Journal articles: 'Nervous system Caenorhabditis elegans'

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Mclntire, Steven L., Erik Jorgensen, Joshua Kaplan, and H. Robert Horvitz. "The GABAergic nervous system of Caenorhabditis elegans." Nature 364, no. 6435 (1993): 337–41. http://dx.doi.org/10.1038/364337a0.

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Meng, Lingfeng, Liang Chen, Zhaoyong Li, Zheng-Xing Wu, and Ge Shan. "Roles of MicroRNAs in the Caenorhabditis elegans Nervous System." Journal of Genetics and Genomics 40, no. 9 (2013): 445–52. http://dx.doi.org/10.1016/j.jgg.2013.07.002.

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Singhvi, Aakanksha, and Shai Shaham. "Glia-Neuron Interactions in Caenorhabditis elegans." Annual Review of Neuroscience 42, no. 1 (2019): 149–68. http://dx.doi.org/10.1146/annurev-neuro-070918-050314.

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Glia are abundant components of animal nervous systems. Recognized 170 years ago, concerted attempts to understand these cells began only recently. From these investigations glia, once considered passive filler material in the brain, have emerged as active players in neuron development and activity. Glia are essential for nervous system function, and their disruption leads to disease. The nematode Caenorhabditis elegans possesses glial types similar to vertebrate glia, based on molecular, morphological, and functional criteria, and has become a powerful model in which to study glia and their neuronal interactions. Facile genetic and transgenic methods in this animal allow the discovery of genes required for glial functions, and effects of glia at single synapses can be monitored by tracking neuron shape, physiology, or animal behavior. Here, we review recent progress in understanding glia-neuron interactions in C. elegans. We highlight similarities with glia in other animals, and suggest conserved emerging principles of glial function.

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Heiman, Maxwell G., and Shai Shaham. "Ancestral roles of glia suggested by the nervous system of Caenorhabditis elegans." Neuron Glia Biology 3, no. 1 (2007): 55–61. http://dx.doi.org/10.1017/s1740925x07000609.

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AbstractThe nematode Caenorhabditis elegans has a simple nervous system with glia restricted primarily to sensory organs. Some of the activities that would be provided by glia in the mammalian nervous system are either absent or provided by non-glial cell types in C. elegans, with only a select set of mammalian glial activities being similarly provided by specialized glial cells in this animal. These observations suggest that ancestral roles of glia may be to modulate neuronal morphology and neuronal sensitivity in sensory organs.

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Pan, Raj Kumar, Nivedita Chatterjee, and Sitabhra Sinha. "Mesoscopic Organization Reveals the Constraints Governing Caenorhabditis elegans Nervous System." PLoS ONE 5, no. 2 (2010): e9240. http://dx.doi.org/10.1371/journal.pone.0009240.

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Ndegwa, Sarah, and Bernard D. Lemire. "Caenorhabditis elegans development requires mitochondrial function in the nervous system." Biochemical and Biophysical Research Communications 319, no. 4 (2004): 1307–13. http://dx.doi.org/10.1016/j.bbrc.2004.05.108.

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Shaham, Shai. "Glia–neuron interactions in the nervous system of Caenorhabditis elegans." Current Opinion in Neurobiology 16, no. 5 (2006): 522–28. http://dx.doi.org/10.1016/j.conb.2006.08.001.

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Metaxakis, Athanasios, Dionysia Petratou, and Nektarios Tavernarakis. "Multimodal sensory processing in Caenorhabditis elegans." Open Biology 8, no. 6 (2018): 180049. http://dx.doi.org/10.1098/rsob.180049.

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Multisensory integration is a mechanism that allows organisms to simultaneously sense and understand external stimuli from different modalities. These distinct signals are transduced into neuronal signals that converge into decision-making neuronal entities. Such decision-making centres receive information through neuromodulators regarding the organism's physiological state and accordingly trigger behavioural responses. Despite the importance of multisensory integration for efficient functioning of the nervous system, and also the implication of dysfunctional multisensory integration in the aetiology of neuropsychiatric disease, little is known about the relative molecular mechanisms. Caenorhabditis elegans is an appropriate model system to study such mechanisms and elucidate the molecular ways through which organisms understand external environments in an accurate and coherent fashion.

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Avery, L. "The genetics of feeding in Caenorhabditis elegans." Genetics 133, no. 4 (1993): 897–917. http://dx.doi.org/10.1093/genetics/133.4.897.

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Abstract The pharynx of Caenorhabditis elegans is a nearly self-contained neuromuscular organ responsible for feeding. To identify genes involved in the development or function of the excitable cells of the pharynx, I screened for worms with visible defects in pharyngeal feeding behavior. Fifty-two mutations identified 35 genes, at least 22 previously unknown. The genes broke down into three broad classes: 2 pha genes, mutations in which caused defects in the shape of the pharynx, 7 phm genes, mutations in which caused defects in the contractile structures of the pharyngeal muscle, and 26 eat genes, mutants in which had abnormal pharyngeal muscle motions, but had normally shaped and normally birefringent pharynxes capable of vigorous contraction. Although the Eat phenotypes were diverse, most resembled those caused by defects in the pharyngeal nervous system. For some of the eat genes there is direct evidence from previous genetic mosaic and pharmacological studies that they do in fact affect nervous system. In eat-5 mutants the motions of the different parts of the pharynx were poorly synchronized. eat-6 and eat-12 mutants failed to relax their pharyngeal muscles properly. These pharyngeal motion defects are most easily explained as resulting from abnormal electrical excitability of the pharyngeal muscle membrane.

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Alkema, Mark J., Melissa Hunter-Ensor, Niels Ringstad, and H. Robert Horvitz. "Tyramine Functions Independently of Octopamine in the Caenorhabditis elegans Nervous System." Neuron 46, no. 2 (2005): 247–60. http://dx.doi.org/10.1016/j.neuron.2005.02.024.

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Hobert, Oliver, Robert J. Johnston, and Sarah Chang. "Left–right asymmetry in the nervous system: the Caenorhabditis elegans model." Nature Reviews Neuroscience 3, no. 8 (2002): 629–40. http://dx.doi.org/10.1038/nrn897.

