Autophagy promotes visceral aging in wild-type C. elegans

We have isolated mini-titin from the nematodes Ascaris lumbricoides and Caenorhabditis elegans under native conditions using a modification in the procedure to prepare this protein from insect muscle. The proteins have an apparent molecular weight of 600,000 and appear in oriented specimens as flexible thin rods with a length around 240–250 nm. The circular dichroism spectrum of the Ascaris protein is dominated by beta-structure. The proteins react with antibodies to insect mini-titin and also with antibodies raised against peptides contained in the sequence predicted for twitchin, the product of the Caenorhabditis elegans unc-22 gene. Antibodies to insect mini-titin decorate the body musculature as well as the pharynx of wild-type C. elegans in immunofluorescence microscopy. In the twitchin mutant E66 only the pharynx is decorated. We conclude that the mini-titins of invertebrate muscles defined earlier by ultrastructural criteria are very likely to be twitchins, i.e. molecules necessary for normal muscle contraction. We discuss the molecular properties of the proteins in the light of the sequence established for twitchin.

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Caenorhabditis elegans triple null mutant lacking UDP-N-acetyl-D-glucosamine:α-3-D-mannoside β1,2-N-acetylglucosaminyltransferase I

Biochemical Journal ◽

10.1042/bj20040793 ◽

2004 ◽

Vol 382 (3) ◽

pp. 995-1001 ◽

Cited By ~ 46

Author(s):

Shaoxian ZHU ◽

Andrew HANNEMAN ◽

Vernon N. REINHOLD ◽

Andrew M. SPENCE ◽

Harry SCHACHTER

Keyword(s):

Caenorhabditis Elegans ◽

Chromosome Number ◽

Null Mutant ◽

Wild Type ◽

Knock Out ◽

C Elegans ◽

In The Wild ◽

Wild Type Worm ◽

Type C ◽

Nematode Worm

We have previously reported, from the nematode worm Caenor-habditis elegans, three genes (gly-12, gly-13 and gly-14) encoding enzymically active UDP-N-acetyl-D-glucosamine:α-3-D-mannoside β1,2-N-acetylglucosaminyltransferase I (GnT I), an enzyme essential for hybrid, paucimannose and complex N-glycan synthesis. We now describe a worm with null mutations in all three GnT I genes, gly-14 (III);gly-12 gly-13 (X) (III and X refer to the chromosome number). The triple-knock-out (TKO) worms have a normal phenotype, although they do not express GnT I activity and do not synthesize 31 paucimannose, complex and fucosylated oligomannose N-glycans present in the wild-type worm. The TKO worm has increased amounts of non-fucosylated oligomannose N-glycan structures, a finding consistent with the site of GnT I action. Five fucosylated oligomannose N-glycan structures were observed in TKO, but not wild-type, worms, indicating the presence of unusual GnT I-independent fucosyltransferases. It is concluded that wild-type C. elegans makes a large number of GnT I-dependent N-glycans that are not essential for normal worm development under laboratory conditions. The TKO worm may be more susceptible to mutations in other genes, thereby providing an approach for the identification of genes that interact with GnT I.

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Katanin controls mitotic and meiotic spindle length

The Journal of Cell Biology ◽

10.1083/jcb.200608117 ◽

2006 ◽

Vol 175 (6) ◽

pp. 881-891 ◽

Cited By ~ 198

Author(s):

Karen McNally ◽

Anjon Audhya ◽

Karen Oegema ◽

Francis J. McNally

Keyword(s):

Chromosome Segregation ◽

Eukaryotic Cell ◽

Meiotic Spindle ◽

Mitotic Spindles ◽

Wild Type ◽

Female Meiosis ◽

C Elegans ◽

Microtubule Severing ◽

Spindle Poles ◽

Type C

Accurate control of spindle length is a conserved feature of eukaryotic cell division. Lengthening of mitotic spindles contributes to chromosome segregation and cytokinesis during mitosis in animals and fungi. In contrast, spindle shortening may contribute to conservation of egg cytoplasm during female meiosis. Katanin is a microtubule-severing enzyme that is concentrated at mitotic and meiotic spindle poles in animals. We show that inhibition of katanin slows the rate of spindle shortening in nocodazole-treated mammalian fibroblasts and in untreated Caenorhabditis elegans meiotic embryos. Wild-type C. elegans meiotic spindle shortening proceeds through an early katanin-independent phase marked by increasing microtubule density and a second, katanin-dependent phase that occurs after microtubule density stops increasing. In addition, double-mutant analysis indicated that γ-tubulin–dependent nucleation and microtubule severing may provide redundant mechanisms for increasing microtubule number during the early stages of meiotic spindle assembly.

