectin (150 micrograms/Kg) repeated once a year leads to a marked reduction in skin microfilaria counts and ocular involvement, although ivermectin has no known long-lasting effects on the adult worms. With treatment there is no significant exacerbation of either anterior or posterior segment eye disease even in those with severe ocular disease. Treatment leads to a marked and prolonged improvement in ocular status. Because of its safety and efficacy, ivermectin can be used on a mass scale and promises to revolutionize the treatment of onchocerciasis.
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Trends in Cell Biology,
1996]
Keeling and Logsdon propose that the y-like sequences from Caenorhabditis elegans and Saccharomyces cerevisiae are bona fide y-tubulins that have undergone rapid evolutionary divergence. Indeed, genetic and localization studies with the yeast epsilon-tubulin (encoded by the TUB4 gene) reveal striking similarities to the bona fide y-tubulins, whereas there is no apparent human analogue to the C. elegans delta-tubulin among the 60 available human y-tubulin expressed-sequence tags. (ESTs).
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Methods Cell Biol,
2011]
Although the general events surrounding fertilization in many species are well described, the molecular underpinnings of fertilization are still poorly understood. Caenorhabditis elegans has emerged as a powerful model system for addressing the molecular and cell biological mechanism of fertilization. A primary advantage is the ability to isolate and propagate mutants that effect gametes and no other cells. This chapter provides conceptual guidelines for the identification, maintenance, and experimental approaches for the study fertility mutants.
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Rev Latinoam Microbiol
]
Onchocerciasis is one of the major causes of blindness in the World, with about 17.7 million infected, particularly in West Africa. In Mexico, onchocerciasis is also present and has been subjected to control since 1923. The standard diagnosis of onchocerciasis is by the detection of microfilariae by skin biopsy and transmission is evaluated by detection of Onchocerca volvulus larvae in the vector. Classically, this was carried out by manual dissection of Simuliumn ochraceun s.l. However, with the use of ivermectin, a drug that kills microfilariae but not the adult worms, the skin biopsy is becoming no longer useful for detecting microfilariae levels and due to the reduced transmission, fly dissection is no longer viable. The subject of this paper is to present the immunological and molecular techniques developed to supersede the skin biopsy and fly dissection, and their diagnostic ability to assess the impact of multiple bi-annual mass ivermectin treatments on O. volvulus transmission in Mexico.
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Neurosci Biobehav Rev,
1996]
The early embryo orients to the antero-posterior axis and differentiates along this, and the dorso-ventral and lateral axes. From Drosophila melanogaster, detailed knowledge has accrued of how segmentation and dorso-ventral differentiation proceed, and of their genic control, mostly by selector and homeobox (Hox) genes. The study of the control of lateral differentiation, instead, has been largely neglected. Yet handed asymmetry (the "obvious" asymmetries of, for example, heart, lung, anatomical features of the nervous system, etc.) is basic and, possibly, universal. In the mouse, two genes control this: the iv gene which, when mutated, leads to random, in the place of biased, asymmetry and so to random situs inversus viscerum: and the inv mutation which, by contrast, results in 100% situs inversus. Both mutants act as autosomal recessives. Human situs inversus is heterogeneous and may be akin to that produced by the murine iv gene. In spite of situs inversus, there is no shift of hand preference; but there is no information on other lateralization, e.g. of language or of dermatoglyphic patterns. Handed asymmetry is known in Drosophila, but there is no information on its control. In the experimental nematode, Caenorhabditis elegans, asymmetry arises when differently programmed cells arrange themselves to the two body sides, and is present already at the six-cell stage; and even the major sensory neurons chains along the body axis are distributed unequally on the two sides of the worm. Experimentally, by embryonic micro-manipulation or the use of chemical mutagens, the normal and invariate direction of handed asymmetry can be reversed.
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Trends in Genetics,
2005]
Eleven of the twelve recognized wingless (Wnt) subfamilies are represented in the sea anemone Nematostelia vectensis, indicating that this developmentally important gene family was already fully diversified in the common ancestor of ''''higher'''' animals. In deuterostomes, although duplications have occurred, no novel subfamilies of Wnts have evolved. By contrast, the protostomes Drosophila and Caenorhabditis have lost half of the ancestral Writs. This pattern - loss of genes from an ancestrally complex state - might be more important in animal evolution than previously recognized.
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WormBook,
2013]
Transforming Growth Factor- (TGF-) superfamily ligands regulate many aspects of cell identity, function, and survival in multicellular animals. Genes encoding five TGF- family members are present in the genome of C. elegans. Two of the ligands, DBL-1 and DAF-7, signal through a canonical receptor-Smad signaling pathway; while a third ligand, UNC-129, interacts with a noncanonical signaling pathway. No function has yet been associated with the remaining two ligands. Here we summarize these signaling pathways and their biological functions.