scholarly journals Caenorhabditis elegans Gastrulation: A Model for Understanding How Cells Polarize, Change Shape, and Journey Toward the Center of an Embryo

Genetics ◽  
2020 ◽  
Vol 214 (2) ◽  
pp. 265-277
Author(s):  
Bob Goldstein ◽  
Jeremy Nance
Keyword(s):  
Caenorhabditis Elegans ◽  
Early Stage ◽  
Future Prospects ◽  
Animal Cells ◽  
Apical Constriction ◽  
C Elegans ◽  
Cell Internalization ◽  
Cell Shapes ◽  
The Rich ◽  
Interior Cell

Gastrulation is fundamental to the development of multicellular animals. Along with neurulation, gastrulation is one of the major processes of morphogenesis in which cells or whole tissues move from the surface of an embryo to its interior. Cell internalization mechanisms that have been discovered to date in Caenorhabditis elegans gastrulation bear some similarity to internalization mechanisms of other systems including Drosophila, Xenopus, and mouse, suggesting that ancient and conserved mechanisms internalize cells in diverse organisms. C. elegans gastrulation occurs at an early stage, beginning when the embryo is composed of just 26 cells, suggesting some promise for connecting the rich array of developmental mechanisms that establish polarity and pattern in embryos to the force-producing mechanisms that change cell shapes and move cells interiorly. Here, we review our current understanding of C. elegans gastrulation mechanisms. We address how cells determine which direction is the interior and polarize with respect to that direction, how cells change shape by apical constriction and internalize, and how the embryo specifies which cells will internalize and when. We summarize future prospects for using this system to discover some of the general principles by which animal cells change shape and internalize during development.

scholarly journals Inducible Systemic RNA Silencing in Caenorhabditis elegans

2003 ◽  
Vol 14 (7) ◽  
pp. 2972-2983 ◽  
Author(s):  
Lisa Timmons ◽  
Hiroaki Tabara ◽  
Craig C. Mello ◽  
Andrew Z. Fire
Keyword(s):  
Rna Interference ◽  
Caenorhabditis Elegans ◽  
Rna Silencing ◽  
Molecular Mechanisms ◽  
Normal Animal ◽  
Cell Types ◽  
Animal Cells ◽  
Tissue Specific ◽  
C Elegans ◽  
Systemic Rna

Introduction of double-stranded RNA (dsRNA) can elicit a gene-specific RNA interference response in a variety of organisms and cell types. In many cases, this response has a systemic character in that silencing of gene expression is observed in cells distal from the site of dsRNA delivery. The molecular mechanisms underlying the mobile nature of RNA silencing are unknown. For example, although cellular entry of dsRNA is possible, cellular exit of dsRNA from normal animal cells has not been directly observed. We provide evidence that transgenic strains of Caenorhabditis elegans transcribing dsRNA from a tissue-specific promoter do not exhibit comprehensive systemic RNA interference phenotypes. In these same animals, modifications of environmental conditions can result in more robust systemic RNA silencing. Additionally, we find that genetic mutations can influence the systemic character of RNA silencing in C. elegans and can separate mechanisms underlying systemic RNA silencing into tissue-specific components. These data suggest that trafficking of RNA silencing signals in C. elegans is regulated by specific physiological and genetic factors.

scholarly journals Intracellular organelles mediate cytoplasmic pulling force for centrosome centration in the Caenorhabditis elegans early embryo

2010 ◽  
Vol 108 (1) ◽  
pp. 137-142 ◽  
Author(s):  
Kenji Kimura ◽  
Akatsuki Kimura
Keyword(s):  
Caenorhabditis Elegans ◽  
Mammalian Cells ◽  
Cytoplasmic Dynein ◽  
Early Embryo ◽  
Organelle Transport ◽  
Animal Cells ◽  
C Elegans ◽  
Cell Functions ◽  
Intracellular Organelles ◽  
Pulling Force