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ACaenorhabditis elegansPheromone Antagonizes Volatile Anesthetic Action Through a Go-Coupled Pathway

Genetics ◽

10.1093/genetics/161.1.109 ◽

2002 ◽

Vol 161 (1) ◽

pp. 109-119 ◽

Cited By ~ 1

Author(s):

Bruno van Swinderen ◽

Laura B Metz ◽

Laynie D Shebester ◽

C Michael Crowder

Keyword(s):

Sensory Neurons ◽

Volatile Anesthetic ◽

Loss Of Function ◽

Wild Type ◽

C Elegans ◽

Pheromone Activity ◽

Dauer Formation ◽

Anesthetic Action ◽

Nervous System Function ◽

Type C

AbstractVolatile anesthetics (VAs) disrupt nervous system function by an ill-defined mechanism with no known specific antagonists. During the course of characterizing the response of the nematode C. elegans to VAs, we discovered that a C. elegans pheromone antagonizes the VA halothane. Acute exposure to pheromone rendered wild-type C. elegans resistant to clinical concentrations of halothane, increasing the EC50 from 0.43 ± 0.03 to 0.90 ± 0.02. C. elegans mutants that disrupt the function of sensory neurons required for the action of the previously characterized dauer pheromone blocked pheromone-induced resistance (Pir) to halothane. Pheromone preparations from loss-of-function mutants of daf-22, a gene required for dauer pheromone production, lacked the halothane-resistance activity, suggesting that dauer and Pir pheromone are identical. However, the pathways for pheromone’s effects on dauer formation and VA action were not identical. Not all mutations that alter dauer formation affected the Pir phenotype. Further, mutations in genes not known to be involved in dauer formation completely blocked Pir, including those altering signaling through the G proteins Goα and Gqα. A model in which sensory neurons transduce the pheromone activity through antagonistic Go and Gq pathways, modulating VA action against neurotransmitter release machinery, is proposed.

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Genetic Differences Affecting the Potency of Stereoisomers of Isoflurane

Anesthesiology ◽

10.1097/00000542-199608000-00021 ◽

1996 ◽

Vol 85 (2) ◽

pp. 385-392 ◽

Cited By ~ 12

Author(s):

Phil G. Morgan ◽

Marianne F. Usiak ◽

Margaret M. Sedensky

Keyword(s):

Volatile Anesthetic ◽

Genetic Differences ◽

Wild Type ◽

C Elegans ◽

Mutant Strains ◽

Anesthetic Action ◽

Type C ◽

Sites Of Action ◽

Standard Techniques

Background In previous studies, researchers demonstrated the ability of a variety of organisms and in vitro sites of anesthetic action to distinguish between stereoisomers of isoflurane or halothane. However, it was not shown whether organisms with differing sensitivities to stereoisomers of one volatile anesthetic are able to distinguish between stereoisomers of another. In this study, the responses of mutants of Caenorbabditis elegans to stereoisomers of isoflurane were determined for comparison to previous results in halothane. Methods Mutant strains of C. elegans were isolated and grown by standard techniques. The EC50s (the effective concentrations of anesthetia at which 50% of the animals are immobilized for 10 s) of stereoisomers of isoflurane and the racemate were determined in wild type and mutant strains of C. elegans. Results Wild type C. elegans and strains with high EC50S of the racemate were more sensitive to the (+) isomer of isoflurane by approximately 30%. The racemate showed a EC50s similar to the less potent isomer, the (-) form. In the strains with low EC50s, one strain showed no ability to differentiate between the stereoisomers, whereas two showed a 60% difference between the (+) and (-) forms. Conclusions The ability to distinguish between stereoisomers of isoflurane is associated with genetic loci separate from those that distinguish between stereoisomers of halothane. These results are consistent with multiple sites of action for these anesthetics.

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A cell that dies during wild-type C. elegans development can function as a neuron in a ced-3 mutant

Cell ◽

10.1016/0092-8674(87)90593-9 ◽

1987 ◽

Vol 51 (6) ◽

pp. 1071-1078 ◽

Cited By ~ 163

Author(s):

Leon Avery ◽

H.Robert Horvitz

Keyword(s):

Wild Type ◽

C Elegans ◽

A Cell ◽

Type C

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Multi-omics analysis identifies essential regulators of mitochondrial stress response in two wild-type C. elegans strains

iScience ◽

10.1016/j.isci.2022.103734 ◽

2022 ◽

pp. 103734

Author(s):

Arwen W. Gao ◽

Gaby El Alam ◽

Amélia Lalou ◽

Terytty Yang Li ◽

Marte Molenaars ◽

...

