Biological effects, translocation, and metabolism of quantum dots in the nematode Caenorhabditis elegans

Anthocyanins have been associated with several health benefits, although the responsible mechanisms are not well established yet. In the present study, an anthocyanin-rich extract from bilberry (Vaccinium myrtillus L.) was tested in order to evaluate its capacity to modulate reactive oxygen species (ROS) production and resistance to thermally induced oxidative stress, using the nematode Caenorhabditis elegans as an in vivo model. The assays were carried out with the wild-type N2 strain and the mutant strains daf-16(mu86) I and hsf-1(sy441), which were grown in the presence of two anthocyanin extract concentrations (5 and 10 μg/mL in the culture medium) and further subjected to thermal stress. The treatment with the anthocyanin extract at 5 μg/mL showed protective effects on the accumulation of ROS and increased thermal resistance in C. elegans, both in stressed and non-stressed young and aged worms. However, detrimental effects were observed in nematodes treated with 10 μg/mL, leading to a higher worm mortality rate compared to controls, which was interpreted as a hormetic response. These findings suggested that the effects of the bilberry extract on C. elegans might not rely on its direct antioxidant capacity, but other mechanisms could also be involved. Additional assays were performed in two mutant strains with loss-of-function for DAF-16 (abnormal DAuer Formation factor 16) and HSF-1 (Heat Shock Factor 1) transcription factors, which act downstream of the insulin/insulin like growth factor-1 (IGF-1) signaling pathway. The results indicated that the modulation of these factors could be behind the improvement in the resistance against thermal stress produced by bilberry anthocyanins in young individuals, whereas they do not totally explain the effects produced in worms in the post-reproductive development stage. Further experiments are needed to continue uncovering the mechanisms behind the biological effects of anthocyanins in living organisms, as well as to establish whether they fall within the hormesis concept.

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Talin requires beta-integrin, but not vinculin, for its assembly into focal adhesion-like structures in the nematode Caenorhabditis elegans.

Molecular Biology of the Cell ◽

10.1091/mbc.7.8.1181 ◽

1996 ◽

Vol 7 (8) ◽

pp. 1181-1193 ◽

Cited By ~ 49

Author(s):

G L Moulder ◽

M M Huang ◽

R H Waterston ◽

R J Barstead

Keyword(s):

Caenorhabditis Elegans ◽

Focal Adhesion ◽

Focal Adhesions ◽

The Body ◽

Nematode Caenorhabditis Elegans ◽

C Elegans ◽

Beta Integrin ◽

Cell Shapes

In cultured cells, the 230-kDa protein talin is found at discrete plasma membrane foci known as focal adhesions, sites that anchor the intracellular actin cytoskeleton to the extracellular matrix. The regulated assembly of focal adhesions influences the direction of cell migrations or the reorientation of cell shapes. Biochemical studies of talin have shown that it binds to the proteins integrin, vinculin, and actin in vitro. To understand the function of talin in vivo and to correlate its in vitro and in vivo biochemical properties, various genetic approaches have been adopted. With the intention of using genetics in the study of talin, we identified a homologue to mouse talin in a genetic model system, the nematode Caenorhabditis elegans. C. elegans talin is 39% identical and 59% similar to mouse talin. In wild-type adult C. elegans, talin colocalizes with integrin, vinculin, and alpha-actinin in the focal adhesion-like structures found in the body-wall muscle. By examining the organization of talin in two different C. elegans mutant strains that do not make either beta-integrin or vinculin, we were able to determine that talin does not require vinculin for its initial organization at the membrane, but that it depends critically on the presence of integrin for its initial assembly at membrane foci.

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Sperm Competition in the Absence of Fertilization in Caenorhabditis elegans

Genetics ◽

10.1093/genetics/152.1.201 ◽

1999 ◽

Vol 152 (1) ◽

pp. 201-208 ◽

Cited By ~ 2

Author(s):

Andrew Singson ◽

Katherine L Hill ◽

Steven W L’Hernault

Keyword(s):

