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Journal articles on the topic 'Elegans synapse'

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Author: Grafiati

Published: 10 December 2022

Last updated: 29 January 2023

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1

Fenyves, Bánk G., Gábor S. Szilágyi, Zsolt Vassy, Csaba Sőti, and Peter Csermely. "Synaptic polarity and sign-balance prediction using gene expression data in the Caenorhabditis elegans chemical synapse neuronal connectome network." PLOS Computational Biology 16, no. 12 (December 21, 2020): e1007974. http://dx.doi.org/10.1371/journal.pcbi.1007974.

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Graph theoretical analyses of nervous systems usually omit the aspect of connection polarity, due to data insufficiency. The chemical synapse network of Caenorhabditis elegans is a well-reconstructed directed network, but the signs of its connections are yet to be elucidated. Here, we present the gene expression-based sign prediction of the ionotropic chemical synapse connectome of C. elegans (3,638 connections and 20,589 synapses total), incorporating available presynaptic neurotransmitter and postsynaptic receptor gene expression data for three major neurotransmitter systems. We made predictions for more than two-thirds of these chemical synapses and observed an excitatory-inhibitory (E:I) ratio close to 4:1 which was found similar to that observed in many real-world networks. Our open source tool (http://EleganSign.linkgroup.hu) is simple but efficient in predicting polarities by integrating neuronal connectome and gene expression data.

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2

Kurup, Naina, Yunbo Li, Alexandr Goncharov, and Yishi Jin. "Intermediate filament accumulation can stabilize microtubules in Caenorhabditis elegans motor neurons." Proceedings of the National Academy of Sciences 115, no. 12 (March 6, 2018): 3114–19. http://dx.doi.org/10.1073/pnas.1721930115.

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Neural circuits utilize a coordinated cellular machinery to form and eliminate synaptic connections, with the neuronal cytoskeleton playing a prominent role. During larval development of Caenorhabditis elegans, synapses of motor neurons are stereotypically rewired through a process facilitated by dynamic microtubules (MTs). Through a genetic suppressor screen on mutant animals that fail to rewire synapses, and in combination with live imaging and ultrastructural studies, we find that intermediate filaments (IFs) stabilize MTs to prevent synapse rewiring. Genetic ablation of IFs or pharmacological disruption of IF networks restores MT growth and rescues synapse rewiring defects in the mutant animals, indicating that IF accumulation directly alters MT stability. Our work sheds light on the impact of IFs on MT dynamics and axonal transport, which is relevant to the mechanistic understanding of several human motor neuron diseases characterized by IF accumulation in axonal swellings.

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3

Narayan, A., G. Laurent, and P. W. Sternberg. "Transfer characteristics of a thermosensory synapse in Caenorhabditis elegans." Proceedings of the National Academy of Sciences 108, no. 23 (May 23, 2011): 9667–72. http://dx.doi.org/10.1073/pnas.1106617108.

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4

Brockie, P. J., and A. V. Maricq. "Building a synapse: genetic analysis of glutamatergic neurotransmission." Biochemical Society Transactions 34, no. 1 (January 20, 2006): 64–67. http://dx.doi.org/10.1042/bst0340064.

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Ionotropic glutamate receptors (iGluRs) are a critical component of the vertebrate central nervous system and mediate the majority of rapid excitatory neurotransmission. However, iGluRs are not self-regulating molecules and require additional proteins in order to function properly. Understanding the molecular architecture of functional glutamatergic synapses is therefore an important challenge in neurobiology. To address this question, we combine the techniques of genetics, molecular biology and electrophysiology in the nematode Caenorhabditis elegans. To date, genetic analysis has identified a number of genes required to build a glutamatergic synapse, including the CUB-domain transmembrane protein, SOL-1, which is thought to act as an auxiliary subunit that directly modifies iGluR function. Identifying and characterizing new proteins, such as SOL-1, in the relatively simple nervous system of the worm can contribute to our understanding of how more complex vertebrate nervous systems function.

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5

Zheng, Zhongfan, Xiumei Zhang, Junqiang Liu, Ping He, Shan Zhang, Yongning Zhang, Jie Gao, et al. "GABAergic synapses suppress intestinal innate immunity via insulin signaling in Caenorhabditis elegans." Proceedings of the National Academy of Sciences 118, no. 20 (May 10, 2021): e2021063118. http://dx.doi.org/10.1073/pnas.2021063118.

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GABAergic neurotransmission constitutes a major inhibitory signaling mechanism that plays crucial roles in central nervous system physiology and immune cell immunomodulation. However, its roles in innate immunity remain unclear. Here, we report that deficiency in the GABAergic neuromuscular junctions (NMJs) of Caenorhabditis elegans results in enhanced resistance to pathogens, whereas pathogen infection enhances the strength of GABAergic transmission. GABAergic synapses control innate immunity in a manner dependent on the FOXO/DAF-16 but not the p38/PMK-1 pathway. Our data reveal that the insulin-like peptide INS-31 level was dramatically decreased in the GABAergic NMJ GABAAR-deficient unc-49 mutant compared with wild-type animals. C. elegans with ins-31 knockdown or loss of function exhibited enhanced resistance to Pseudomonas aeruginosa PA14 exposure. INS-31 may act downstream of GABAergic NMJs and in body wall muscle to control intestinal innate immunity in a cell-nonautonomous manner. Our results reveal a signaling axis of synapse–muscular insulin–intestinal innate immunity in vivo.

