scholarly journals Neuronally Produced Betaine Acts via a Novel Ligand Gated Ion Channel to Control Behavioural States

2021 ◽  
Author(s):  
Iris Hardege ◽  
Julia Morud ◽  
Jingfang Yu ◽  
Tatiana S Wilson ◽  
Frank Schroeder ◽  
...  
Keyword(s):  
Nervous System ◽  
Ion Channel ◽  
Molecular Mechanisms ◽  
Amino Acid Derivative ◽  
Single Pair ◽  
Complex Behaviour ◽  
Functional Roles ◽  
C Elegans ◽  
Nematode Worm ◽  
Control Complex

Trimethyl glycine, or betaine, is an amino acid derivative found in diverse organisms, from bacteria to plants and animals. It can function as an osmolyte to protect cells against osmotic stress, and building evidence suggests betaine may also play important functional roles in the nervous system. However, despite growing interest in betaine's roles in the nervous system, few molecular mechanisms have been elucidated. Here we identify the expression of betaine synthesis pathway genes in the nervous system of the nematode worm, C. elegans. We show that betaine, produced in a single pair of interneurons, the RIMs, can control complex behavioural states. Moreover, we also identify and characterise a new betaine-gated inhibitory ligand gated ion channel, LGC-41, which is required for betaine related behavioural changes. Intriguingly we observed expression of LGC-41 in punctate structures across several sensory and interneurons, including those synaptically connected to the RIMs. Our data presents a neuronal molecular mechanism for the action of betaine, via a specific receptor, in the control of complex behaviour within the nervous system of C. elegans. This may suggest a much broader role for betaine in the regulation of animal nervous systems than previously recognised.

Sensory activity affects sensory axon development in C. elegans

Development ◽  
1999 ◽  
Vol 126 (9) ◽  
pp. 1891-1902 ◽  
Author(s):  
E.L. Peckol ◽  
J.A. Zallen ◽  
J.C. Yarrow ◽  
C.I. Bargmann
Keyword(s):  
Nervous System ◽  
Molecular Mechanisms ◽  
Sensory Deprivation ◽  
Axon Growth ◽  
System Structure ◽  
Sensory Axon ◽  
C Elegans ◽  
Sensory Axons ◽  
Axon Development ◽  
Sensory Activity

The simple nervous system of the nematode C. elegans consists of 302 neurons with highly reproducible morphologies, suggesting a hard-wired program of axon guidance. Surprisingly, we show here that sensory activity shapes sensory axon morphology in C. elegans. A class of mutants with deformed sensory cilia at their dendrite endings have extra axon branches, suggesting that sensory deprivation disrupts axon outgrowth. Mutations that alter calcium channels or membrane potential cause similar defects. Cell-specific perturbations of sensory activity can cause cell-autonomous changes in axon morphology. Although the sensory axons initially reach their targets in the embryo, the mutations that alter sensory activity cause extra axon growth late in development. Thus, perturbations of activity affect the maintenance of sensory axon morphology after an initial pattern of innervation is established. This system provides a genetically tractable model for identifying molecular mechanisms linking neuronal activity to nervous system structure.

scholarly journals Erratum: Betaine acts on a ligand-gated ion channel in the nervous system of the nematode C. elegans

2014 ◽  
Vol 17 (12) ◽  
pp. 1840-1840
Author(s):  
Aude S Peden ◽  
Patrick Mac ◽  
You-Jun Fei ◽  
Cecilia Castro ◽  
Guoliang Jiang ◽  
...  
Keyword(s):  
Nervous System ◽  
Ion Channel ◽  
C Elegans

Multiple Roles of RNA Regulatory Factors in Neuronal Development and Function in C. elegans

2020 ◽  
Author(s):  
Matthew G. Andrusiak ◽  
Yishi Jin
Keyword(s):  
Nervous System ◽  
Cell Biology ◽  
Molecular Mechanisms ◽  
Neuronal Development ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Model Organism ◽  
Nervous System Development ◽  
Forward Genetics ◽  
C Elegans

Recent evidence has highlighted the dynamic nature of mRNA regulation, particularly in the nervous system, from complex pre-mRNA processing to long-range transport and long-term storage of mature mRNAs. In accordance with the importance for mRNA-mediated regulation of nervous system development and maintenance, various mutations in RNA-binding proteins are associated with a range of human disorders. C. elegans express many RNA-binding factors that have human orthologs and perform similar biochemical functions. This chapter focuses on the research using C. elegans to dissect molecular mechanisms involving mRNA-mediated pathways. It highlights the key approaches and findings that integrate genetic and genomic studies in the nervous system. The analyses of genetic mutants, primarily using forward genetics, offer functional insights for genes important for neuronal development, synaptic transmission, and neuronal repair. In combination with single-neuron cell biology and cell-type genomics, the knowledge learned from this model organism has continued to lead to ground-breaking discoveries.

scholarly journals Dietary supplementation with PUFAs rescues the eggshell defects caused by seipin mutations in C. elegans