Caenorhabditis Elegans ◽

Sperm Competition ◽

Sperm Function ◽

Sperm Precedence ◽

Wild Type ◽

Nematode Caenorhabditis Elegans ◽

C Elegans ◽

Normal Sperm ◽

Self Fertilization ◽

Competition Assays

Abstract Hermaphrodite self-fertilization is the primary mode of reproduction in the nematode Caenorhabditis elegans. However, when a hermaphrodite is crossed with a male, nearly all of the oocytes are fertilized by male-derived sperm. This sperm precedence during reproduction is due to the competitive superiority of male-derived sperm and results in a functional suppression of hermaphrodite self-fertility. In this study, mutant males that inseminate fertilization-defective sperm were used to reveal that sperm competition within a hermaphrodite does not require successful fertilization. However, sperm competition does require normal sperm motility. Additionally, sperm competition is not an absolute process because oocytes not fertilized by male-derived sperm can sometimes be fertilized by hermaphrodite-derived sperm. These results indicate that outcrossed progeny result from a wild-type cross because male-derived sperm are competitively superior and hermaphrodite-derived sperm become unavailable to oocytes. The sperm competition assays described in this study will be useful in further classifying the large number of currently identified mutations that alter sperm function and development in C. elegans.

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Genetic, Behavioral and Environmental Determinants of Male Longevity in Caenorhabditis elegans

Genetics ◽

10.1093/genetics/154.4.1597 ◽

2000 ◽

Vol 154 (4) ◽

pp. 1597-1610 ◽

Cited By ~ 1

Author(s):

David Gems ◽

Donald L Riddle

Keyword(s):

Caenorhabditis Elegans ◽

Life Span ◽

Wild Type ◽

Neuronal Function ◽

Nematode Caenorhabditis Elegans ◽

Wild Isolate ◽

Young Males ◽

C Elegans ◽

Single Sex ◽

Solitary Males

Abstract Males of the nematode Caenorhabditis elegans are shorter lived than hermaphrodites when maintained in single-sex groups. We observed that groups of young males form clumps and that solitary males live longer, indicating that male-male interactions reduce life span. By contrast, grouped or isolated hermaphrodites exhibited the same longevity. In one wild isolate of C. elegans, AB2, there was evidence of copulation between males. Nine uncoordinated (unc) mutations were used to block clumping behavior. These mutations had little effect on hermaphrodite life span in most cases, yet many increased male longevity even beyond that of solitary wild-type males. In one case, the neuronal function mutant unc-64(e246), hermaphrodite life span was also increased by up to 60%. The longevity of unc-4(e120), unc-13(e51), and unc-32(e189) males exceeded that of hermaphrodites by 70–120%. This difference appears to reflect a difference in sex-specific life span potential revealed in the absence of male behavior that is detrimental to survival. The greater longevity of males appears not to be affected by daf-2, but is influenced by daf-16. In the absence of male-male interactions, median (but not maximum) male life span was variable. This variability was reduced when dead bacteria were used as food. Maintenance on dead bacteria extended both male and hermaphrodite longevity.

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A genetic mapping system in Caenorhabditis elegans based on polymorphic sequence-tagged sites.

Genetics ◽

10.1093/genetics/131.3.609 ◽

1992 ◽

Vol 131 (3) ◽

pp. 609-624 ◽

Cited By ~ 13

Author(s):

B D Williams ◽

B Schrank ◽

C Huynh ◽

R Shownkeen ◽

R H Waterston

Keyword(s):

Caenorhabditis Elegans ◽

Genetic Mapping ◽

Physical Map ◽

Nematode Caenorhabditis Elegans ◽

C Elegans ◽

Sequence Tagged Sites ◽

Mapping System ◽

Polymerase Chain ◽

Tc1 Element ◽

Single Reaction

Abstract We devised an efficient genetic mapping system in the nematode Caenorhabditis elegans which is based upon the differences in number and location of the transposable element Tc1 between the Bristol and Bergerac strains. Using the nearly completed physical map of the C. elegans genome, we selected 40 widely distributed sites which contain a Tc1 element in the Bergerac strain, but not in the Bristol strain. For each site a polymerase chain reaction assay was designed that can distinguish between the Bergerac Tc1-containing site and the Bristol "empty" site. By combining appropriate assays in a single reaction, one can score multiple sites within single worms. This permits a mutation to be rapidly mapped, first to a linkage group and then to a chromosomal subregion, through analysis of only a small number of progeny from a single interstrain cross.