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Pathak, Anand, Nivedita Chatterjee, and Sitabhra Sinha. "Developmental trajectory of Caenorhabditis elegans nervous system governs its structural organization." PLOS Computational Biology 16, no. 1 (2020): e1007602. http://dx.doi.org/10.1371/journal.pcbi.1007602.

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PILON, Marc, and Catarina MORCK. "Development of Caenorhabditis elegans pharynx, with emphasis on its nervous system." Acta Pharmacologica Sinica 26, no. 4 (2005): 396–404. http://dx.doi.org/10.1111/j.1745-7254.2005.00070.x.

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Gleeson, Padraig, David Lung, Radu Grosu, Ramin Hasani, and Stephen D. Larson. "c302: a multiscale framework for modelling the nervous system of Caenorhabditis elegans." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1758 (2018): 20170379. http://dx.doi.org/10.1098/rstb.2017.0379.

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The OpenWorm project has the ambitious goal of producing a highly detailed in silico model of the nematode Caenorhabditis elegans . A crucial part of this work will be a model of the nervous system encompassing all known cell types and connections. The appropriate level of biophysical detail required in the neuronal model to reproduce observed high-level behaviours in the worm has yet to be determined. For this reason, we have developed a framework, c302, that allows different instances of neuronal networks to be generated incorporating varying levels of anatomical and physiological detail, which can be investigated and refined independently or linked to other tools developed in the OpenWorm modelling toolchain. This article is part of a discussion meeting issue ‘Connectome to behaviour: modelling C. elegans at cellular resolution’.

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Venkatachalam, Vivek, Ni Ji, Xian Wang, et al. "Pan-neuronal imaging in roaming Caenorhabditis elegans." Proceedings of the National Academy of Sciences 113, no. 8 (2015): E1082—E1088. http://dx.doi.org/10.1073/pnas.1507109113.

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We present an imaging system for pan-neuronal recording in crawling Caenorhabditis elegans. A spinning disk confocal microscope, modified for automated tracking of the C. elegans head ganglia, simultaneously records the activity and position of ∼80 neurons that coexpress cytoplasmic calcium indicator GCaMP6s and nuclear localized red fluorescent protein at 10 volumes per second. We developed a behavioral analysis algorithm that maps the movements of the head ganglia to the animal’s posture and locomotion. Image registration and analysis software automatically assigns an index to each nucleus and calculates the corresponding calcium signal. Neurons with highly stereotyped positions can be associated with unique indexes and subsequently identified using an atlas of the worm nervous system. To test our system, we analyzed the brainwide activity patterns of moving worms subjected to thermosensory inputs. We demonstrate that our setup is able to uncover representations of sensory input and motor output of individual neurons from brainwide dynamics. Our imaging setup and analysis pipeline should facilitate mapping circuits for sensory to motor transformation in transparent behaving animals such as C. elegans and Drosophila larva.

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Qu, Man, Yan Kong, Yujie Yuan, and Dayong Wang. "Neuronal damage induced by nanopolystyrene particles in nematode Caenorhabditis elegans." Environmental Science: Nano 6, no. 8 (2019): 2591–601. http://dx.doi.org/10.1039/c9en00473d.

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Jin, Eugene Jennifer, Seungmee Park, Xiaohui Lyu, and Yishi Jin. "Gap junctions: historical discoveries and new findings in the Caenorhabditiselegans nervous system." Biology Open 9, no. 8 (2020): bio053983. http://dx.doi.org/10.1242/bio.053983.

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ABSTRACTGap junctions are evolutionarily conserved structures at close membrane contacts between two cells. In the nervous system, they mediate rapid, often bi-directional, transmission of signals through channels called innexins in invertebrates and connexins in vertebrates. Connectomic studies from Caenorhabditis elegans have uncovered a vast number of gap junctions present in the nervous system and non-neuronal tissues. The genome also has 25 innexin genes that are expressed in spatial and temporal dynamic pattern. Recent findings have begun to reveal novel roles of innexins in the regulation of multiple processes during formation and function of neural circuits both in normal conditions and under stress. Here, we highlight the diverse roles of gap junctions and innexins in the C. elegans nervous system. These findings contribute to fundamental understanding of gap junctions in all animals.

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Geng, Wei, Pamela Cosman, Joong-Hwan Baek, Charles C. Berry, and William R. Schafer. "Quantitative Classification and Natural Clustering of Caenorhabditis elegans Behavioral Phenotypes." Genetics 165, no. 3 (2003): 1117–26. http://dx.doi.org/10.1093/genetics/165.3.1117.

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Abstract Genetic analysis of nervous system function relies on the rigorous description of behavioral phenotypes. However, standard methods for classifying the behavioral patterns of mutant Caenorhabditis elegans rely on human observation and are therefore subjective and imprecise. Here we describe the application of machine learning to quantitatively define and classify the behavioral patterns of C. elegans nervous system mutants. We have used an automated tracking and image processing system to obtain measurements of a wide range of morphological and behavioral features from recordings of representative mutant types. Using principal component analysis, we represented the behavioral patterns of eight mutant types as data clouds distributed in multidimensional feature space. Cluster analysis using the k-means algorithm made it possible to quantitatively assess the relative similarities between different behavioral phenotypes and to identify natural phenotypic clusters among the data. Since the patterns of phenotypic similarity identified in this study closely paralleled the functional similarities of the mutant gene products, the complex phenotypic signatures obtained from these image data appeared to represent an effective diagnostic of the mutants' underlying molecular defects.

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SAKAGUCHI, Aisa, Naoki HISAMOTO, and Kunihiro MATSUMOTO. "MAP Kinase Cascades Regulating Development, Differentiation and Nervous System in Caenorhabditis elegans." Kagaku To Seibutsu 41, no. 8 (2003): 522–27. http://dx.doi.org/10.1271/kagakutoseibutsu1962.41.522.

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Toth, M. L., I. Melentijevic, L. Shah, et al. "Neurite Sprouting and Synapse Deterioration in the Aging Caenorhabditis elegans Nervous System." Journal of Neuroscience 32, no. 26 (2012): 8778–90. http://dx.doi.org/10.1523/jneurosci.1494-11.2012.