The centrosome is generally maintained at the center of the cell. In animal cells, centrosome centration is powered by the pulling force of microtubules, which is dependent on cytoplasmic dynein. However, it is unclear how dynein brings the centrosome to the cell center, i.e., which structure inside the cell functions as a substrate to anchor dynein. Here, we provide evidence that a population of dynein, which is located on intracellular organelles and is responsible for organelle transport toward the centrosome, generates the force required for centrosome centration in Caenorhabditis elegans embryos. By using the database of full-genome RNAi in C. elegans, we identified dyrb-1, a dynein light chain subunit, as a potential subunit involved in dynein anchoring for centrosome centration. DYRB-1 is required for organelle movement toward the minus end of the microtubules. The temporal correlation between centrosome centration and the net movement of organelle transport was found to be significant. Centrosome centration was impaired when Rab7 and RILP, which mediate the association between organelles and dynein in mammalian cells, were knocked down. These results indicate that minus end-directed transport of intracellular organelles along the microtubules is required for centrosome centration in C. elegans embryos. On the basis of this finding, we propose a model in which the reaction forces of organelle transport generated along microtubules act as a driving force that pulls the centrosomes toward the cell center. This is the first model, to our knowledge, providing a mechanical basis for cytoplasmic pulling force for centrosome centration.

scholarly journals A deletion polymorphism in the Caenorhabditis elegans RIG-I homolog disables viral RNA dicing and antiviral immunity

eLife ◽  
2013 ◽  
Vol 2 ◽  
Author(s):  
Alyson Ashe ◽  
Tony Bélicard ◽  
Jérémie Le Pen ◽  
Peter Sarkies ◽  
Lise Frézal ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Genome Wide Association Study ◽  
Rna Virus ◽  
Rnai Pathway ◽  
Animal Cells ◽  
C Elegans ◽  
Base Pair Deletion ◽  
A Genome ◽  
Positive Strand Rna ◽  
Viral Recognition

RNA interference defends against viral infection in plant and animal cells. The nematode Caenorhabditis elegans and its natural pathogen, the positive-strand RNA virus Orsay, have recently emerged as a new animal model of host-virus interaction. Using a genome-wide association study in C. elegans wild populations and quantitative trait locus mapping, we identify a 159 base-pair deletion in the conserved drh-1 gene (encoding a RIG-I-like helicase) as a major determinant of viral sensitivity. We show that DRH-1 is required for the initiation of an antiviral RNAi pathway and the generation of virus-derived siRNAs (viRNAs). In mammals, RIG-I-domain containing proteins trigger an interferon-based innate immunity pathway in response to RNA virus infection. Our work in C. elegans demonstrates that the RIG-I domain has an ancient role in viral recognition. We propose that RIG-I acts as modular viral recognition factor that couples viral recognition to different effector pathways including RNAi and interferon responses.

TRPM channel function in Caenorhabditis elegans

2007 ◽  
Vol 35 (1) ◽  
pp. 129-132 ◽  
Author(s):  
H.A. Baylis ◽  
K. Goyal
Keyword(s):  
Caenorhabditis Elegans ◽  
Mammalian Cells ◽  
Transient Receptor Potential ◽  
Early Stage ◽  
Animal Experiments ◽  
Receptor Potential ◽  
Transient Receptor Potential Channels ◽  
Growth Defect ◽  
C Elegans

The nematode Caenorhabditis elegans contains over 20 genes for TRP (transient receptor potential) channels which include members of all of the subclasses identified in mammalian cells. These proteins include three members of the TRPM (TRP melastatin) family: gon-2 (abnormal gonad development), gtl-1 (gon-2-like 1) and gtl-2. Although studies of these genes are at an early stage, we are beginning to understand their functions in the life of C. elegans. Mutations in gon-2 have defective gonad formation because of failures in the cell division of the somatic gonad precursor cells. gon-2 and gtl-1 are both expressed in the intestine of the animal. Experiments on gon-2,gtl-1 double mutants show that they have a severe growth defect that is ameliorated by the addition of high levels of Mg2+ to the growth medium. gon-2,gtl-1 double mutants have defective magnesium homoeostasis and also have altered sensitivity to toxic levels of Ni2+. Furthermore gon-2 mutants have reduced levels of IORCa (outwardly rectifying calcium current) in the intestinal cells. Thus these two channels appear to play an important role in cation homoeostasis in C. elegans. In addition, perturbing the function of gon-2 and gtl-1 disrupts the ultradian defecation rhythm in C. elegans, suggesting that these channels play an important role in regulating this calcium-dependent rhythmic process. The tractability of C. elegans as an experimental animal and its amenability to techniques such as RNAi (RNA interference) and in vivo imaging make it an excellent system for an integrative analysis of TRPM function.