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Caenorhabditis elegans as an in vivo Model to Assess Amphetamine Tolerance

Brain Behavior and Evolution ◽

10.1159/000514858 ◽

2021 ◽

pp. 1-9

Author(s):

Dayana Torres Valladares ◽

Sirisha Kudumala ◽

Murad Hossain ◽

Lucia Carvelli

Keyword(s):

Caenorhabditis Elegans ◽

Molecular Mechanisms ◽

Drugs Of Abuse ◽

Genetic Model ◽

In Vivo Model ◽

C Elegans ◽

Hyperactivity Disorder ◽

In Vitro Data

Amphetamine is a potent psychostimulant also used to treat attention deficit/hyperactivity disorder and narcolepsy. In vivo and in vitro data have demonstrated that amphetamine increases the amount of extra synaptic dopamine by both inhibiting reuptake and promoting efflux of dopamine through the dopamine transporter. Previous studies have shown that chronic use of amphetamine causes tolerance to the drug. Thus, since the molecular mechanisms underlying tolerance to amphetamine are still unknown, an animal model to identify the neurochemical mechanisms associated with drug tolerance is greatly needed. Here we took advantage of a unique behavior caused by amphetamine in <i>Caenorhabditis elegans</i> to investigate whether this simple, but powerful, genetic model develops tolerance following repeated exposure to amphetamine. We found that at least 3 treatments with 0.5 mM amphetamine were necessary to see a reduction in the amphetamine-induced behavior and, thus, to promote tolerance. Moreover, we found that, after intervals of 60/90 minutes between treatments, animals were more likely to exhibit tolerance than animals that underwent 10-minute intervals between treatments. Taken together, our results show that <i>C. elegans</i> is a suitable system to study tolerance to drugs of abuse such as amphetamines.

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Specific collagens maintain the cuticle permeability barrier in Caenorhabditis elegans

Genetics ◽

10.1093/genetics/iyaa047 ◽

2021 ◽

Author(s):

Anjali Sandhu ◽

Divakar Badal ◽

Riya Sheokand ◽

Shalini Tyagi ◽

Varsha Singh

Keyword(s):

Transcription Factor ◽

Caenorhabditis Elegans ◽

Barrier Function ◽

Permeability Barrier ◽

Nematode Caenorhabditis Elegans ◽

Zinc Finger Transcription Factor ◽

Outermost Layer ◽

C Elegans ◽

Receptor Mutant ◽

Antioxidant Machinery

Abstract Collagen enriched cuticle forms the outermost layer of skin in nematode Caenorhabditis elegans. The nematode’s genome encodes 177 collagens, but little is known about their role in maintaining the structure or barrier function of the cuticle. In this study, we found six permeability determining (PD) collagens. Loss of any of these PD collagens- DPY-2, DPY-3, DPY-7, DPY-8, DPY-9, and DPY-10- led to enhanced susceptibility of nematodes to paraquat (PQ) and antihelminthic drugs levamisole and ivermectin. Upon exposure to paraquat, PD collagen mutants accumulated more PQ and incurred more damage and death despite the robust activation of antioxidant machinery. We find that BLMP-1, a zinc finger transcription factor, maintains the barrier function of the cuticle by regulating the expression of PD collagens. We show that the permeability barrier maintained by PD collagens acts in parallel to FOXO transcription factor DAF-16 to enhance survival of insulin-like receptor mutant, daf-2. In all, this study shows that PD collagens regulate cuticle permeability by maintaining the structure of C. elegans cuticle and thus provide protection against exogenous toxins.

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Microtubules and microtubule-associated proteins from the nematode Caenorhabditis elegans: periodic cross-links connect microtubules in vitro.

The Journal of Cell Biology ◽

10.1083/jcb.103.1.23 ◽

1986 ◽

Vol 103 (1) ◽

pp. 23-31 ◽

Cited By ~ 35

Author(s):

E J Aamodt ◽

J G Culotti

Keyword(s):