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Gainutdinov, M. Kh, A. Kh Timoshenko, A. M. Petrov, T. M. Gainutdinov, and T. B. Kalinnikova. "Ethanol Sensitizes the Nervous System of Caenorhabditis elegans Nematode to Heat Stress." Bulletin of Experimental Biology and Medicine 150, no. 1 (2010): 55–57. http://dx.doi.org/10.1007/s10517-010-1067-0.

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Avery, L., C. I. Bargmann, and H. R. Horvitz. "The Caenorhabditis elegans unc-31 gene affects multiple nervous system-controlled functions." Genetics 134, no. 2 (1993): 455–64. http://dx.doi.org/10.1093/genetics/134.2.455.

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Abstract We have devised a method for selecting Caenorhabditis elegans mutants that execute feeding motions in the absence of food. One mutation isolated in this way is an allele of the gene unc-31, first discovered by S. Brenner in 1974, because of its effects on locomotion. We find that strong unc-31 mutations cause defects in four functions controlled by the nervous system. Mutant worms are lethargic, feed constitutively, are defective in egg-laying and produce dauer larvae that fail to recover. We discuss two extreme models to explain this pleiotropy: either unc-31 affects one or a few neurons that coordinately control several different functions, or it affects many neurons that independently control different functions.

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Guziewicz, Megan, Toni Vitullo, Bethany Simmons, and Rebecca Eustance Kohn. "Analyzing Defects in the Caenorhabditis elegans Nervous System Using Organismal and Cell Biological Approaches." Cell Biology Education 1, no. 1 (2002): 18–25. http://dx.doi.org/10.1187/cbe.01-08-0001.

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The goal of this laboratory exercise is to increase student understanding of the impact of nervous system function at both the organismal and cellular levels. This inquiry-based exercise is designed for an undergraduate course examining principles of cell biology. After observing the movement of Caenorhabditis elegans with defects in their nervous system, students examine the structure of the nervous system to categorize the type of defect. They distinguish between defects in synaptic vesicle transport and defects in synaptic vesicle fusion with membranes. The synaptic vesicles are tagged with green fluorescent protein (GFP), simplifying cellular analysis. The expected outcome of this experiment is that students will better understand the concepts of vesicle transport, neurotransmitter release, GFP, and the relation between the nervous system and behavior.

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Crowder, Michael C., Laynie D. Shebester, and Tim Schedl. "Behavioral Effects of Volatile Anesthetics in Caenorhabditis elegans." Anesthesiology 85, no. 4 (1996): 901–12. http://dx.doi.org/10.1097/00000542-199610000-00027.

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Background The nematode Caenorhabditis elegans offers many advantages as a model organism for studying volatile anesthetic actions. It has a simple, well-understood nervous system; it allows the researcher to do forward genetics; and its genome will soon be completely sequenced. C. elegans is immobilized by volatile anesthetics only at high concentrations and with an unusually slow time course. Here other behavioral dysfunctions are considered as anesthetic endpoints in C. elegans. Methods The potency of halothane for disrupting eight different behaviors was determined by logistic regression of concentration and response data. Other volatile anesthetics were also tested for some behaviors. Established protocols were used for behavioral endpoints that, except for pharyngeal pumping, were set as complete disruption of the behavior. Time courses were measured for rapid behaviors. Recovery from exposure to 1 or 4 vol% halothane was determined for mating, chemotaxis, and gross movement. All experiments were performed at 20 to 22 degrees C. Results The median effective concentration values for halothane inhibition of mating (0.30 vol%-0.21 mM), chemotaxis (0.34 vol%-0.24 mM), and coordinated movement (0.32 vol% - 0.23 mM) were similar to the human minimum alveolar concentration (MAC; 0.21 mM). In contrast, halothane produced immobility with a median effective concentration of 3.65 vol% (2.6 mM). Other behaviors had intermediate sensitivities. Halothane's effects reached steady-state in 10 min for all behaviors tested except immobility, which required 2 h. Recovery was complete after exposure to 1 vol% halothane but was significantly reduced after exposure to immobilizing concentrations. Conclusions Volatile anesthetics selectively disrupt C. elegans behavior. The potency, time course, and recovery characteristics of halothane's effects on three behaviors are similar to its anesthetic properties in vertebrates. The affected nervous system molecules may express structural motifs similar to those on vertebrate anesthetic targets.

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Suzuki, Michiyo, Zu Soh, Hiroki Yamashita, Toshio Tsuji, and Tomoo Funayama. "Targeted Central Nervous System Irradiation of Caenorhabditis elegans Induces a Limited Effect on Motility." Biology 9, no. 9 (2020): 289. http://dx.doi.org/10.3390/biology9090289.

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To clarify the tissue responsible for a biological function, that function can be experimentally perturbed by an external stimulus, such as radiation. Radiation can be precisely and finely administered and any subsequent change in function examined. To investigate the involvement of the central nervous system (CNS) in Caenorhabditis elegans’ locomotion, we irradiated a limited 20-µm-diameter area of the CNS with a single dose and evaluated the resulting effects on motility. However, whether irradiated area (beam size)-dependent or dose-dependent effects on motility occur via targeted irradiation remain unknown. In the present study, we examined the irradiated area- and dose-dependent effects of CNS-targeted irradiation on the motility of C. elegans using a collimating microbeam system and confirmed the involvement of the CNS and body-wall muscle cells around the CNS in motility. After CNS-targeted microbeam irradiation, C. elegans’ motility was assayed. The results demonstrated a dose-dependent effect of CNS-targeted irradiation on motility reflecting direct effects on the irradiated CNS. In addition, when irradiated with 1000-Gy irradiation, irradiated area (beam size)-dependent effects were observed. This method has two technical advantages: Performing a series of on-chip imaging analyses before and after irradiation and targeted irradiation using a distinct ion-beam size.

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Xiao, Yi, Fang Liu, Pei-ji Zhao, Cheng-Gang Zou, and Ke-Qin Zhang. "PKA/KIN-1 mediates innate immune responses to bacterial pathogens in Caenorhabditis elegans." Innate Immunity 23, no. 8 (2017): 656–66. http://dx.doi.org/10.1177/1753425917732822.