2020 ◽  
Author(s):  
Xiaofei Bai ◽  
Leng-Jie Huang ◽  
Sheng-Wen Chen ◽  
Ben Nebenfuehr ◽  
Brian Wysolmerski ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Fatty Acid Biosynthesis ◽  
Gene Expression Pattern ◽  
Dietary Supplementation ◽  
Embryonic Lethality ◽  
Permeability Barrier ◽  
Deletion Mutants ◽  
Functional Roles ◽  
C Elegans ◽  
Barrier Formation

AbstractSEIPIN, an ER membrane protein, plays critical roles in lipid droplet (LD) formation and lipid storage. Dysfunction of SEIPIN causes a variety of human diseases, including lipodystrophy, neuropathies, and male and female infertility. However, the cellular and molecular mechanisms of SEIPIN in causing these diseases are poorly understood. To address such mechanisms, we investigated the functional roles of R01B10.6 (seip-1), the sole SEIPIN1 ortholog in C. elegans, using CRISPR/Cas9 gene editing, and transcriptional assays. SEIP-1::mScarlet is widely expressed throughout development in C. elegans. Three full gene deletion mutants, generated by CRISPR/Cas9, displayed penetrant embryonic lethality. EM imaging and the visualization of reporter genes revealed that the lipid-rich permeability barrier, the innermost layer of the C. elegans embryonic eggshell, was defective or missing. Intriguingly, depletion of SEIP-1 revealed a perturbed gene expression pattern for fatty acid biosynthesis enzymes, in agreement with the disrupted permeability barrier formation phenotype of the embryos. Lastly, dietary supplementation of PUFAs rescued the embryonic lethality and defective permeability barrier in the deletion mutants. In sum, our study suggests that SEIP-1 may maternally regulate LD biogenesis and maintain lipid homeostasis to orchestrate the formation of the lipid-rich permeability barrier, which is crucial for eggshell formation and embryogenesis.

scholarly journals Regulation of Gliogenesis by lin-32/Atoh1 in Caenorhabditis elegans

2020 ◽  
Vol 10 (9) ◽  
pp. 3271-3278 ◽  
Author(s):  
Albert Zhang ◽  
Kentaro Noma ◽  
Dong Yan
Keyword(s):  
Nervous System ◽  
Caenorhabditis Elegans ◽  
Embryonic Development ◽  
Molecular Mechanisms ◽  
System Development ◽  
Nervous System Development ◽  
Proneural Gene ◽  
C Elegans ◽  
Fundamental Process ◽  
Mutant Phenotypes

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.

scholarly journals Betaine acts on a ligand-gated ion channel in the nervous system of the nematode C. elegans

2013 ◽  
Vol 16 (12) ◽  
pp. 1794-1801 ◽  
Author(s):  
Aude S Peden ◽  
Patrick Mac ◽  
You-Jun Fei ◽  
Cecilia Castro ◽  
Guoliang Jiang ◽  
...  
Keyword(s):  
Nervous System ◽  
Ion Channel ◽  
C Elegans

scholarly journals The nematode worm C. elegans chooses between bacterial foods exactly as if maximizing economic utility

2021 ◽  
Author(s):  
Abraham Katzen ◽  
Hui-Kuan Chung ◽  
William Harbaugh ◽  
Christina Della Iacono ◽  
Nicholas Jackson ◽  
...  
Keyword(s):  
Decision Making ◽  
Nervous System ◽  
Utility Maximization ◽  
Sufficient Conditions ◽  
Food Choices ◽  
Growth Potential ◽  
C Elegans ◽  
Dopamine Signaling ◽  
Nematode Worm ◽  
As If

In value-based decision making, options are selected according to subjective values assigned by the individual to available goods and actions. Despite the importance of this faculty of the mind, the neural mechanisms of value assignments, and how choices are directed by them, remain obscure. To investigate this problem, we used a classic measure of utility maximization, the Generalized Axiom of Revealed Preference, to quantify internal consistency of food preferences in Caenorhabditis elegans, a nematode worm with a nervous system of only 302 neurons. Using a novel combination of microfluidics and electrophysiology, we found that C. elegans food choices fulfill the necessary and sufficient conditions for utility maximization, indicating that nematodes behave exactly as if they maintain, and attempt to maximize, an underlying representation of subjective value. Food choices are well-fit by a utility function widely used to model human consumers. Moreover, as in many other animals, subjective values in C. elegans are learned, a process we now find requires intact dopamine signaling. Differential responses of identified chemosensory neurons to foods with distinct growth potential are amplified by prior consumption of these foods, suggesting that these neurons may be part of a value-assignment system. The demonstration of utility maximization in an organism with a nervous system of only 302 neurons sets a new lower bound on the computational requirements for its execution, and offers the prospect of an essentially complete explanation of value-based decision making at single neuron resolution.

scholarly journals Sleep homeostasis regulated by 5HT2b receptor in a small subset of neurons in the dorsal fan-shaped body of drosophila

