scholarly journals Chemosensory signal transduction in Caenorhabditis elegans

Genetics ◽  
2021 ◽  
Author(s):  
Denise M Ferkey ◽  
Piali Sengupta ◽  
Noelle D L’Etoile

Abstract Chemosensory neurons translate perception of external chemical cues, including odorants, tastants, and pheromones, into information that drives attraction or avoidance motor programs. In the laboratory, robust behavioral assays, coupled with powerful genetic, molecular and optical tools, have made Caenorhabditis elegans an ideal experimental system in which to dissect the contributions of individual genes and neurons to ethologically relevant chemosensory behaviors. Here, we review current knowledge of the neurons, signal transduction molecules and regulatory mechanisms that underlie the response of C. elegans to chemicals, including pheromones. The majority of identified molecules and pathways share remarkable homology with sensory mechanisms in other organisms. With the development of new tools and technologies, we anticipate that continued study of chemosensory signal transduction and processing in C. elegans will yield additional new insights into the mechanisms by which this animal is able to detect and discriminate among thousands of chemical cues with a limited sensory neuron repertoire.

2002 ◽  
Vol 69 ◽  
pp. 117-134 ◽  
Author(s):  
Stuart M. Haslam ◽  
David Gems ◽  
Howard R. Morris ◽  
Anne Dell

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.


eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Lukas Landler ◽  
Simon Nimpf ◽  
Tobias Hochstoeger ◽  
Gregory C Nordmann ◽  
Artemis Papadaki-Anastasopoulou ◽  
...  

A diverse array of species on the planet employ the Earth's magnetic field as a navigational aid. As the majority of these animals are migratory, their utility to interrogate the molecular and cellular basis of the magnetic sense is limited. Vidal-Gadea and colleagues recently argued that the worm Caenorhabditis elegans possesses a magnetic sense that guides their vertical movement in soil. In making this claim, they relied on three different behavioral assays that involved magnetic stimuli. Here, we set out to replicate their results employing blinded protocols and double wrapped coils that control for heat generation. We find no evidence supporting the existence of a magnetic sense in C. elegans. We further show that the Vidal-Gadea hypothesis is problematic as the adoption of a correction angle and a fixed trajectory relative to the Earth's magnetic inclination does not necessarily result in vertical movement.


Genetics ◽  
2021 ◽  
Vol 217 (1) ◽  
Author(s):  
Chia-En Tsai ◽  
Fang-Jung Yang ◽  
Ching-Han Lee ◽  
Yen-Ping Hsueh ◽  
Cheng-Ju Kuo ◽  
...  

Abstract Infection with antibiotic-resistant bacteria is an emerging life-threatening issue worldwide. Enterohemorrhagic Escherichia coli O157: H7 (EHEC) causes hemorrhagic colitis and hemolytic uremic syndrome via contaminated food. Treatment of EHEC infection with antibiotics is contraindicated because of the risk of worsening the syndrome through the secreted toxins. Identifying the host factors involved in bacterial infection provides information about how to combat this pathogen. In our previous study, we showed that EHEC colonizes in the intestine of Caenorhabditis elegans. However, the host factors involved in EHEC colonization remain elusive. Thus, in this study, we aimed to identify the host factors involved in EHEC colonization. We conducted forward genetic screens to isolate mutants that enhanced EHEC colonization and named this phenotype enhanced intestinal colonization (Inc). Intriguingly, four mutants with the Inc phenotype showed significantly increased EHEC-resistant survival, which contrasts with our current knowledge. Genetic mapping and whole-genome sequencing (WGS) revealed that these mutants have loss-of-function mutations in unc-89. Furthermore, we showed that the tolerance of unc-89(wf132) to EHEC relied on HLH-30/TFEB activation. These findings suggest that hlh-30 plays a key role in pathogen tolerance in C. elegans.