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The genetically tractable organism Caenorhabditis elegans is a powerful model animal for the study of host innate immunity. Although the intestine and the epidermis of C. elegans that is in contact with pathogens are likely to function as sites for the immune function, recent studies indicate that the nervous system could control innate immunity in C. elegans. In this report, we demonstrated that protein kinase A (PKA)/KIN-1 in the neurons contributes to resistance against Salmonella enterica infection in C. elegans. Microarray analysis revealed that PKA/KIN-1 regulates the expression of a set of antimicrobial effectors in the non-neuron tissues, which are required for innate immune responses to S. enterica. Furthermore, PKA/KIN-1 regulated the expression of lysosomal genes during S. enterica infection. Our results suggest that the lysosomal signaling molecules are involved in autophagy by controlling autophagic flux, rather than formation of autophagosomes. As autophagy is crucial for host defense against S. enterica infection in a metazoan, the lysosomal pathway also acts as a downstream effector of the PKA/KIN-1 signaling for innate immunity. Our data indicate that the PKA pathway contributes to innate immunity in C. elegans by signaling from the nervous system to periphery tissues to protect the host against pathogens.

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Zhang, Albert, Kentaro Noma, and Dong Yan. "Regulation of Gliogenesis by lin-32/Atoh1 in Caenorhabditis elegans." G3 Genes|Genomes|Genetics 10, no. 9 (2020): 3271–78. http://dx.doi.org/10.1534/g3.120.401547.

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Abstract The regulation of gliogenesis is a fundamental process for nervous system development, as the appropriate glial number and identity is required for a functional nervous system. To investigate the molecular mechanisms involved in gliogenesis, we used C. elegans as a model and identified the function of the proneural gene lin-32/Atoh1 in gliogenesis. We found that lin-32 functions during embryonic development to negatively regulate the number of AMsh glia. The ectopic AMsh cells at least partially arise from cells originally fated to become CEPsh glia, suggesting that lin-32 is involved in the specification of specific glial subtypes. Moreover, we show that lin-32 acts in parallel with cnd-1/ NeuroD1 and ngn-1/ Neurog1 in negatively regulating an AMsh glia fate. Furthermore, expression of murine Atoh1 fully rescues lin-32 mutant phenotypes, suggesting lin-32/Atoh1 may have a conserved role in glial specification.

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Kovács, István A., Dániel L. Barabási, and Albert-László Barabási. "Uncovering the genetic blueprint of the C. elegans nervous system." Proceedings of the National Academy of Sciences 117, no. 52 (2020): 33570–77. http://dx.doi.org/10.1073/pnas.2009093117.

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Despite rapid advances in connectome mapping and neuronal genetics, we lack theoretical and computational tools to unveil, in an experimentally testable fashion, the genetic mechanisms that govern neuronal wiring. Here we introduce a computational framework to link the adjacency matrix of a connectome to the expression patterns of its neurons, helping us uncover a set of genetic rules that govern the interactions between neurons in contact. The method incorporates the biological realities of the system, accounting for noise from data collection limitations, as well as spatial restrictions. The resulting methodology allows us to infer a network of 19 innexin interactions that govern the formation of gap junctions in Caenorhabditis elegans, five of which are already supported by experimental data. As advances in single-cell gene expression profiling increase the accuracy and the coverage of the data, the developed framework will allow researchers to systematically infer experimentally testable connection rules, offering mechanistic predictions for synapse and gap junction formation.

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Emmons, Scott W. "Neural Circuits of Sexual Behavior inCaenorhabditis elegans." Annual Review of Neuroscience 41, no. 1 (2018): 349–69. http://dx.doi.org/10.1146/annurev-neuro-070815-014056.

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The recently determined connectome of the Caenorhabditis elegans adult male, together with the known connectome of the hermaphrodite, opens up the possibility for a comprehensive description of sexual dimorphism in this species and the identification and study of the neural circuits underlying sexual behaviors. The C. elegans nervous system consists of 294 neurons shared by both sexes plus neurons unique to each sex, 8 in the hermaphrodite and 91 in the male. The sex-specific neurons are well integrated within the remainder of the nervous system; in the male, 16% of the input to the shared component comes from male-specific neurons. Although sex-specific neurons are involved primarily, but not exclusively, in controlling sex-unique behavior—egg-laying in the hermaphrodite and copulation in the male—these neurons act together with shared neurons to make navigational choices that optimize reproductive success. Sex differences in general behaviors are underlain by considerable dimorphism within the shared component of the nervous system itself, including dimorphism in synaptic connectivity.

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Alqadah, Amel, Yi-Wen Hsieh, Rui Xiong, and Chiou-Fen Chuang. "Stochastic left–right neuronal asymmetry in Caenorhabditis elegans." Philosophical Transactions of the Royal Society B: Biological Sciences 371, no. 1710 (2016): 20150407. http://dx.doi.org/10.1098/rstb.2015.0407.

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Left–right asymmetry in the nervous system is observed across species. Defects in left–right cerebral asymmetry are linked to several neurological diseases, but the molecular mechanisms underlying brain asymmetry in vertebrates are still not very well understood. The Caenorhabditis elegans left and right amphid wing ‘C’ (AWC) olfactory neurons communicate through intercellular calcium signalling in a transient embryonic gap junction neural network to specify two asymmetric subtypes, AWC OFF (default) and AWC ON (induced), in a stochastic manner. Here, we highlight the molecular mechanisms that establish and maintain stochastic AWC asymmetry. As the components of the AWC asymmetry pathway are highly conserved, insights from the model organism C. elegans may provide a window onto how brain asymmetry develops in humans. This article is part of the themed issue ‘Provocative questions in left–right asymmetry’.

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Emmons, Scott W. "The beginning of connectomics: a commentary on White et al. (1986) ‘The structure of the nervous system of the nematode Caenorhabditis elegans ’." Philosophical Transactions of the Royal Society B: Biological Sciences 370, no. 1666 (2015): 20140309. http://dx.doi.org/10.1098/rstb.2014.0309.