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6

Yook, Karen J., Stephen R. Proulx, and Erik M. Jorgensen. "Rules of Nonallelic Noncomplementation at the Synapse in Caenorhabditis elegans." Genetics 158, no. 1 (May 1, 2001): 209–20. http://dx.doi.org/10.1093/genetics/158.1.209.

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Abstract Nonallelic noncomplementation occurs when recessive mutations in two different loci fail to complement one another, in other words, the double heterozygote exhibits a phenotype. We observed that mutations in the genes encoding the physically interacting synaptic proteins UNC-13 and syntaxin/UNC-64 failed to complement one another in the nematode Caenorhabditis elegans. Noncomplementation was not observed between null alleles of these genes and thus this genetic interaction does not occur with a simple decrease in dosage at the two loci. However, noncomplementation was observed if at least one gene encoded a partially functional gene product. Thus, this genetic interaction requires a poisonous gene product to sensitize the genetic background. Nonallelic noncomplementation was not limited to interacting proteins: Although the strongest effects were observed between loci encoding gene products that bind to one another, interactions were also observed between proteins that do not directly interact but are members of the same complex. We also observed noncomplementation between genes that function at distant points in the same pathway, implying that physical interactions are not required for nonallelic noncomplementation. Finally, we observed that mutations in genes that function in different processes such as neurotransmitter synthesis or synaptic development complement one another. Thus, this genetic interaction is specific for genes acting in the same pathway, that is, for genes acting in synaptic vesicle trafficking.

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7

Broadie, Kendal S., and Janet E. Richmond. "Establishing and sculpting the synapse in Drosophila and C. elegans." Current Opinion in Neurobiology 12, no. 5 (October 2002): 491–98. http://dx.doi.org/10.1016/s0959-4388(02)00359-8.

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8

Seifert, Mark, Enrico Schmidt, and Ralf Baumeister. "The genetics of synapse formation and function in Caenorhabditis elegans." Cell and Tissue Research 326, no. 2 (August 3, 2006): 273–85. http://dx.doi.org/10.1007/s00441-006-0277-2.

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9

Allen, Peter B., Allyson E. Sgro, Daniel L. Chao, Byron E. Doepker, J. Scott Edgar, Kang Shen, and Daniel T. Chiu. "Single-synapse ablation and long-term imaging in live C. elegans." Journal of Neuroscience Methods 173, no. 1 (August 2008): 20–26. http://dx.doi.org/10.1016/j.jneumeth.2008.05.007.

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10

Kreyden, Victoria A., Elly B. Mawi, Kristen M. Rush, and Jennifer R. Kowalski. "UBC-9 Acts in GABA Neurons to Control Neuromuscular Signaling in C. elegans." Neuroscience Insights 15 (January 2020): 263310552096279. http://dx.doi.org/10.1177/2633105520962792.

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Regulation of excitatory to inhibitory signaling balance is essential to nervous system health and is maintained by numerous enzyme systems that modulate the activity, localization, and abundance of synaptic proteins. SUMOylation is a key post-translational regulator of protein function in diverse cells, including neurons. There, its role in regulating synaptic transmission through pre- and postsynaptic effects has been shown primarily at glutamatergic central nervous system synapses, where the sole SUMO-conjugating enzyme Ubc9 is a critical player. However, whether Ubc9 functions globally at other synapses, including inhibitory synapses, has not been explored. Here, we investigated the role of UBC-9 and the SUMOylation pathway in controlling the balance of excitatory cholinergic and inhibitory GABAergic signaling required for muscle contraction in Caenorhabditis elegans. We found inhibition or overexpression of UBC-9 in neurons modestly increased muscle excitation. Similar and even stronger phenotypes were seen with UBC-9 overexpression specifically in GABAergic neurons, but not in cholinergic neurons. These effects correlated with accumulation of synaptic vesicle-associated proteins at GABAergic presynapses, where UBC-9 and the C. elegans SUMO ortholog SMO-1 localized, and with defects in GABA-dependent behaviors. Experiments involving expression of catalytically inactive UBC-9 [UBC-9(C93S)], as well as co-expression of UBC-9 and SMO-1, suggested wild type UBC-9 overexpressed alone may act via substrate sequestration in the absence of sufficient free SUMO, underscoring the importance of tightly regulated SUMO enzyme function. Similar effects on muscle excitation, GABAergic signaling, and synaptic vesicle localization occurred with overexpression of the SUMO activating enzyme subunit AOS-1. Together, these data support a model in which UBC-9 and the SUMOylation system act at presynaptic sites in inhibitory motor neurons to control synaptic signaling balance in C. elegans. Future studies will be important to define UBC-9 targets at this synapse, as well as mechanisms by which UBC-9 and the SUMO pathway are regulated.