Caenorhabditis Elegans ◽

Apparent Molecular Weight ◽

Cross Link ◽

Nematode Caenorhabditis Elegans ◽

Microtubule Associated Proteins ◽

C Elegans ◽

Associated Proteins ◽

Cross Links ◽

The Cross

The nematode Caenorhabditis elegans should be an excellent model system in which to study the role of microtubules in mitosis, embryogenesis, morphogenesis, and nerve function. It may be studied by the use of biochemical, genetic, molecular biological, and cell biological approaches. We have purified microtubules and microtubule-associated proteins (MAPs) from C. elegans by the use of the anti-tumor drug taxol (Vallee, R. B., 1982, J. Cell Biol., 92:435-44). Approximately 0.2 mg of microtubules and 0.03 mg of MAPs were isolated from each gram of C. elegans. The C. elegans microtubules were smaller in diameter than bovine microtubules assembled in vitro in the same buffer. They contained primarily 9-11 protofilaments, while the bovine microtubules contained 13 protofilaments. The principal MAP had an apparent molecular weight of 32,000 and the minor MAPs were 30,000, 45,000, 47,000, 50,000, 57,000, and 100,000-110,000 mol wt as determined by SDS-gel electrophoresis. The microtubules were observed, by electron microscopy of negatively stained preparations, to be connected by stretches of highly periodic cross-links. The cross-links connected the adjacent protofilaments of aligned microtubules, and occurred at a frequency of one cross-link every 7.7 +/- 0.9 nm, or one cross-link per tubulin dimer along the protofilament. The cross-links were removed when the MAPs were extracted from the microtubules with 0.4 M NaCl. The cross-links then re-formed when the microtubules and the MAPs were recombined in a low salt buffer. These results strongly suggest that the cross-links are composed of MAPs.

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MPA-capped CdTe quantum dots exposure causes neurotoxic effects in nematode Caenorhabditis elegans by affecting the transporters and receptors of glutamate, serotonin and dopamine at the genetic level, or by increasing ROS, or both

Nanoscale ◽

10.1039/c5nr05914c ◽

2015 ◽

Vol 7 (48) ◽

pp. 20460-20473 ◽

Cited By ~ 21

Author(s):

Tianshu Wu ◽

Keyu He ◽

Qinglin Zhan ◽

Shengjun Ang ◽

Jiali Ying ◽

...

Keyword(s):

Quantum Dots ◽

Caenorhabditis Elegans ◽

Biomedical Applications ◽

Biological Properties ◽

Cdte Quantum Dots ◽

Nematode Caenorhabditis Elegans ◽

Neurotoxic Effects ◽

Genetic Level

As quantum dots (QDs) are widely used in biomedical applications, the number of studies focusing on their biological properties is increasing.

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lag-1, a gene required for lin-12 and glp-1 signaling in Caenorhabditis elegans, is homologous to human CBF1 and Drosophila Su(H)

Development ◽

10.1242/dev.122.5.1373 ◽

1996 ◽

Vol 122 (5) ◽

pp. 1373-1383 ◽

Cited By ~ 12

Author(s):

S. Christensen ◽

V. Kodoyianni ◽

M. Bosenberg ◽

L. Friedman ◽

J. Kimble

Keyword(s):

Caenorhabditis Elegans ◽

Binding Sites ◽

Feedback Loop ◽

Target Genes ◽

Sequence Similarity ◽

Nematode Caenorhabditis Elegans ◽

C Elegans ◽

Downstream Target ◽

Binding Factor ◽

Flanking Regions

The homologous receptors LIN-12 and GLP-1 mediate diverse cell-signaling events during development of the nematode Caenorhabditis elegans. These two receptors appear to be functionally interchangeable and have sequence similarity to Drosophila Notch. Here we focus on a molecular analysis of the lag-1 gene (lin-12 -and glp-1), which plays a central role in LIN-12 and GLP-1-mediated signal transduction. We find that the predicted LAG-1 protein is homologous to two DNA-binding proteins: human C Promoter Binding Factor (CBF1) and Drosophila Suppressor of Hairless (Su(H)). Furthermore, we show that LAG-1 binds specifically to the DNA sequence RTGGGAA, previously identified as a CBF-1/Su(H)-binding site. Finally, we report that the 5′ flanking regions and first introns of the lin-12, glp-1 and lag-1 genes are enriched for potential LAG-1-binding sites. We propose that LAG-1 is a transcriptional regulator that serves as a primary link between the LIN-12 and GLP-1 receptors and downstream target genes in C. elegans. In addition, we propose that LAG-1 may be a key component of a positive feedback loop that amplifies activity of the LIN-12/GLP-1 pathway.

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