Keyword(s):

Stress Response ◽

Wild Type ◽

Mitochondrial Stress ◽

C Elegans ◽

Omics Analysis ◽

Type C

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A parthenogenetic quasi-program causes teratoma-like tumors during aging in wild-type C. elegans

npj Aging and Mechanisms of Disease ◽

10.1038/s41514-018-0025-3 ◽

2018 ◽

Vol 4 (1) ◽

Cited By ~ 13

Author(s):

Hongyuan Wang ◽

Yuan Zhao ◽

Marina Ezcurra ◽

Alexandre Benedetto ◽

Ann F. Gilliat ◽

...

Keyword(s):

Wild Type ◽

C Elegans ◽

Type C

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Early Exposure is Necessary for the Lifespan Extension Effects of Cocoa in C. elegans

Nutrition and Metabolic Insights ◽

10.1177/11786388211029443 ◽

2021 ◽

Vol 14 ◽

pp. 117863882110294

Author(s):

Mihiri Munasinghe ◽

Abdullah Almotayri ◽

Jency Thomas ◽

Deniz Heydarian ◽

Markandeya Jois

Keyword(s):

Lifespan Extension ◽

Early Exposure ◽

Mechanistic Studies ◽

Wild Type ◽

Survival Curves ◽

E Coli ◽

C Elegans ◽

Larval Stages ◽

Mutant Strains ◽

Type C

Background: We previously showed that cocoa, a rich source of polyphenols improved the age-associated health and extended the lifespan in C. elegans when supplemented starting from L1 stage. Aim: In this study, we aimed to find out the effects of timing of cocoa exposure on longevity improving effects and the mechanisms and pathways involved in lifespan extension in C. elegans. Methods: The standard E. coli OP50 diet of wild type C. elegans was supplemented with cocoa powder starting from different larval stages (L1, L2, L3, and L4) till the death, from L1 to adult day 1 and from adult day 1 till the death. For mechanistic studies, different mutant strains of C. elegans were supplemented with cocoa starting from L1 stage till the death. Survival curves were plotted, and mean lifespan was reported. Results: Cocoa exposure starting from L1 stage till the death and till adult day 1 significantly extended the lifespan of worms. However, cocoa supplementation at other larval stages as well as at adulthood could not extend the lifespan, instead the lifespan was significantly reduced. Cocoa could not extend the lifespan of daf-16, daf-2, sir-2.1, and clk-1 mutants. Conclusion: Early-start supplementation is essential for cocoa-mediated lifespan extension which is dependent on insulin/IGF-1 signaling pathway and mitochondrial respiration.

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The Effect of Mianserin on Lifespan of Caenorhabditis elegans is Abolished by Glucose

Current Aging Science ◽

10.2174/1874609813999210104203614 ◽

2021 ◽

Vol 13 ◽

Author(s):

Abdullah Almotayri ◽

Jency Thomas ◽

Mihiri Munasinghe ◽

Markandeya Jois

Keyword(s):

Caenorhabditis Elegans ◽

Scaffolding Protein ◽

Lifespan Extension ◽

Wild Type ◽

E Coli ◽

C Elegans ◽

Risk Of Death ◽

Increased Risk ◽

Antidepressant Use ◽

Extension Effect

Background: The antidepressant mianserin has been shown to extend the lifespan of Caenorhabditis elegans (C. elegans), a well-established model organism used in aging research. The extension of lifespan in C. elegans was shown to be dependent on increased expression of the scaffolding protein (ANK3/unc-44). In contrast, antidepressant use in humans is associated with an increased risk of death. The C. elegans in the laboratory are fed Escherichia coli (E. coli), a diet high in protein and low in carbohydrate, whereas a typical human diet is high in carbohydrates. We hypothesized that dietary carbohydrates might mitigate the lifespan-extension effect of mianserin. Objective: To investigate the effect of glucose added to the diet of C. elegans on the lifespan-extension effect of mianserin. Methods: Wild-type Bristol N2 and ANK3/unc-44 inactivating mutants were cultured on agar plates containing nematode growth medium and fed E. coli. Treatment groups included (C) control, (M50) 50 μM mianserin, (G) 73 mM glucose, and (M50G) 50 μM mianserin and 73 mM glucose. Lifespan was determined by monitoring the worms until they died. Statistical analysis was performed using the Kaplan-Meier version of the log-rank test. Results: Mianserin treatment resulted in a 12% increase in lifespan (P<0.05) of wild-type Bristol N2 worms but reduced lifespan by 6% in ANK3/unc-44 mutants, consistent with previous research. The addition of glucose to the diet reduced the lifespan of both strains of worms and abolished the lifespan-extension by mianserin. Conclusion: The addition of glucose to the diet of C. elegans abolishes the lifespan-extension effects of mianserin.

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