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The article ‘Structure of the nervous system of the nematode Caenorhabditis elegans ' (aka ‘The mind of a worm’) by White et al. , published for the first time the complete set of synaptic connections in the nervous system of an animal. The work was carried out as part of a programme to begin to understand how genes determine the structure of a nervous system and how a nervous system creates behaviour. It became a major stimulus to the field of C. elegans research, which has since contributed insights into all areas of biology. Twenty-six years elapsed before developments, notably more powerful computers, made new studies of this kind possible. It is hoped that one day knowledge of synaptic structure, the connectome , together with results of many other investigations, will lead to an understanding of the human brain. This commentary was written to celebrate the 350th anniversary of the journal Philosophical Transactions of the Royal Society .

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Knobel, Karla M., Warren S. Davis, Erik M. Jorgensen, and Michael J. Bastiani. "UNC-119 suppresses axon branching inC. elegans." Development 128, no. 20 (2001): 4079–92. http://dx.doi.org/10.1242/dev.128.20.4079.

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The architecture of the differentiated nervous system is stable but the molecular mechanisms that are required for stabilization are unknown. We characterized the gene unc-119 in the nematode Caenorhabditis elegans and demonstrate that it is required to stabilize the differentiated structure of the nervous system. In unc-119 mutants, motor neuron commissures are excessively branched in adults. However, live imaging demonstrated that growth cone behavior during extension was fairly normal with the exception that the overall rate of migration was reduced. Later, after development was complete, secondary growth cones sprouted from existing motor neuron axons and cell bodies. These new growth cones extended supernumerary branches to the dorsal nerve cord at the same time the previously formed axons retracted. These defects could be suppressed by expressing the UNC-119 protein after embryonic development; thus demonstrating that UNC-119 is required for the maintenance of the nervous system architecture. Finally, UNC-119 is located in neuron cell bodies and axons and acts cell-autonomously to inhibit axon branching.

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Towlson, Emma K., Petra E. Vértes, Gang Yan, et al. "Caenorhabditis elegans and the network control framework—FAQs." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1758 (2018): 20170372. http://dx.doi.org/10.1098/rstb.2017.0372.

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Control is essential to the functioning of any neural system. Indeed, under healthy conditions the brain must be able to continuously maintain a tight functional control between the system's inputs and outputs. One may therefore hypothesize that the brain's wiring is predetermined by the need to maintain control across multiple scales, maintaining the stability of key internal variables, and producing behaviour in response to environmental cues. Recent advances in network control have offered a powerful mathematical framework to explore the structure–function relationship in complex biological, social and technological networks, and are beginning to yield important and precise insights on neuronal systems. The network control paradigm promises a predictive, quantitative framework to unite the distinct datasets necessary to fully describe a nervous system, and provide mechanistic explanations for the observed structure and function relationships. Here, we provide a thorough review of the network control framework as applied to Caenorhabditis elegans (Yan et al. 2017 Nature 550 , 519–523. ( doi:10.1038/nature24056 )), in the style of Frequently Asked Questions. We present the theoretical, computational and experimental aspects of network control, and discuss its current capabilities and limitations, together with the next likely advances and improvements. We further present the Python code to enable exploration of control principles in a manner specific to this prototypical organism. This article is part of a discussion meeting issue ‘Connectome to behaviour: modelling C. elegans at cellular resolution’.

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Liu, Hexuan, Jimin Kim, and Eli Shlizerman. "Functional connectomics from neural dynamics: probabilistic graphical models for neuronal network of Caenorhabditis elegans." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1758 (2018): 20170377. http://dx.doi.org/10.1098/rstb.2017.0377.

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We propose an approach to represent neuronal network dynamics as a probabilistic graphical model (PGM). To construct the PGM, we collect time series of neuronal responses produced by the neuronal network and use singular value decomposition to obtain a low-dimensional projection of the time-series data. We then extract dominant patterns from the projections to get pairwise dependency information and create a graphical model for the full network. The outcome model is a functional connectome that captures how stimuli propagate through the network and thus represents causal dependencies between neurons and stimuli. We apply our methodology to a model of the Caenorhabditis elegans somatic nervous system to validate and show an example of our approach. The structure and dynamics of the C. elegans nervous system are well studied and a model that generates neuronal responses is available. The resulting PGM enables us to obtain and verify underlying neuronal pathways for known behavioural scenarios and detect possible pathways for novel scenarios. This article is part of a discussion meeting issue ‘Connectome to behaviour: modelling C. elegans at cellular resolution’.

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Maruyama, H., T. L. Rakow, and I. N. Maruyama. "Synaptic exocytosis and nervous system development impaired in Caenorhabditis elegans unc-13 mutants." Neuroscience 104, no. 2 (2001): 287–97. http://dx.doi.org/10.1016/s0306-4522(01)00097-5.

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Herman, Robert K. "Mosaic Analysis of Two Genes That Affect Nervous System Structure in Caenorhabditis elegans." Genetics 116, no. 3 (1987): 377–88. http://dx.doi.org/10.1093/genetics/116.3.377.

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ABSTRACT The mutation mec-4(e1611), identified by M. Chalfie, leads to the degeneration and death of the six neurons, called the microtubule cells, that mediate the response of wild-type animals to light touch. The fates of two of these cells, PLML and PLMR, which are responsible for response to light touch in the tail of the animal, have been monitored in animals mosaic for the mec-4(e1611) mutation. The results are consistent with the view that the mutation behaves cell autonomously in its killing effect; in particular, none of the neurons that make either chemical synapses or gap junctions to PLML or PLMR is responsible for the deaths of PLML or PLMR. The results of gene dosage and dominance tests suggest that the mec-4(+) gene product, which is required for wild-type microtubule cell function, is altered by the e1611 mutation into a novel product that kills the microtubule cells. Mutation in the gene unc-3 leads to the derangement of the processes of the motor neurons of the ventral cord. Mosaic analysis strongly suggests that unc-3(+) expression is required only in the motor neurons themselves for normal neuronal development. In particular, the hypodermis surrounding the ventral cord is not the primary focus of unc-3 action (body muscle was excluded in earlier work). Finally, the mosaic analysis supports an earlier suggestion that a sensory defect caused by a daf-6 mutation is localized to a non-neuronal cell called the sheath cell.