scholarly journals Natural variation in the roles of C. elegans autophagy components during microsporidia infection

2018 ◽  
Author(s):  
Keir M. Balla ◽  
Vladimir Lažetić ◽  
Emily Troemel
Keyword(s):  
Genetic Variation ◽  
Caenorhabditis Elegans ◽  
Natural Variation ◽  
Early Stage ◽  
Laboratory Strain ◽  
Host Strain ◽  
Standard Laboratory ◽  
Natural Genetic Variation ◽  
C Elegans ◽  
Natural Variant

AbstractNatural genetic variation can determine the outcome of an infection, and often reflects the co-evolutionary battle between hosts and pathogens. We previously found that a natural variant of the nematode Caenorhabditis elegans from Hawaii (HW) has increased resistance against natural microsporidian pathogens in the Nematocida genus, when compared to the standard laboratory strain of N2. In particular, HW animals can clear infection, while N2 animals cannot. In addition, HW animals have lower levels of intracellular colonization of Nematocida compared to N2. Here we investigate how this natural variation in resistance relates to autophagy. We found that there is much better targeting of autophagy-related machinery to parasites under conditions where they are cleared. In particular, ubiquitin targeting to Nematocida cells correlates very well with their subsequent clearance in terms of timing, host strain and age, as well as Nematocida species. Furthermore, clearance correlates with targeting of the LGG-2/LC3 autophagy protein to parasite cells, with HW animals having much more efficient targeting of LGG-2 to parasite cells than N2 animals. Surprisingly, however, we found that lgg-2 is not required to clear infection. Instead we found that loss of lgg-2 leads to increased intracellular colonization in the HW background, although interestingly, it does not affect colonization in the N2 background. Altogether our results suggest that there is natural genetic variation in an lgg-2-dependent process that regulates intracellular levels of microsporidia at a very early stage of infection prior to clearance.

scholarly journals RACK-1 Directs Dynactin-dependent RAB-11 Endosomal Recycling during Mitosis in Caenorhabditis elegans

2009 ◽  
Vol 20 (6) ◽  
pp. 1629-1638 ◽  
Author(s):  
Erkang Ai ◽  
Daniel S. Poole ◽  
Ahna R. Skop
Keyword(s):  
Cell Cycle ◽  
Caenorhabditis Elegans ◽  
Membrane Trafficking ◽  
Animal Cells ◽  
Recycling Endosomes ◽  
C Elegans ◽  
Astral Microtubule ◽  
Endosomal Recycling ◽  
Chromosome Separation ◽  
Dynactin Complex

Membrane trafficking pathways are necessary for the addition and removal of membrane during cytokinesis. In animal cells, recycling endosomes act as a major source of the additional membranes during furrow progression and abscission. However, the mechanisms and factors that regulate recycling endosomes during the cell cycle remain poorly understood. Here, we show that the Caenorhabditis elegans Receptor of Activated C Kinase 1 (RACK-1) is required for cytokinesis, germline membrane organization, and the recruitment of RAB-11–labeled recycling endosomes to the pericentrosomal region and spindle. RACK-1 is also required for proper chromosome separation and astral microtubule length. RACK-1 localizes to the centrosomes, kinetochores, the midbody, and nuclear envelopes during the cell cycle. We found that RACK-1 directly binds to DNC-2, the C. elegans p50/dynamitin subunit of the dynactin complex. Last, RACK-1 may facilitate the sequestration of recycling endosomes by targeting DNC-2 to centrosomes and the spindle. Our findings suggest a mechanism by which RACK-1 directs the dynactin-dependent redistribution of recycling endosomes during the cell cycle, thus ensuring proper membrane trafficking events during cytokinesis.