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11

Labrousse, Arnaud M., Dixie-Lee Shurland, and Alexander M. van der Bliek. "Contribution of the GTPase Domain to the Subcellular Localization of Dynamin in the Nematode Caenorhabditis elegans." Molecular Biology of the Cell 9, no. 11 (November 1998): 3227–39. http://dx.doi.org/10.1091/mbc.9.11.3227.

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Caenorhabditis elegans dynamin is expressed at high levels in neurons and at lower levels in other cell types, consistent with the important role that dynamin plays in the recycling of synaptic vesicles. Indirect immunofluorescence showed that dynamin is concentrated along the dorsal and ventral nerve cords and in the synapse-rich nerve ring. Green fluorescent protein (GFP) fused to the N terminus of dynamin is localized to synapse-rich regions. Furthermore, this chimera was detected along the apical membrane of intestinal cells, in spermathecae, and in coelomocytes. Dynamin localization was not affected by disrupting axonal transport of synaptic vesicles in the unc-104 (kinesin) mutant. To investigate the alternative mechanisms that dynamin might use for translocation to the synapse, we systematically tested the localization of different protein domains by fusion to GFP. Localization of each chimera was measured in one specific neuron, the ALM. The GTPase, a middle domain, and the putative coiled coil each contribute to synaptic localization. Surprisingly, the pleckstrin homology domain and the proline-rich domain, which are known to bind to coated-pit constituents, did not contribute to synaptic localization. The GFP-GTPase chimera was most strongly localized, although the GTPase domain has no known interactions with proteins other than with dynamin itself. Our results suggest that different dynamin domains contribute to axonal transport and the sequestration of a pool of dynamin molecules in synaptic cytosol.

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12

Hendi, Ardalan, Mizuki Kurashina, and Kota Mizumoto. "Intrinsic and extrinsic mechanisms of synapse formation and specificity in C. elegans." Cellular and Molecular Life Sciences 76, no. 14 (April 29, 2019): 2719–38. http://dx.doi.org/10.1007/s00018-019-03109-1.

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13

Toth, M. L., I. Melentijevic, L. Shah, A. Bhatia, K. Lu, A. Talwar, H. Naji, et al. "Neurite Sprouting and Synapse Deterioration in the Aging Caenorhabditis elegans Nervous System." Journal of Neuroscience 32, no. 26 (June 27, 2012): 8778–90. http://dx.doi.org/10.1523/jneurosci.1494-11.2012.

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14

Klassen, Matthew P., and Kang Shen. "Wnt Signaling Positions Neuromuscular Connectivity by Inhibiting Synapse Formation in C. elegans." Cell 130, no. 4 (August 2007): 704–16. http://dx.doi.org/10.1016/j.cell.2007.06.046.

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15

Oliver, Devyn, Shankar Ramachandran, Alison Philbrook, Christopher M. Lambert, Ken C. Q. Nguyen, David H. Hall, and Michael M. Francis. "Kinesin-3 mediated axonal delivery of presynaptic neurexin stabilizes dendritic spines and postsynaptic components." PLOS Genetics 18, no. 1 (January 28, 2022): e1010016. http://dx.doi.org/10.1371/journal.pgen.1010016.

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The functional properties of neural circuits are defined by the patterns of synaptic connections between their partnering neurons, but the mechanisms that stabilize circuit connectivity are poorly understood. We systemically examined this question at synapses onto newly characterized dendritic spines of C. elegans GABAergic motor neurons. We show that the presynaptic adhesion protein neurexin/NRX-1 is required for stabilization of postsynaptic structure. We find that early postsynaptic developmental events proceed without a strict requirement for synaptic activity and are not disrupted by deletion of neurexin/nrx-1. However, in the absence of presynaptic NRX-1, dendritic spines and receptor clusters become destabilized and collapse prior to adulthood. We demonstrate that NRX-1 delivery to presynaptic terminals is dependent on kinesin-3/UNC-104 and show that ongoing UNC-104 function is required for postsynaptic maintenance in mature animals. By defining the dynamics and temporal order of synapse formation and maintenance events in vivo, we describe a mechanism for stabilizing mature circuit connectivity through neurexin-based adhesion.

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16

Baran, Renee, Liliana Castelblanco, Garland Tang, Ian Shapiro, Alexandr Goncharov, and Yishi Jin. "Motor Neuron Synapse and Axon Defects in a C. elegans Alpha-Tubulin Mutant." PLoS ONE 5, no. 3 (March 11, 2010): e9655. http://dx.doi.org/10.1371/journal.pone.0009655.

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17

Spilker, Kerri A., George J. Wang, Madina S. Tugizova, and Kang Shen. "Caenorhabditis elegans Muscleblind homolog mbl-1 functions in neurons to regulate synapse formation." Neural Development 7, no. 1 (2012): 7. http://dx.doi.org/10.1186/1749-8104-7-7.

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18

Husson, Steven J., Alexander Gottschalk, and Andrew M. Leifer. "Optogenetic manipulation of neural activity inC. elegans: From synapse to circuits and behaviour." Biology of the Cell 105, no. 6 (April 26, 2013): 235–50. http://dx.doi.org/10.1111/boc.201200069.