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Yongjun Qian ◽  
Yue Cao ◽  
Bowen Deng ◽  
Guang Yang ◽  
Jiayun Li ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Expression Patterns ◽  
Sleep Time ◽  
Small Subset ◽  
Single Pair ◽  
Functional Roles ◽  
Genetic Ablation ◽  
Shaped Body ◽  
Sleep Homeostasis ◽  
Impaired Sleep

Our understanding of the molecular mechanisms underlying sleep homeostasis is limited. We have taken a systematic approach to study neural signaling by the transmitter 5-hydroxytryptamine (5-HT) in drosophila. We have generated knockout and knockin lines for Trh, the 5-HT synthesizing enzyme and all five 5-HT receptors, making it possible for us to determine their expression patterns and to investigate their functional roles. Loss of the Trh, 5HT1a or 5HT2b gene decreased sleep time whereas loss of the Trh or 5HT2b gene diminished sleep rebound after sleep deprivation. 5HT2b expression in a small subset of, probably a single pair of, neurons in the dorsal fan-shaped body (dFB) is functionally essential: elimination of the 5HT2b gene from these neurons led to loss of sleep homeostasis. Genetic ablation of 5HT2b neurons in the dFB decreased sleep and impaired sleep homeostasis. Our results have shown that serotonergic signaling in specific neurons is required for the regulation of sleep homeostasis.

scholarly journals Conserved gene regulatory module specifies lateral neural borders across bilaterians

2017 ◽  
Vol 114 (31) ◽  
pp. E6352-E6360 ◽  
Author(s):  
Yongbin Li ◽  
Di Zhao ◽  
Takeo Horie ◽  
Geng Chen ◽  
Hongcun Bao ◽  
...  
Keyword(s):  
Nervous System ◽  
Molecular Mechanisms ◽  
Neural Progenitors ◽  
Expression Domain ◽  
Lateral Border ◽  
C Elegans ◽  
Regulatory Module ◽  
Neural Plate Border ◽  
Gene Regulatory ◽  
Conserved Gene

The lateral neural plate border (NPB), the neural part of the vertebrate neural border, is composed of central nervous system (CNS) progenitors and peripheral nervous system (PNS) progenitors. In invertebrates, PNS progenitors are also juxtaposed to the lateral boundary of the CNS. Whether there are conserved molecular mechanisms determining vertebrate and invertebrate lateral neural borders remains unclear. Using single-cell-resolution gene-expression profiling and genetic analysis, we present evidence that orthologs of the NPB specification module specify the invertebrate lateral neural border, which is composed of CNS and PNS progenitors. First, like in vertebrates, the conserved neuroectoderm lateral border specifier Msx/vab-15 specifies lateral neuroblasts in Caenorhabditis elegans. Second, orthologs of the vertebrate NPB specification module (Msx/vab-15, Pax3/7/pax-3, and Zic/ref-2) are significantly enriched in worm lateral neuroblasts. In addition, like in other bilaterians, the expression domain of Msx/vab-15 is more lateral than those of Pax3/7/pax-3 and Zic/ref-2 in C. elegans. Third, we show that Msx/vab-15 regulates the development of mechanosensory neurons derived from lateral neural progenitors in multiple invertebrate species, including C. elegans, Drosophila melanogaster, and Ciona intestinalis. We also identify a novel lateral neural border specifier, ZNF703/tlp-1, which functions synergistically with Msx/vab-15 in both C. elegans and Xenopus laevis. These data suggest a common origin of the molecular mechanism specifying lateral neural borders across bilaterians.

scholarly journals Preconditioning of Caenorhabditis elegans to Anoxic Insult by Inactivation of Cholinergic, GABAergic, and Muscle Activity

2020 ◽  
Author(s):  
Heather L. Bennett ◽  
Patrick D. McClanahan ◽  
Christopher Fang-Yen ◽  
Robert G. Kalb
Keyword(s):  
Nervous System ◽  
Chloride Channels ◽  
Body Wall ◽  
Molecular Mechanisms ◽  
Oxygen Deprivation ◽  
C Elegans ◽  
Cell Dysfunction ◽  
Sublethal Stress ◽  
Body Wall Muscles

AbstractFor most metazoans, oxygen deprivation leads to cell dysfunction and if severe, death. Sublethal stress prior to a hypoxic or anoxic insult (“preconditioning”) can protect cells from subsequent oxygen deprivation. The molecular mechanisms by which sublethal stress can buffer against a subsequent toxic insult and the role of the nervous system in the response are not well understood. We studied the role of neuronal activity preconditioning to oxygen deprivation in C. elegans. Animals expressing the histamine gated chloride channels (HisCl1) in select cell populations were used to temporally and spatially inactivate the nervous system or tissue prior to an anoxic insult. We find that inactivation of the nervous system for 3 hours prior to the insult confers resistance to a 48-hour anoxic insult in 4th-stage larval animals. Experiments show that this resistance can be attributed to loss of activity in cholinergic and GABAergic neurons as well as in body wall muscles. These observations indicate that the nervous system activity can mediate the organism’s response to anoxia.

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