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Suzuki, Michiyo, Yuya Hattori, Tetsuya Sakashita, Yuichiro Yokota, Yasuhiko Kobayashi, and Tomoo Funayama. "Region-specific irradiation system with heavy-ion microbeam for active individuals of Caenorhabditis elegans." Journal of Radiation Research 58, no. 6 (2017): 881–86. http://dx.doi.org/10.1093/jrr/rrx043.

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Abstract Radiation may affect essential functions and behaviors such as locomotion, feeding, learning and memory. Although whole-body irradiation has been shown to reduce motility in the nematode Caenorhabditis elegans, the detailed mechanism responsible for this effect remains unknown. Targeted irradiation of the nerve ring responsible for sensory integration and information processing would allow us to determine whether the reduction of motility following whole-body irradiation reflects effects on the central nervous system or on the muscle cells themselves. We therefore addressed this issue using a collimating microbeam system. However, radiation targeting requires the animal to be immobilized, and previous studies have anesthetized animals to prevent their movement, thus making it impossible to assess their locomotion immediately after irradiation. We developed a method in which the animal was enclosed in a straight, microfluidic channel in a polydimethylsiloxane chip to inhibit free motion during irradiation, thus allowing locomotion to be observed immediately after irradiation. The head region (including the central nervous system), mid region around the intestine and uterus, and tail region were targeted independently. Each region was irradiated with 12 000 carbon ions (12C; 18.3 MeV/u; linear energy transfer = 106.4 keV/μm), corresponding to 500 Gy at a φ20 μm region. Motility was significantly decreased by whole-body irradiation, but not by irradiation of any of the individual regions, including the central nervous system. This suggests that radiation inhibits locomotion by a whole-body mechanism, potentially involving motoneurons and/or body-wall muscle cells, rather than affecting motor control via the central nervous system and the stimulation response.

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DiLoreto, Chute, Bryce, and Srinivasan. "Novel Technological Advances in Functional Connectomics in C. elegans." Journal of Developmental Biology 7, no. 2 (2019): 8. http://dx.doi.org/10.3390/jdb7020008.

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The complete structure and connectivity of the Caenorhabditis elegans nervous system (“mind of a worm”) was first published in 1986, representing a critical milestone in the field of connectomics. The reconstruction of the nervous system (connectome) at the level of synapses provided a unique perspective of understanding how behavior can be coded within the nervous system. The following decades have seen the development of technologies that help understand how neural activity patterns are connected to behavior and modulated by sensory input. Investigations on the developmental origins of the connectome highlight the importance of role of neuronal cell lineages in the final connectivity matrix of the nervous system. Computational modeling of neuronal dynamics not only helps reconstruct the biophysical properties of individual neurons but also allows for subsequent reconstruction of whole-organism neuronal network models. Hence, combining experimental datasets with theoretical modeling of neurons generates a better understanding of organismal behavior. This review discusses some recent technological advances used to analyze and perturb whole-organism neuronal function along with developments in computational modeling, which allows for interrogation of both local and global neural circuits, leading to different behaviors. Combining these approaches will shed light into how neural networks process sensory information to generate the appropriate behavioral output, providing a complete understanding of the worm nervous system.

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Kohn, Rebecca Eustance, Janet S. Duerr, John R. McManus, et al. "Expression of Multiple UNC-13 Proteins in theCaenorhabditis elegans Nervous System." Molecular Biology of the Cell 11, no. 10 (2000): 3441–52. http://dx.doi.org/10.1091/mbc.11.10.3441.

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The Caenorhabditis elegans UNC-13 protein and its mammalian homologues are important for normal neurotransmitter release. We have identified a set of transcripts from the unc-13locus in C. elegans resulting from alternative splicing and apparent alternative promoters. These transcripts encode proteins that are identical in their C-terminal regions but that vary in their N-terminal regions. The most abundant protein form is localized to most or all synapses. We have analyzed the sequence alterations, immunostaining patterns, and behavioral phenotypes of 31 independentunc-13 alleles. Many of these mutations are transcript-specific; their phenotypes suggest that the different UNC-13 forms have different cellular functions. We have also isolated a deletion allele that is predicted to disrupt all UNC-13 protein products; animals homozygous for this null allele are able to complete embryogenesis and hatch, but they die as paralyzed first-stage larvae. Transgenic expression of the entire gene rescues the behavior of mutants fully; transgenic overexpression of one of the transcripts can partially compensate for the genetic loss of another. This finding suggests some degree of functional overlap of the different protein products.

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Hall, David H. "The Nematode Caenorhabditis elegans A Model Animal “Made for Microscopy”." Microscopy Today 12, no. 2 (2004): 8–13. http://dx.doi.org/10.1017/s1551929500069807.

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The small unassuming nematode, Caenorhabditis elegans is only one millimeter long and lives in the soil munching on bacteria. While many nematode (roundworm) species are parasites with medical or agricultural importance, C. elegans seems to harm no one. Yet, this animal has attained a status in medical science that compares to more complex organisms such as the mouse or fruit fly in its utility for scientific discovery. It has been the subject of thousands of studies dealing with topics as diverse as nutrition, aging, and nervous system development. About 5000 scientists are now pursuing this single species in hundreds of laboratories worldwide. In 2002, the Nobel Prize in Medicine was awarded to three of the pioneers in establishing C. elegans as a “model organism“: Sydney Brenner, John Sulston, and H. Robert Horvitz. Why study worms?Sydney Brenner first turned his attention to C. elegans in the 1960's. Working at the Medical Research Council in England, he was looking for a small animal with inexpensive tastes that could be easily cultured in the laboratory.

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McCloskey, Richard J., Anthony D. Fouad, Matthew A. Churgin, and Christopher Fang-Yen. "Food responsiveness regulates episodic behavioral states in Caenorhabditis elegans." Journal of Neurophysiology 117, no. 5 (2017): 1911–34. http://dx.doi.org/10.1152/jn.00555.2016.

