Hsu PC et al. (2012) Environ Toxicol Chem "Quantum dot nanoparticles affect the reproductive system of Caenorhabditis elegans."

Al-Salim N, Hsu PC, Hurst MR, O'Callaghan M

[Environ Toxicol Chem, 2012]

Quantum dots (QDs) are an increasingly important class of nanoparticle, but little ecotoxicological data for QDs has been published to date. The effects of mercaptosuccinic acid (MSA)-capped QDs (QDs-MSA) and equivalent concentrations of cadmium (Cd) from cadmium chloride on growth and reproduction of the nematode Caenorhabditis elegans (Rhabditidae) were assessed in laboratory experiments. Growth from larvae to adults of C. elegans was unaffected by exposure to 1M fluorescent QDs-MSA, but adults produced more embryos and laid them prematurely. Furthermore, C. elegans exposed to QDs-MSA (1M) showed a high percentage of embryo mortality (19.2+/-0.5, p<0.001, percentage+/-standard deviation) compared with unexposed nematodes (11.6+/-0.4). An egg-laying defect phenotype was also observed at high frequency in response to 1M QDs-MSA exposure (38.3+/-3.6%, p<0.01; control 10.0+/-2.2%). This resulted in a reduced mean life span (20.5+/-1.1 d, p<0.05) compared with the control (24.6+/-1.0 d). Cadmium also caused reduced life span in C. elegans, but a low incidence of egg-laying defects was observed, suggesting that Cd and QDs-MSA affected C. elegans by different mechanisms. Furthermore, egg-laying defects caused by QDs-MSA responded to the addition of the anticonvulsant ethosuximide and to a lesser extent to the neurotransmitter serotonin, suggesting that QDs-MSA might have disrupted motor neurons during the reproduction process.

Ge YL et al. (2002) Anticancer Res "Effects of adenoviral gene transfer of C. elegans n-3 fatty acid desaturase on the lipid profile and growth of human breast cancer cells."

Kang ZB, Chen Z, Leaf A, Kang JX, Cluette-Brown J, Laposata M, Ge YL

[Anticancer Res, 2002]

Background: Current evidence from both experimental and human studies indicates that omega-6 polyunsaturated fatty acids (n-6 PUFAs) promote breast tumor development, whereas long-chain n-3 polyunsaturated fatty acids (n-3 PUFAs) exert suppressive effects. The ratio of n-6 to n-3 fatty acids appears to be an important factor in controlling tumor development. Human cells usually have a very high n-6/n-3 fatty acid ratio because they cannot convert n-6 PUFAs to n-3 PUFAs due to lack of an n-3 desaturase found in C. elegans. Materials and Methods: Adenoviral strategies were used to introduce the C. elegans fat-1 gene encoding an n-3 fatty acid desaturase into human breast cancer cells followed by examination of the n-6/n-3 fatty acid ratio and growth of the cells. Results: Infection of MCF-7 cells with an adenovirus carrying the fat-1 gene resulted in a high expression of the n-3 fatty acid desaturase. Lipid analysis indicated a remarkable increase in the levels of n-3 PUFAs accompanied with a large decrease in the contents of n-6 PUFAs, leading to a change of the n-6/n-3 ratio from 12.0 to 0.8. Accordingly, production of the eicosanoids derived from n-6 PUFA was reduced significantly in cells expressing the fat-1 gene. Importantly, the gene transfer induced mass cell death and inhibited cell proliferation. Conclusion: The gene transfer of the n-3 fatty acid desaturase, as a novel approach, can effectively modify the n-6/n-3 fatty acid ratio of human tumor cells and provide an anticancer effect, without the need of exogenous n-3 PUFA supplementation. These data also increase the understanding of the effects of n-3 fatty acids and the n-6/n-3 ratio on cancer prevention and treatment.

Warren CE et al. (2000) Glycobiology "Caenorhabditis elegans gly-1, a core 2/I N-acetylglucosaminyltransferase homologue, is a glucosyltransferase."

Partridge EA, Krizus A, Warren CE, Dennis JW

[Glycobiology, 2000]

We recently reported the initial characterisation of a family of 6 C. elegans genes that were homologous to mammalian core 2 N-acetylglucosaminyltransferases (Warren et al, 2001).

Seo J et al. (2005) Arch Environ Contam Toxicol "Biodegradation of the insecticide N,N-diethyl-m-toluamide by fungi: identification and toxicity of metabolites."