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19

Burgess, Robert W., Kevin A. Peterson, Michael J. Johnson, Jeffrey J. Roix, Ian C. Welsh, and Timothy P. O'Brien. "Evidence for a Conserved Function in Synapse Formation Reveals Phr1 as a Candidate Gene for Respiratory Failure in Newborn Mice." Molecular and Cellular Biology 24, no. 3 (February 1, 2004): 1096–105. http://dx.doi.org/10.1128/mcb.24.3.1096-1105.2004.

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ABSTRACT Genetic studies using a set of overlapping deletions centered at the piebald locus on distal mouse chromosome 14 have defined a genomic region associated with respiratory distress and lethality at birth. We have isolated and characterized the candidate gene Phr1 that is located within the respiratory distress critical genomic interval. Phr1 is the ortholog of the human Protein Associated with Myc as well as Drosophila highwire and Caenorhabditis elegans regulator of presynaptic morphology 1. Phr1 is expressed in the embryonic and postnatal nervous system. In mice lacking Phr1, the phrenic nerve failed to completely innervate the diaphragm. In addition, nerve terminal morphology was severely disrupted, comparable with the synaptic defects seen in the Drosophila hiw and C. elegans rpm-1 mutants. Although intercostal muscles were completely innervated, they also showed dysmorphic nerve terminals. In addition, sensory neuron terminals in the diaphragm were abnormal. The neuromuscular junctions showed excessive sprouting of nerve terminals, consistent with inadequate presynaptic stimulation of the muscle. On the basis of the abnormal neuronal morphology seen in mice, Drosophila, and C. elegans, we propose that Phr1 plays a conserved role in synaptic development and is a candidate gene for respiratory distress and ventilatory disorders that arise from defective neuronal control of breathing.

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20

Snider, Joseph. "Indistinguishable Synapses Lead to Sparse Networks." Neural Computation 30, no. 3 (March 2018): 708–22. http://dx.doi.org/10.1162/neco_a_01052.

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Neurons integrate information from many neighbors when they process information. Inputs to a given neuron are thus indistinguishable from one another. Under the assumption that neurons maximize their information storage, indistinguishability is shown to place a strong constraint on the distribution of strengths between neurons. The distribution of individual synapse strengths is found to follow a modified Boltzmann distribution with strength proportional to [Formula: see text]. The model is shown to be consistent with experimental data from Caenorhabditis elegans connectivity and in vivo synaptic strength measurements. The [Formula: see text] dependence helps account for the observation of many zero or weak connections between neurons or sparsity of the neural network.

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21

Shui, Yuan, Ping Liu, Haiying Zhan, Bojun Chen, and Zhao-Wen Wang. "Molecular basis of junctional current rectification at an electrical synapse." Science Advances 6, no. 27 (July 2020): eabb3076. http://dx.doi.org/10.1126/sciadv.abb3076.

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Rectifying electrical synapses (RESs) exist across animal species, but their rectification mechanism is largely unknown. We investigated why RESs between AVA premotor interneurons and A-type cholinergic motoneurons (A-MNs) in Caenorhabditis elegans escape circuit conduct junctional currents (Ij) only in the antidromic direction. These RESs consist of UNC-7 innexin in AVA and UNC-9 innexin in A-MNs. UNC-7 has multiple isoforms differing in the length and sequence of the amino terminus. In a heterologous expression system, only one UNC-7 isoform, UNC-7b, can form heterotypic gap junctions (GJs) with UNC-9 that strongly favor Ij in the UNC-9 to UNC-7 direction. Knockout of unc-7b alone almost eliminated the Ij, whereas AVA-specific expression of UNC-7b substantially rescued the coupling defect of unc-7 mutant. Neutralizing charged residues in UNC-7b amino terminus abolished the rectification property of UNC-7b/UNC-9 GJs. Our results suggest that the rectification property results from electrostatic interactions between charged residues in UNC-7b amino terminus.

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22

Ericson, Vivian R., Kerri A. Spilker, Madina S. Tugizova, and Kang Shen. "MTM-6, a Phosphoinositide Phosphatase, is Required to Promote Synapse Formation in Caenorhabditis elegans." PLoS ONE 9, no. 12 (December 5, 2014): e114501. http://dx.doi.org/10.1371/journal.pone.0114501.

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23

Nelson, J. C., and D. A. Colon-Ramos. "Serotonergic Neurosecretory Synapse Targeting Is Controlled by Netrin-Releasing Guidepost Neurons in Caenorhabditis elegans." Journal of Neuroscience 33, no. 4 (January 23, 2013): 1366–76. http://dx.doi.org/10.1523/jneurosci.3471-12.2012.

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24

Van Epps, H., Y. Dai, Y. Qi, A. Goncharov, and Y. Jin. "Nuclear pre-mRNA 3'-end processing regulates synapse and axon development in C. elegans." Development 137, no. 13 (June 8, 2010): 2237–50. http://dx.doi.org/10.1242/dev.049692.

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25

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 (December 14, 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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26

Baran, R., R. Aronoff, and G. Garriga. "The C. elegans homeodomain gene unc-42 regulates chemosensory and glutamate receptor expression." Development 126, no. 10 (May 15, 1999): 2241–51. http://dx.doi.org/10.1242/dev.126.10.2241.