scholarly journals A Caenorhabditis elegans behavioral assay distinguishes early stage prostate cancer patient urine from controls

Biology Open ◽  
2021 ◽  
Vol 10 (3) ◽  
Author(s):  
Morgan Thompson ◽  
Noemi Sarabia Feria ◽  
Ally Yoshioka ◽  
Eugene Tu ◽  
Fehmi Civitci ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Caenorhabditis Elegans ◽  
Early Stage ◽  
False Positive Rate ◽  
Specific Antigen ◽  
Dependent Manner ◽  
C Elegans ◽  
Non Invasive ◽  
Volatile Organic ◽  
Positive Rate

ABSTRACT Current methods for non-invasive prostate cancer (PrCa) detection have a high false-positive rate and often result in unnecessary biopsies. Previous work has suggested that urinary volatile organic compound (VOC) biomarkers may be able to distinguish PrCa cases from benign disease. The behavior of the nematode Caenorhabditis elegans has been proposed as a tool to take advantage of these potential VOC profiles. To test the ability of C. elegans Bristol N2 to distinguish PrCa cases from controls, we performed chemotaxis assays using human urine samples collected from men screened for PrCa. Behavioral response of nematodes towards diluted urine from PrCa cases was compared to response to samples from cancer-free controls. Overall, we observed a significant attraction of young adult-stage C. elegans nematodes to 1:100 diluted urine from confirmed PrCa cases and repulsion of C. elegans to urine from controls. When C. elegans chemotaxis index was considered alongside prostate-specific antigen levels for distinguishing cancer from cancer-free controls, the accuracy of patient classification was 81%. We also observed behavioral attraction of C. elegans to two previously reported VOCs to be increased in PrCa patient urine. We conclude nematode behavior distinguishes PrCa case urine from controls in a dilution-dependent manner.

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

1996 ◽  
Vol 7 (8) ◽  
pp. 1181-1193 ◽  
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.

The glycomes of Caenorhabditis elegans and other model organisms

2002 ◽  
Vol 69 ◽  
pp. 117-134 ◽  
Author(s):  
Stuart M. Haslam ◽  
David Gems ◽  
Howard R. Morris ◽  
Anne Dell
Keyword(s):  
Caenorhabditis Elegans ◽  
Current Knowledge ◽  
Structural Data ◽  
Model Organisms ◽  
Entire Genome ◽  
C Elegans ◽  
The Face ◽  
Area Of Concern ◽  
Nematode Worm

There is no doubt that the immense amount of information that is being generated by the initial sequencing and secondary interrogation of various genomes will change the face of glycobiological research. However, a major area of concern is that detailed structural knowledge of the ultimate products of genes that are identified as being involved in glycoconjugate biosynthesis is still limited. This is illustrated clearly by the nematode worm Caenorhabditis elegans, which was the first multicellular organism to have its entire genome sequenced. To date, only limited structural data on the glycosylated molecules of this organism have been reported. Our laboratory is addressing this problem by performing detailed MS structural characterization of the N-linked glycans of C. elegans; high-mannose structures dominate, with only minor amounts of complex-type structures. Novel, highly fucosylated truncated structures are also present which are difucosylated on the proximal N-acetylglucosamine of the chitobiose core as well as containing unusual Fucα1–2Gal1–2Man as peripheral structures. The implications of these results in terms of the identification of ligands for genomically predicted lectins and potential glycosyltransferases are discussed in this chapter. Current knowledge on the glycomes of other model organisms such as Dictyostelium discoideum, Saccharomyces cerevisiae and Drosophila melanogaster is also discussed briefly.

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

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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