Kim SD, Cha CJ, Hur HG, Lee YG, Seo J, Ahn JH

[Arch Environ Contam Toxicol, 2005]

Fungi (Cunninghamella elegans ATCC 9245, Mucor ramannianus R-56, Aspergillus niger VKMF-1119, and Phanerochaete chrysosporium BKMF-1767) were tested to elucidate the biologic fate of the topical insect repellent N,N-diethyl-m-toluamide (DEET). The elution profile obtained from analysis by high-pressure liquid chromatography equipped with a reverse-phase C-18 column, showed that three peaks occurred after incubation of C. elegans, with which 1 mM DEET was combined as a final concentration. The peaks were not detected in the control experiments with either DEET alone or tested fungus alone. The metabolites produced by C. elegans exhibited a molecular mass of 207 with a fragment ion (m/z) at 135, a molecular mass of 179 with an m/z at 135, and a molecular mass of 163 with an m/z at 119, all of which correspond to N,N-diethyl-m-toluamide-N-oxide, N-ethyl-m-toluamide-N-oxide, and N-ethyl-m-toluamide, respectively. M. ramannianus R-56 also produced N, N-diethyl-m-toluamide-N-oxide and N-ethyl-m-toluamide but did not produce N-ethyl-m-toluamide-N-oxide. For the biologic toxicity test with DEET and its metabolites, the freshwater zooplankton Daphnia magna was used. The biologic sensitivity in decreasing order was DEET > N-ethyl-m-toluamide > N,N-diethyl-m-toluamide-N-oxide. Although DEET and its fungal metabolites showed relatively low mortality compared with other insecticides, the toxicity was increased at longer exposure periods. These are the first reports of the metabolism of DEET by fungi and of the biologic toxicity of DEET and its fungal metabolites to the freshwater zooplankton D. magna.

Kang ZB et al. (2001) Proc Natl Acad Sci U S A "Adenoviral gene transfer of Caenorhabditis elegans n--3 fatty acid desaturase optimizes fatty acid composition in mammalian cells."

Leaf A, Laposata M, Kang ZB, Kang JX, Chen Z, Ge Y, Cluette-Brown J

[Proc Natl Acad Sci U S A, 2001]

Omega-3 polyunsaturated fatty acids (PUFAs) are essential components required for normal cellular function and have been shown to exert many preventive and therapeutic actions. The amount of n-3 PUFAs is insufficient in most Western people, whereas the level of n-6 PUFAs is relatively too high, with an n-6/n-3 ratio of >18. These two classes of PUFAs are metabolically and functionally distinct and often have important opposing physiological functions; their balance is important for homeostasis and normal development. Elevating tissue concentrations of n-3 PUFAs in mammals relies on chronic dietary intake of fat rich in n-3 PUFAs, because mammalian cells lack enzymatic activities necessary either to synthesize the precursor of n-3 PUFAs or to convert n-6 to n-3 PUFAs. Here we report that adenovirus-mediated introduction of the Caenorhabditis elegans fat-1 gene encoding an n-3 fatty acid desaturase into mammalian cells can quickly and effectively elevate the cellular n - 3 PUFA contents and dramatically balance the ratio of n-6/n-3 PUFAs, Heterologous expression of the fat-1 gene in rat cardiac myocytes rendered cells capable of converting various n-6 PUFAs to the corresponding n-3 PUFAs, and changed the n-6/n-3 ratio from about 15:1 to 1:1. In addition, an eicosanoid derived from n-6 PUFA (i.e., arachidonic acid) was reduced significantly in the transgenic cells. This study demonstrates an effective approach to modifying fatty acid composition of mammalian cells and also provides a basis for potential applications of this gene transfer in experimental and clinical settings.

De Stasio E et al. (1994) Worm Breeder's Gazette "Mutagenesis of C. elegans Using N-ethyl-N-nitrosourea."

De Stasio E, Stanislaus D, Lephoto C

[Worm Breeder's Gazette, 1994]

Mutagenesis of C. elegans using N-ethyl-N-nitrosourea Elizabeth De Stasio, Dinesh Stanislaus and Catherine Lephoto. Department of Biology, Lawrence University, Appleton, Wl 54911

Kang JX et al. (2004) Nature "Transgenic mice: fat-1 mice convert n-6 to n-3 fatty acids."

Kang JX, Wang J, Kang ZB, Wu L

[Nature, 2004]

Mammals cannot naturally produce omega-3 (n-3) fatty acids--beneficial nutrients found mainly in fish oil--from the more abundant omega-6 (n-6) fatty acids and so they must rely on a dietary supply. Here we show that mice engineered to carry a fat-1 gene from the roundworm Caenorhabditis elegans can add a double bond into an unsaturated fatty-acid hydrocarbon chain and convert n-6 to n-3 fatty acids. This results in an abundance of n-3 and a reduction in n-6 fatty acids in the organs and tissues of these mice, in the absence of dietary n-3. As well as presenting an opportunity to investigate the roles played by n-3 fatty acids in the body, our discovery indicates that this technology might be adapted to enrich n-3 fatty acids in animal products such as meat, milk and eggs.