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Genes that specify cell fate can influence multiple aspects of neuronal differentiation, including axon guidance, target selection and synapse formation. Mutations in the unc-42 gene disrupt axon guidance along the C. elegans ventral nerve cord and cause distinct functional defects in sensory-locomotory neural circuits. Here we show that unc-42 encodes a novel homeodomain protein that specifies the fate of three classes of neurons in the Caenorhabditis elegans nervous system: the ASH polymodal sensory neurons, the AVA, AVD and AVE interneurons that mediate repulsive sensory stimuli to the nematode head and anterior body, and a subset of motor neurons that innervate head and body-wall muscles. unc-42 is required for the expression of cell-surface receptors that are essential for the mature function of these neurons. In mutant animals, the ASH sensory neurons fail to express SRA-6 and SRB-6, putative chemosensory receptors. The AVA, AVD and AVE interneurons and RME and RMD motor neurons of unc-42 mutants similarly fail to express the GLR-1 glutamate receptor. These results show that unc-42 performs an essential role in defining neuron identity and contributes to the establishment of neural circuits in C. elegans by regulating the transcription of glutamate and chemosensory receptor genes.

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Edwards, Stacey L., Rosalina M. Yorks, Logan M. Morrison, Christopher M. Hoover, and Kenneth G. Miller. "Synapse-Assembly Proteins Maintain Synaptic Vesicle Cluster Stability and Regulate Synaptic Vesicle Transport inCaenorhabditis elegans." Genetics 201, no. 1 (September 2015): 91–116. http://dx.doi.org/10.1534/genetics.115.177337.

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28

Tulgren, Erik D., Scott T. Baker, Laramie Rapp, Allison M. Gurney, and Brock Grill. "PPM-1, a PP2Cα/β phosphatase, Regulates Axon Termination and Synapse Formation in Caenorhabditis elegans." Genetics 189, no. 4 (October 3, 2011): 1297–307. http://dx.doi.org/10.1534/genetics.111.134791.

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29

Yeh, E., S. Ng, T. Starich, J. Shaw, and M. Zhen. "[P64]: The C. elegans gap junction protein UNC‐7 is required for chemical synapse formation." International Journal of Developmental Neuroscience 24, no. 8 (November 16, 2006): 523. http://dx.doi.org/10.1016/j.ijdevneu.2006.09.127.

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30

Margeta, Milica A., Kang Shen, and Brock Grill. "Building a synapse: lessons on synaptic specificity and presynaptic assembly from the nematode C. elegans." Current Opinion in Neurobiology 18, no. 1 (February 2008): 69–76. http://dx.doi.org/10.1016/j.conb.2008.04.003.

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Meng, Lingfeng, Ben Mulcahy, Steven J. Cook, Marianna Neubauer, Airong Wan, Yishi Jin, and Dong Yan. "The Cell Death Pathway Regulates Synapse Elimination through Cleavage of Gelsolin in Caenorhabditis elegans Neurons." Cell Reports 11, no. 11 (June 2015): 1737–48. http://dx.doi.org/10.1016/j.celrep.2015.05.031.

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32

Mano, Itzhak, Sarah Straud, and Monica Driscoll. "Caenorhabditis elegans Glutamate Transporters Influence Synaptic Function and Behavior at Sites Distant from the Synapse." Journal of Biological Chemistry 282, no. 47 (November 2007): 34412–19. http://dx.doi.org/10.1074/jbc.m704134200.

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Pandey, Pratima, Anuradha Singh, Harjot Kaur, Anindya Ghosh-Roy, and Kavita Babu. "Increased dopaminergic neurotransmission results in ethanol dependent sedative behaviors in Caenorhabditis elegans." PLOS Genetics 17, no. 2 (February 1, 2021): e1009346. http://dx.doi.org/10.1371/journal.pgen.1009346.

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Ethanol is a widely used drug, excessive consumption of which could lead to medical conditions with diverse symptoms. Ethanol abuse causes dysfunction of memory, attention, speech and locomotion across species. Dopamine signaling plays an essential role in ethanol dependent behaviors in animals ranging from C. elegans to humans. We devised an ethanol dependent assay in which mutants in the dopamine autoreceptor, dop-2, displayed a unique sedative locomotory behavior causing the animals to move in circles while dragging the posterior half of their body. Here, we identify the posterior dopaminergic sensory neuron as being essential to modulate this behavior. We further demonstrate that in dop-2 mutants, ethanol exposure increases dopamine secretion and functions in a DVA interneuron dependent manner. DVA releases the neuropeptide NLP-12 that is known to function through cholinergic motor neurons and affect movement. Thus, DOP-2 modulates dopamine levels at the synapse and regulates alcohol induced movement through NLP-12.

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Lu, Ningning, Bo Chen, Jiao Qing, Jinhong Lei, Tongliang Wang, Haitao Shi, and Jichao Wang. "Transcriptome Analyses Provide Insights into the Auditory Function in Trachemys scripta elegans." Animals 12, no. 18 (September 14, 2022): 2410. http://dx.doi.org/10.3390/ani12182410.