2021 ◽  
Author(s):  
Jiseon Lim ◽  
Jun Kim ◽  
Junho Lee

Although reproductive capacity is a major factor in individual fitness, aging of the reproductive system precedes somatic aging and may reduce the total brood size. Genetic studies have led to the development of a body of evolutionary theory in the nematode Caenorhabditis elegans, but these studies did not take into account current knowledge about the natural history of C. elegans. To enhance our understanding of reproductive aging in C. elegans, we measured and compared two reproductive aging-related traitsthe number of progeny and the X-chromosome nondisjunction rateof 96 wild strains during early, late and total reproductive periods. We found that the two traits exhibited natural phenotypic variation, with few outliers, and that the brood size and the X-chromosome nondisjunction rate were not genetically correlated. Contrary to a previous hypothesis, that reproductive aging contributes to the generation of an optimal total number of offspring, we found that the total brood size did not converge to an optimal value, and early brood size was more constant than total brood size among wild strains. We speculate that reproductive aging is a by-product of a rapid increase in the initial population size, which might be related to the boom-and-bust lifestyle of C. elegans. We also identified loci and candidate genetic variants significantly associated with X-chromosome nondisjunction rate in the late and total reproductive periods. Our results provide an insight into reproductive aging in wild C. elegans strains.


2021 ◽  
Author(s):  
Rachael J Chandler ◽  
Susanna Cogo ◽  
Patrick A Lewis ◽  
Eva Kevei

For decades, Parkinson’s disease (PD) cases have been genetically categorised into familial, when caused by mutations in single genes with a clear inheritance pattern in affected families, or idiopathic, in the absence of an evident monogenic determinant. Recently, genome-wide association studies (GWAS) have revealed how common genetic variability can explain up to 36% of PD heritability and that PD manifestation is often determined by multiple variants at different genetic loci. Thus, one of the current challenges in PD research stands in modelling the complex genetic architecture of this condition and translating this into functional studies. Caenorhabditis elegans provide a profound advantage as a reductionist, economical model for PD research, with a short lifecycle, straightforward genome engineering and high conservation of PD relevant neural, cellular and molecular pathways. Functional models of PD genes utilising C. elegans, show many phenotypes recapitulating pathologies observed in PD. When contrasted with mammalian in vivo and in vitro models, these are frequently validated, suggesting relevance of C. elegans in the development of novel PD functional models. This review will discuss how the nematode C. elegans PD models have contributed to the uncovering of molecular and cellular mechanisms of disease, with a focus on the genes most commonly found as causative in familial PD and risk factors in idiopathic PD. Specifically, we will examine the current knowledge on a central player in both familial and idiopathic PD, Leucine-rich repeat kinase 2 (LRRK2) and how it connects to multiple PD associated GWAS candidates and Mendelian disease-causing genes.


eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Andres Vidal-Gadea ◽  
Chance Bainbridge ◽  
Ben Clites ◽  
Bridgitte E Palacios ◽  
Layla Bakhtiari ◽  
...  

Many animals can orient using the earth’s magnetic field. In a recent study, we performed three distinct behavioral assays providing evidence that the nematode Caenorhabditis elegans orients to earth-strength magnetic fields (<xref ref-type="bibr" rid="bib28">Vidal-Gadea et al., 2015</xref>). A new study by Landler et al. suggests that C. elegans does not orient to magnetic fields (<xref ref-type="bibr" rid="bib10">Landler et al., 2018</xref>). They also raise conceptual issues that cast doubt on our study. Here, we explain how they appear to have missed positive results in part by omitting controls and running assays longer than prescribed, so that worms switched their preferred migratory direction within single tests. We also highlight differences in experimental methods and interpretations that may explain our different results and conclusions. Together, these findings provide guidance on how to achieve robust magnetotaxis and reinforce our original finding that C. elegans is a suitable model system to study magnetoreception.


2010 ◽  
Vol 26 (4) ◽  
pp. 249-256 ◽  
Author(s):  
Cai Kezhou ◽  
Ren Chong ◽  
Yu Zengliang