Kang JX (2007) Prostaglandins Leukot Essent Fatty Acids "Fat-1 transgenic mice: a new model for omega-3 research."

Kang JX

[Prostaglandins Leukot Essent Fatty Acids, 2007]

An appropriate animal model that can eliminate confounding factors of diet would be very helpful for evaluation of the health effects of nutrients such as n-3 fatty acids. We recently generated a fat-1 transgenic mouse expressing the Caenorhabditis elegans fat-1 gene encoding an n-3 fatty acid desaturase that converts n-6 to n-3 fatty acids (which is absent in mammals). The fat-1 transgenic mice are capable of producing n-3 fatty acids from the n-6 type, leading to abundant n-3 fatty acids with reduced levels of n-6 fatty acids in their organs and tissues, without the need of a dietary n-3 supply. Feeding an identical diet (high in n-6) to the transgenic and wild-type littermates can produce different fatty acid profiles in these animals. Thus, this model allows well-controlled studies to be performed, without the interference of the potential confounding factors of diet. The transgenic mice are now being used widely and are emerging as a new tool for studying the benefits of n-3 fatty acids and the molecular mechanisms of their action.

Vincenz L et al. (2014) Cell "Sugarcoating ER Stress."

Vincenz L, Hartl FU

[Cell, 2014]

The hexosamine biosynthetic pathway (HBP) generates metabolites for protein N- and O-glycosylation. Wang et al. and Denzel et al. report a hitherto unknown link between the HBP and stress in the endoplasmic reticulum. These studies establish the HBP as a critical component of the cellular machinery of protein homeostasis.

ZHANG, Gaotian et al. (2015) International Worm Meeting "Characterization of nematode-infecting microsporidia and natural variation in sensitivity of Caenorhabditis nematodes to microsporidia."

Zhang, Gaotian, Felix, Marie-Anne

[International Worm Meeting, 2015]

The microsporidian Nematocida parisii is the first characterized intracellular pathogen of Caenorhabditis elegans; and a second Nematocida species, called N. sp. 1, was also reported from an Indian C. briggsae isolate (Troemel et al. 2008). In our lab we further established a collection of wild rhabditid nematodes suspected with microsporidian infection. Here, we characterize molecularly these wild microsporidia and study their specificity of infection.First, the potentially infected rhabditid isolates were characterized using newly designed PCR primers specific for 18S and beta-tubulin genes of microsporidia. In addition to C. elegans, we found wild C. briggsae and Oscheius tipulae as natural hosts for N. parisii; in addition to C. briggsae, we found C. elegans and C. remanei as natural hosts of N. sp. 1. We further found three new microsporidian species. Two of them are close to the Nematocida species in microsporidian clade II and preliminarily named N.-like sp. 2 and N.-like sp. 3. The third species (or group of species), infecting Oscheius, is very distant, and found in microsporidian clade IV, that includes most human pathogens. They are closest to Orthosomella operophterae (with 18S), and thus preliminarily named Orthosomella-like spp.. Phylogenetic analyses with the 18S and beta-tubulin genes provide the same relationships of Nematocida spp. and the three putative new microsporidia species. Co-infections of two microsporidian species occurr in two wild O. tipulae strains, of which one infected with N. parisii and O.-like spp., the other infected with N. sp. 1 and O.-like spp. (confirmed by specific FISH probes).Secondly, two transgenic C. elegans strains ERT54 jyIs8[C17H1.6p::gfp; myo-2p::mCherry] and ERT72 jyIs15[F26F2.1p::gfp; myo-2::mCherry], which express a constitutive fluorescent Cherry marker and will induce GFP upon infection with N. parisii (Bakowski et al. 2014), were used in infection tests. Our results show that N. parisii, N. sp. 1, N.-like sp. 2 and N.-like sp. 3 can infect ERT54 and ERT72, forming meronts and spores; N. sp. 1 does not induce the GFP reporter (or only rarely), while the other three induce it consistently, suggesting that C. elegans has a different transcriptional response to the infection of N. sp. 1 than to other Nematocida spp. (see also abstract of Luallen et al.). The results also showed that O.-like spp. could not infect the two transgenic C. elegans strains (nor induce the GFP signals).