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An auditory ability is essential for communication in vertebrates, and considerable attention has been paid to auditory sensitivity in mammals, birds, and frogs. Turtles were thought to be deaf for a long time; however, recent studies have confirmed the presence of an auditory ability in Trachemys scripta elegans as well as sex-related differences in hearing sensitivity. Earlier studies mainly focused on the morphological and physiological functions of the hearing organ in turtles; thus, the gene expression patterns remain unclear. In this study, 36 transcriptomes from six tissues (inner ear, tympanic membrane, brain, eye, lung, and muscle) were sequenced to explore the gene expression patterns of the hearing system in T. scripta elegans. A weighted gene co-expression network analysis revealed that hub genes related to the inner ear and tympanic membrane are involved in development and signal transduction. Moreover, we identified six differently expressed genes (GABRA1, GABRG2, GABBR2, GNAO1, SLC38A1, and SLC12A5) related to the GABAergic synapse pathway as candidate genes to explain the differences in sexually dimorphic hearing sensitivity. Collectively, this study provides a critical foundation for genetic research on auditory functions in turtles.

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35

Yan, Xiaojie, and Yuequan Shen. "Preliminary crystallographic analysis of the kinase domain of SAD-1, a protein essential for presynaptic differentiation inCaenorhabditis elegans." Acta Crystallographica Section F Structural Biology and Crystallization Communications 69, no. 4 (March 28, 2013): 449–52. http://dx.doi.org/10.1107/s1744309113006088.

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SAD-1 is a serine/threonine kinase which plays an important role in the regulation of both neuronal polarity and synapse formation inCaenorhabditis elegans. The kinase domain of SAD-1 fromC. eleganswas overexpressed inEscherichia coliBL21 (DE3) cells and purified to homogeneity using nickel–nitrilotriacetic acid metal-affinity, ion-exchange and gel-filtration chromatography. Diffraction-quality crystals were grown using the sitting-drop vapour-diffusion technique from a condition consisting of 1 MCAPSO pH 9.6, 10%(w/v) polyethylene glycol 3350. The crystals belonged to the monoclinic space groupC2, with unit-cell parametersa= 205.4,b= 57.1,c= 71.7 Å, β = 106.1°. X-ray diffraction data were recorded to 3.0 Å resolution from a single crystal using synchrotron radiation.

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Luo, S., A. M. Schaefer, S. Dour, and M. L. Nonet. "The conserved LIM domain-containing focal adhesion protein ZYX-1 regulates synapse maintenance in Caenorhabditis elegans." Journal of Cell Science 127, no. 21 (October 31, 2014): e1-e1. http://dx.doi.org/10.1242/jcs.164327.

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Jin, YiShi. "Unraveling the mechanisms of synapse formation and axon regeneration: the awesome power of C. elegans genetics." Science China Life Sciences 58, no. 11 (November 2015): 1084–88. http://dx.doi.org/10.1007/s11427-015-4962-9.

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Luo, S., A. M. Schaefer, S. Dour, and M. L. Nonet. "The conserved LIM domain-containing focal adhesion protein ZYX-1 regulates synapse maintenance in Caenorhabditis elegans." Development 141, no. 20 (September 24, 2014): 3922–33. http://dx.doi.org/10.1242/dev.108217.

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Miller, D. M., and C. J. Niemeyer. "Expression of the unc-4 homeoprotein in Caenorhabditis elegans motor neurons specifies presynaptic input." Development 121, no. 9 (September 1, 1995): 2877–86. http://dx.doi.org/10.1242/dev.121.9.2877.

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In the nematode, Caenorhabditis elegans, VA and VB motor neurons arise from a common precursor cell but adopt different morphologies and synapse with separate sets of interneurons in the ventral nerve cord. A mutation that inactivates the unc-4 homeodomain gene causes VA motor neurons to assume the VB pattern of synaptic input while retaining normal axonal polarity and output; the disconnection of VA motor neurons from their usual presynaptic partners blocks backward locomotion. We show that expression of a functional unc-4-beta-galactosidase chimeric protein in VA motor neurons restores wild-type movement to an unc-4 mutant. We propose that unc-4 controls a differentiated characteristic of the VA motor neurons that distinguishes them from their VB sisters, thus dictating recognition by the appropriate interneurons. Our results show that synaptic choice can be controlled at the level of transcription in the post-synaptic neuron and identify a homeoprotein that defines a subset of cell-specific traits required for this choice.

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Mahoney, Timothy R., Qiang Liu, Takashi Itoh, Shuo Luo, Gayla Hadwiger, Rose Vincent, Zhao-Wen Wang, Mitsunori Fukuda, and Michael L. Nonet. "Regulation of Synaptic Transmission by RAB-3 and RAB-27 in Caenorhabditis elegans." Molecular Biology of the Cell 17, no. 6 (June 2006): 2617–25. http://dx.doi.org/10.1091/mbc.e05-12-1170.