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Animals optimize survival and reproduction in part through control of behavioral states, which depend on an organism’s internal and external environments. In the nematode Caenorhabditis elegans a variety of behavioral states have been described, including roaming, dwelling, quiescence, and episodic swimming. These states have been considered in isolation under varied experimental conditions, making it difficult to establish a unified picture of how they are regulated. Using long-term imaging, we examined C. elegans episodic behavioral states under varied mechanical and nutritional environments. We found that animals alternate between high-activity (active) and low-activity (sedentary) episodes in any mechanical environment, while the incidence of episodes and their behavioral composition depend on food levels. During active episodes, worms primarily roam, as characterized by continuous whole body movement. During sedentary episodes, animals exhibit dwelling (slower movements confined to the anterior half of the body) and quiescence (a complete lack of movement). Roaming, dwelling, and quiescent states are manifest not only through locomotory characteristics but also in pharyngeal pumping (feeding) and in egg-laying behaviors. Next, we analyzed the genetic basis of behavioral states. We found that modulation of behavioral states depends on neuropeptides and insulin-like signaling in the nervous system. Sensory neurons and the Foraging homolog EGL-4 regulate behavior through control of active/sedentary episodes. Optogenetic stimulation of dopaminergic and serotonergic neurons induced dwelling, implicating dopamine as a dwell-promoting neurotransmitter. Our findings provide a more unified description of behavioral states and suggest that perception of nutrition is a conserved mechanism for regulating animal behavior. NEW & NOTEWORTHY One strategy by which animals adapt to their internal states and external environments is by adopting behavioral states. The roundworm Caenorhabditis elegans is an attractive model for investigating how behavioral states are genetically and neuronally controlled. Here we describe the hierarchical organization of behavioral states characterized by locomotory activity, feeding, and egg-laying. We show that decisions to engage in these behaviors are controlled by the nervous system through insulin-like signaling and the perception of food.

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Hedgecock, E. M., J. G. Culotti, D. H. Hall, and B. D. Stern. "Genetics of cell and axon migrations in Caenorhabditis elegans." Development 100, no. 3 (1987): 365–82. http://dx.doi.org/10.1242/dev.100.3.365.

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The Caenorhabditis elegans epidermis comprises 78 cells which cover the external surface of the embryo as a single cell layer. These cells secrete the cuticle from their exterior faces and support the body wall muscles and most of the nervous system on their interior faces. The epidermal cells arise by autonomous embryonic cell lineages but show regulative interactions after their assembly into an epithelium. It is believed that the various epidermal cells express different kinds or amounts of surface molecules that govern their mutual assembly and also guide the attachments and migrations of the underlying body muscles and neurones. The first muscles and neurones may in turn express new surface molecules that refine later cell movements. Mutations in some 30 known genes disrupt the movements of cells or axons along the body wall.

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Kondo, K., J. Hodgkin, and R. H. Waterston. "Differential expression of five tRNA(UAGTrp) amber suppressors in Caenorhabditis elegans." Molecular and Cellular Biology 8, no. 9 (1988): 3627–35. http://dx.doi.org/10.1128/mcb.8.9.3627.

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Caenorhabditis elegans has 12 tRNA(UGGTrp) genes as defined by Southern analysis. In order to evaluate the function of the individual members of this multigene family, we sought to recover amber (UAG)-suppressing mutations from reversion experiments with animals carrying amber mutations in a nervous system-affecting gene (unc-13) or a sex-determining gene (tra-3). Revertants were analyzed by Southern blot, exploiting the fact that the CCA to CTA change at the anticodon creates a new XbaI site. Five different members of the tRNATrp gene family were identified as suppressors: sup-7 X, sup-5 III, sup-24 IV, sup-28 X, and sup-29 IV. All five suppressor genes were sequenced and found to encode identical tRNA(UAGTrp) molecules with a single base change (CCA to CTA) at the anticodon compared with their wild-type counterparts. The flanking sequences had only limited homology. The relative expression of these five genes was determined by measuring the efficiencies of suppressers against amber mutations in genes affecting the nervous system, hypodermis, muscle, and sex determination. The results of these cross-suppression tests showed that the five members of the tRNA(Trp) gene family were differentially regulated in a tissue- or development stage-specific manner.

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Kondo, K., J. Hodgkin, and R. H. Waterston. "Differential expression of five tRNA(UAGTrp) amber suppressors in Caenorhabditis elegans." Molecular and Cellular Biology 8, no. 9 (1988): 3627–35. http://dx.doi.org/10.1128/mcb.8.9.3627-3635.1988.

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Caenorhabditis elegans has 12 tRNA(UGGTrp) genes as defined by Southern analysis. In order to evaluate the function of the individual members of this multigene family, we sought to recover amber (UAG)-suppressing mutations from reversion experiments with animals carrying amber mutations in a nervous system-affecting gene (unc-13) or a sex-determining gene (tra-3). Revertants were analyzed by Southern blot, exploiting the fact that the CCA to CTA change at the anticodon creates a new XbaI site. Five different members of the tRNATrp gene family were identified as suppressors: sup-7 X, sup-5 III, sup-24 IV, sup-28 X, and sup-29 IV. All five suppressor genes were sequenced and found to encode identical tRNA(UAGTrp) molecules with a single base change (CCA to CTA) at the anticodon compared with their wild-type counterparts. The flanking sequences had only limited homology. The relative expression of these five genes was determined by measuring the efficiencies of suppressers against amber mutations in genes affecting the nervous system, hypodermis, muscle, and sex determination. The results of these cross-suppression tests showed that the five members of the tRNA(Trp) gene family were differentially regulated in a tissue- or development stage-specific manner.

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Hutter, Harald, and Donald Moerman. "Big Data in Caenorhabditis elegans: quo vadis?" Molecular Biology of the Cell 26, no. 22 (2015): 3909–14. http://dx.doi.org/10.1091/mbc.e15-05-0312.