Many investigations have shown that nickel exposure can induce micronuclei generation, inhibit DNA repair and induce cell apoptosis, both in cells and tissues. However, there is a lack of appropriate in vivo animal models to study the underlying mechanisms of nickel-induced apoptosis. The model organism, Caenorhabditis elegans, has been shown to be a good model for investigating many biological processes. In the present study, we detected 0.01 mM nickel induced significantly germline cell apoptosis after treatment for 12 hours, which demonstrated that C. elegans could be a mammalian in vivo substitute model to study the mechanisms of apoptosis. Then gene knockout C. elegans strains were utilized to investigate the relationship between nickel-induced apoptosis and relevant signal pathways, which were involved in DNA damage and repair, apoptosis regulation and damage signal transduction. The results presented here demonstrated that nickel-induced apoptosis was independent of the DNA damage response gene, such as hus-1, p53/cep-1 and egl-1. The loss-of-function of the genes that related to Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinases (MAPK) signaling cascades suppressed nickel-induced germline apoptosis, while ERK signaling cascades have no effects on the nickel-induced germline apoptosis.


2018 ◽  
Author(s):  
M. Dal Bello ◽  
A. Pérez-Escudero ◽  
F. C. Schroeder ◽  
J. Gore

AbstractDespite the ubiquity and importance of chemical signaling, we have only limited insight about the role of learning in the response to pheromones. Here, we demonstrate that responses to pheromones can be reprogrammed through associative learning. In particular, we show that attraction to ascaroside pheromones in the model nematode Caenorhabditis elegans can be reversed by training the animals to associate either a pheromone blend or single synthetic ascarosides with the lack of food. This behavioral plasticity alters worm preference for pheromones following consumption of a food patch, possibly improving foraging in natural environments. By bridging the gap between the current knowledge on the chemical language and the learning abilities of C. elegans, we provide insight on the possible links between learning and chemical signaling in animals.


2017 ◽  
Vol 114 (9) ◽  
pp. 2289-2294 ◽  
Author(s):  
Shashi Thutupalli ◽  
Sravanti Uppaluri ◽  
George W. A. Constable ◽  
Simon A. Levin ◽  
Howard A. Stone ◽  
...  

The ecological and evolutionary dynamics of populations are shaped by the strategies they use to produce and use resources. However, our understanding of the interplay between the genetic, behavioral, and environmental factors driving these strategies is limited. Here, we report on a Caenorhabditis elegans–Escherichia coli (worm–bacteria) experimental system in which the worm-foraging behavior leads to a redistribution of the bacterial food source, resulting in a growth advantage for both organisms, similar to that achieved via farming. We show experimentally and theoretically that the increased resource growth represents a public good that can benefit all other consumers, regardless of whether or not they are producers. Mutant worms that cannot farm bacteria benefit from farming by other worms in direct proportion to the fraction of farmers in the worm population. The farming behavior can therefore be exploited if it is associated with either energetic or survival costs. However, when the individuals compete for resources with their own type, these costs can result in an increased population density. Altogether, our findings reveal a previously unrecognized mechanism of public good production resulting from the foraging behavior of C. elegans, which has important population-level consequences. This powerful system may provide broad insight into exploration–exploitation tradeoffs, the resultant ecoevolutionary dynamics, and the underlying genetic and neurobehavioral driving forces of multispecies interactions.


2021 ◽  
Vol 15 ◽  
Author(s):  
Iris Marchal ◽  
Baris Tursun

Cell fate conversion by the forced overexpression of transcription factors (TFs) is a process known as reprogramming. It leads to de-differentiation or trans-differentiation of mature cells, which could then be used for regenerative medicine applications to replenish patients suffering from, e.g., neurodegenerative diseases, with healthy neurons. However, TF-induced reprogramming is often restricted due to cell fate safeguarding mechanisms, which require a better understanding to increase reprogramming efficiency and achieve higher fidelity. The germline of the nematode Caenorhabditis elegans has been a powerful model to investigate the impediments of generating neurons from germ cells by reprogramming. A number of conserved factors have been identified that act as a barrier for TF-induced direct reprogramming of germ cells to neurons. In this review, we will first summarize our current knowledge regarding cell fate safeguarding mechanisms in the germline. Then, we will focus on the molecular mechanisms underlying neuronal induction from germ cells upon TF-mediated reprogramming. We will shortly discuss the specific characteristics that might make germ cells especially fit to change cellular fate and become neurons. For future perspectives, we will look at the potential of C. elegans research in advancing our knowledge of the mechanisms that regulate cellular identity, and what implications this has for therapeutic approaches such as regenerative medicine.


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