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Rab small GTPases are involved in the transport of vesicles between different membranous organelles. RAB-3 is an exocytic Rab that plays a modulatory role in synaptic transmission. Unexpectedly, mutations in the Caenorhabditis elegans RAB-3 exchange factor homologue, aex-3, cause a more severe synaptic transmission defect as well as a defecation defect not seen in rab-3 mutants. We hypothesized that AEX-3 may regulate a second Rab that regulates these processes with RAB-3. We found that AEX-3 regulates another exocytic Rab, RAB-27. Here, we show that C. elegans RAB-27 is localized to synapse-rich regions pan-neuronally and is also expressed in intestinal cells. We identify aex-6 alleles as containing mutations in rab-27. Interestingly, aex-6 mutants exhibit the same defecation defect as aex-3 mutants. aex-6; rab-3 double mutants have behavioral and pharmacological defects similar to aex-3 mutants. In addition, we demonstrate that RBF-1 (rabphilin) is an effector of RAB-27. Therefore, our work demonstrates that AEX-3 regulates both RAB-3 and RAB-27, that both RAB-3 and RAB-27 regulate synaptic transmission, and that RAB-27 potentially acts through its effector RBF-1 to promote soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) function.

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Tanis, J. E., A. Bellemer, J. J. Moresco, B. Forbush, and M. R. Koelle. "The Potassium Chloride Cotransporter KCC-2 Coordinates Development of Inhibitory Neurotransmission and Synapse Structure in Caenorhabditis elegans." Journal of Neuroscience 29, no. 32 (August 12, 2009): 9943–54. http://dx.doi.org/10.1523/jneurosci.1989-09.2009.

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Kurup, Naina, Dong Yan, Karina Kono, and Yishi Jin. "Differential regulation of polarized synaptic vesicle trafficking and synapse stability in neural circuit rewiring in Caenorhabditis elegans." PLOS Genetics 13, no. 6 (June 21, 2017): e1006844. http://dx.doi.org/10.1371/journal.pgen.1006844.

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Holden-Dye, Lindy, and Robert J. Walker. "Invertebrate models of behavioural plasticity and human disease." Brain and Neuroscience Advances 2 (January 2018): 239821281881806. http://dx.doi.org/10.1177/2398212818818068.

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The fundamental processes of neural communication have been largely conserved through evolution. Throughout the last century, researchers have taken advantage of this, and the experimental tractability of invertebrate animals, to advance understanding of the nervous system that translates to mammalian brain. This started with the inspired analysis of the ionic basis of neuronal excitability and neurotransmission using squid during the 1940s and 1950s and has progressed to detailed insight into the molecular architecture of the synapse facilitated by the genetic tractability of the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster. Throughout this time, invertebrate preparations have provided a means to link neural mechanisms to behavioural plasticity and thus key insight into fundamental aspects of control systems, learning, and memory. This article captures key highlights that exemplify the historical and continuing invertebrate contribution to neuroscience.

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Grill, B., L. Chen, E. D. Tulgren, S. T. Baker, W. Bienvenut, M. Anderson, M. Quadroni, Y. Jin, and C. C. Garner. "RAE-1, a Novel PHR Binding Protein, Is Required for Axon Termination and Synapse Formation in Caenorhabditis elegans." Journal of Neuroscience 32, no. 8 (February 22, 2012): 2628–36. http://dx.doi.org/10.1523/jneurosci.2901-11.2012.

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Jin, YiShi. "Erratum to: Unraveling the mechanisms of synapse formation and axon regeneration: the awesome power of C. elegans genetics." Science China Life Sciences 58, no. 12 (December 2015): 1306. http://dx.doi.org/10.1007/s11427-015-4978-1.

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Juo, Peter, Tom Harbaugh, Gian Garriga, and Joshua M. Kaplan. "CDK-5 Regulates the Abundance of GLR-1 Glutamate Receptors in the Ventral Cord of Caenorhabditis elegans." Molecular Biology of the Cell 18, no. 10 (October 2007): 3883–93. http://dx.doi.org/10.1091/mbc.e06-09-0818.

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The proline-directed kinase Cdk5 plays a role in several aspects of neuronal development. Here, we show that CDK-5 activity regulates the abundance of the glutamate receptor GLR-1 in the ventral cord of Caenorhabditis elegans and that it produces corresponding changes in GLR-1–dependent behaviors. Loss of CDK-5 activity results in decreased abundance of GLR-1 in the ventral cord, accompanied by accumulation of GLR-1 in neuronal cell bodies. Genetic analysis of cdk-5 and the clathrin adaptin unc-11 AP180 suggests that CDK-5 functions prior to endocytosis at the synapse. The scaffolding protein LIN-10/Mint-1 also regulates GLR-1 abundance in the nerve cord. CDK-5 phosphorylates LIN-10/Mint-1 in vitro and bidirectionally regulates the abundance of LIN-10/Mint-1 in the ventral cord. We propose that CDK-5 promotes the anterograde trafficking of GLR-1 and that phosphorylation of LIN-10 may play a role in this process.

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Chew, Yee Lian, Laura J. Grundy, André E. X. Brown, Isabel Beets, and William R. Schafer. "Neuropeptides encoded by nlp-49 modulate locomotion, arousal and egg-laying behaviours in Caenorhabditis elegans via the receptor SEB-3." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1758 (September 10, 2018): 20170368. http://dx.doi.org/10.1098/rstb.2017.0368.