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A clear definition of what constitutes “Big Data” is difficult to identify, but we find it most useful to define Big Data as a data collection that is complete. By this criterion, researchers on Caenorhabditis elegans have a long history of collecting Big Data, since the organism was selected with the idea of obtaining a complete biological description and understanding of development. The complete wiring diagram of the nervous system, the complete cell lineage, and the complete genome sequence provide a framework to phrase and test hypotheses. Given this history, it might be surprising that the number of “complete” data sets for this organism is actually rather small—not because of lack of effort, but because most types of biological experiments are not currently amenable to complete large-scale data collection. Many are also not inherently limited, so that it becomes difficult to even define completeness. At present, we only have partial data on mutated genes and their phenotypes, gene expression, and protein–protein interaction—important data for many biological questions. Big Data can point toward unexpected correlations, and these unexpected correlations can lead to novel investigations; however, Big Data cannot establish causation. As a result, there is much excitement about Big Data, but there is also a discussion on just what Big Data contributes to solving a biological problem. Because of its relative simplicity, C. elegans is an ideal test bed to explore this issue and at the same time determine what is necessary to build a multicellular organism from a single cell.

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Rose, Simon, Maria Grazia Malabarba, Claudia Krag, et al. "Caenorhabditis elegans Intersectin: A Synaptic Protein Regulating Neurotransmission." Molecular Biology of the Cell 18, no. 12 (2007): 5091–99. http://dx.doi.org/10.1091/mbc.e07-05-0460.

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Intersectin is a multifunctional protein that interacts with components of the endocytic and exocytic pathways, and it is also involved in the control of actin dynamics. Drosophila intersectin is required for viability, synaptic development, and synaptic vesicle recycling. Here, we report the characterization of intersectin function in Caenorhabditis elegans. Nematode intersectin (ITSN-1) is expressed in the nervous system, and it is enriched in presynaptic regions. The C. elegans intersectin gene (itsn-1) is nonessential for viability. In addition, itsn-1-null worms do not display any evident phenotype, under physiological conditions. However, they display aldicarb-hypersensitivity, compatible with a negative regulatory role of ITSN-1 on neurotransmission. ITSN-1 physically interacts with dynamin and EHS-1, two proteins involved in synaptic vesicle recycling. We have previously shown that EHS-1 is a positive modulator of synaptic vesicle recycling in the nematode, likely through modulation of dynamin or dynamin-controlled pathways. Here, we show that ITSN-1 and EHS-1 have opposite effects on aldicarb sensitivity, and on dynamin-dependent phenotypes. Thus, the sum of our results identifies dynamin, or a dynamin-controlled pathway, as a potential target for the negative regulatory role of ITSN-1.

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Díaz-Balzac, Carlos A., María I. Lázaro-Peña, Eillen Tecle, Nathali Gomez, and Hannes E. Bülow. "Complex Cooperative Functions of Heparan Sulfate Proteoglycans Shape Nervous System Development in Caenorhabditis elegans." G3: Genes|Genomes|Genetics 4, no. 10 (2014): 1859–70. http://dx.doi.org/10.1534/g3.114.012591.

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Philippsen, Daniela Frizzo, Wagner Antonio Tamagno, Ana Paula Vanin, et al. "Copper uses in organic production are safe to the nervous system of Caenorhabditis elegans ?" Environmental Quality Management 30, no. 4 (2021): 61–70. http://dx.doi.org/10.1002/tqem.21736.

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Wen, Quan, Shangbang Gao, and Mei Zhen. "Caenorhabditis elegans excitatory ventral cord motor neurons derive rhythm for body undulation." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1758 (2018): 20170370. http://dx.doi.org/10.1098/rstb.2017.0370.

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The intrinsic oscillatory activity of central pattern generators underlies motor rhythm. We review and discuss recent findings that address the origin of Caenorhabditis elegans motor rhythm. These studies propose that the A- and mid-body B-class excitatory motor neurons at the ventral cord function as non-bursting intrinsic oscillators to underlie body undulation during reversal and forward movements, respectively. Proprioception entrains their intrinsic activities, allows phase-coupling between members of the same class motor neurons, and thereby facilitates directional propagation of undulations. Distinct pools of premotor interneurons project along the ventral nerve cord to innervate all members of the A- and B-class motor neurons, modulating their oscillations, as well as promoting their bi-directional coupling. The two motor sub-circuits, which consist of oscillators and descending inputs with distinct properties, form the structural base of dynamic rhythmicity and flexible partition of the forward and backward motor states. These results contribute to a continuous effort to establish a mechanistic and dynamic model of the C. elegans sensorimotor system. C. elegans exhibits rich sensorimotor functions despite a small neuron number. These findings implicate a circuit-level functional compression. By integrating the role of rhythm generation and proprioception into motor neurons, and the role of descending regulation of oscillators into premotor interneurons, this numerically simple nervous system can achieve a circuit infrastructure analogous to that of anatomically complex systems. C. elegans has manifested itself as a compact model to search for general principles of sensorimotor behaviours. This article is part of a discussion meeting issue ‘Connectome to behaviour: modelling C. elegans at cellular resolution’.

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Dillon, J., N. A. Hopper, L. Holden-Dye, and V. O'Connor. "Molecular characterization of the metabotropic glutamate receptor family in Caenorhabditis elegans." Biochemical Society Transactions 34, no. 5 (2006): 942–48. http://dx.doi.org/10.1042/bst0340942.

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mGluRs (metabotropic glutamate receptors) are G-protein-coupled receptors that play an important neuromodulatory role in the brain. Glutamatergic transmission itself plays a fundamental role in the simple nervous system of the model organism Caenorhabditis elegans, but little is known about the contribution made by mGluR signalling. The sequenced genome of C. elegans predicts three distinct genes, mgl-1, mgl-2 and mgl-3 (designated Y4C6A.2). We have used in silico and cDNA analyses to investigate the genes encoding mgls. Our results indicate that mgl genes constitute a gene family made up of three distinct subclasses of receptor. Our transcript analysis highlights potential for complex gene regulation with respect to both expression and splicing. Further, we identify that the predicted proteins encoded by mgls harbour structural motifs that are likely to regulate function. Taken together, this molecular characterization provides a platform to further investigate mGluR function in the model organism C. elegans.

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Journal articles on the topic 'Nervous system Caenorhabditis elegans'

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