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Neuropeptide signalling has been implicated in a wide variety of biological processes in diverse organisms, from invertebrates to humans. The Caenorhabditis elegans genome has at least 154 neuropeptide precursor genes, encoding over 300 bioactive peptides. These neuromodulators are thought to largely signal beyond ‘wired’ chemical/electrical synapse connections, therefore creating a ‘wireless’ network for neuronal communication. Here, we investigated how behavioural states are affected by neuropeptide signalling through the G protein-coupled receptor SEB-3, which belongs to a bilaterian family of orphan secretin receptors. Using reverse pharmacology, we identified the neuropeptide NLP-49 as a ligand of this evolutionarily conserved neuropeptide receptor. Our findings demonstrate novel roles for NLP-49 and SEB-3 in locomotion, arousal and egg-laying. Specifically, high-content analysis of locomotor behaviour indicates that seb-3 and nlp-49 deletion mutants cause remarkably similar abnormalities in movement dynamics, which are reversed by overexpression of wild-type transgenes. Overexpression of NLP-49 in AVK interneurons leads to heightened locomotor arousal, an effect that is dependent on seb-3. Finally, seb-3 and nlp-49 mutants also show constitutive egg-laying in liquid medium and alter the temporal pattern of egg-laying in similar ways. Together, these results provide in vivo evidence that NLP-49 peptides act through SEB-3 to modulate behaviour, and highlight the importance of neuropeptide signalling in the control of behavioural states. This article is part of a discussion meeting issue ‘Connectome to behaviour: modelling C. elegans at cellular resolution’.

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Starich, Todd A., Ji Xu, I. Martha Skerrett, Bruce J. Nicholson, and Jocelyn E. Shaw. "Interactions between innexins UNC-7 and UNC-9 mediate electrical synapse specificity in the Caenorhabditis elegans locomotory nervous system." Neural Development 4, no. 1 (2009): 16. http://dx.doi.org/10.1186/1749-8104-4-16.

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Fieseler, Charles, Manuel Zimmer, and J. Nathan Kutz. "Unsupervised learning of control signals and their encodings in Caenorhabditis elegans whole-brain recordings." Journal of The Royal Society Interface 17, no. 173 (December 2020): 20200459. http://dx.doi.org/10.1098/rsif.2020.0459.

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A major goal of computational neuroscience is to understand the relationship between synapse-level structure and network-level functionality. Caenorhabditis elegans is a model organism to probe this relationship due to the historic availability of the synaptic structure (connectome) and recent advances in whole brain calcium imaging techniques. Recent work has applied the concept of network controllability to neuronal networks, discovering some neurons that are able to drive the network to a certain state. However, previous work uses a linear model of the network dynamics, and it is unclear if the real neuronal network conforms to this assumption. Here, we propose a method to build a global, low-dimensional model of the dynamics, whereby an underlying global linear dynamical system is actuated by temporally sparse control signals. A key novelty of this method is discovering candidate control signals that the network uses to control itself. We analyse these control signals in two ways, showing they are interpretable and biologically plausible. First, these control signals are associated with transitions between behaviours, which were previously annotated via expert-generated features. Second, these signals can be predicted both from neurons previously implicated in behavioural transitions but also additional neurons previously unassociated with these behaviours. The proposed mathematical framework is generic and can be generalized to other neurosensory systems, potentially revealing transitions and their encodings in a completely unsupervised way.

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Thoreson, Wallace B., and Dwight A. Burkhardt. "Effects of synaptic blocking agents on the depolarizing responses of turtle cones evoked by surround illumination." Visual Neuroscience 5, no. 6 (December 1990): 571–83. http://dx.doi.org/10.1017/s0952523800000730.

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AbstractThe effects of synaptic blocking agents on the antagonistic surround of the receptive field of cone photoreceptors were studied intracellular recording in the retina of hte turtle (Pseudemys scripta elegans) Illumination of a cone's receptive-field surround typically evoked a hybriid depolarizing response composed of two componests: (1) the graded synaptic feedback depolarization and (2) the prolonged depolarization a distinctive, intrinsic response of the cone. The locus of action of synaptic blocking agents was analyzed by comparing their effects on the light-evoked response of horizontal cells, the hybrid cone depolarization evoked by surround illumination, and the pure prolonged depolarization evoked by intracellular current injection.The excitatory amino-acid antagonists, d-O-phosphoserine (DOS) and kynurenic acid (KynA), suppressed the light responses of horizontal cells and eliminated the surround-evoked, hybrid cone depolarization without affecting the prolonged depolarization evoked by current injection. Cobalt at 5–10 mM suppressed horizontal cell responses and thereby eliminated surround-evoked cone depolarizations. Cobalt (5–10 mM) also blocked the current-evoked prolonged depolarization, suggesting that the intrinsic cone mechanisms responsible for the prolonged depolarization are likely to be calcium-dependent.Various GABA agonists and antagonists were found to have no effect on the surround-evoked depolarizations of cones. In contrast, a very low concentration of cobalt (0.5 mM) selectively suppressed the light-evoked feedback depolarization of cones without affecting horizontal cell responses or the current-evoked prolonged depolarization. Cobalt at 0.5 mM thus blocks the light-evoked action of the cone feedback synapse while sparing feedforward synaptic transmission from cones to horizontal cells. The implications of the present work for the possible neurotransmitters used at these synapses is discussed.

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