scholarly journals Structural and functional diversity in the neuronal microtubules of Caenorhabditis elegans.

1982 ◽  
Vol 93 (1) ◽  
pp. 15-23 ◽  
Author(s):  
M Chalfie ◽  
J N Thomson
Keyword(s):  
Caenorhabditis Elegans ◽  
Colchicine Treatment ◽  
Variable Number ◽  
Sensory Transduction ◽  
Partial Replacement ◽  
C Elegans ◽  
Touch Receptor Neurons ◽  
Touch Sensitivity ◽  
Receptor Neurons

Tannic acid fixation reveals differences in the number of protofilaments between microtubules (MTs) in the nematode Caenorhabditis elegans. Most cells have MTs with 11 protofilaments but the six touch receptor neurons (the microtubule cells) have MTs with 15 protofilaments. No 13-protofilament (13-p) MT has been seen. The modified cilia of sensory neurons also possess unusual structures. The cilia contain nine outer doublets with A subfibers of 13 protofilaments and B subfibers of 11 protofilaments and a variable number of inner singlet MTs containing 11 protofilaments. The 15-p MTs but not the 11-p MTs are eliminated by colchicine-treatment or by mutation of the gene mec-7. Concomitantly, touch sensitivity is also lost. However, whereas colchicine treatment leads to the loss of all MTs from the microtubule cells, mutations in mec-7 result in the partial replacement of the 15-p MTs with 11-p MTs. Benzimidazoles (benomyl and nocodazole) have more general effects on C. elegans (slow growth, severe uncoordination, and loss of processes from the ventral cord) but do not affect the 15-p MTs. Benomyl will, however, disrupt the replacement 11-p MTs found in the microtubule cells of mec-7 mutants. The 11-p and 15-p MTs also respond differently to temperature and fixation conditions. It is likely that either type of MT will suffice for the proper outgrowth of the microtubule cell process, but only the 15-p MT can function in the specialized role of sensory transduction of the microtubule cells.

scholarly journals Identification of Nonviable Genes Affecting Touch Sensitivity in Caenorhabditis elegans Using Neuronally Enhanced Feeding RNA Interference

2015 ◽  
Vol 5 (3) ◽  
pp. 467-475 ◽  
Author(s):  
Xiaoyin Chen ◽  
Margarete Diaz Cuadros ◽  
Martin Chalfie
Keyword(s):  
Rna Interference ◽  
Caenorhabditis Elegans ◽  
The Body ◽  
Genetic Screens ◽  
Tubulin Acetylation ◽  
Touch Receptor Neurons ◽  
Touch Sensitivity ◽  
Touch Response ◽  
Receptor Neurons ◽  
Neuronal Functions

Abstract Caenorhabditis elegans senses gentle touch along the body via six touch receptor neurons. Although genetic screens and microarray analyses have identified several genes needed for touch sensitivity, these methods miss pleiotropic genes that are essential for the viability, movement, or fertility of the animals. We used neuronally enhanced feeding RNA interference to screen genes that cause lethality or paralysis when mutated, and we identified 61 such genes affecting touch sensitivity, including five positive controls. We confirmed 18 genes by using available alleles, and further studied one of them, tag-170, now renamed txdc-9. txdc-9 preferentially affects anterior touch response but is needed for tubulin acetylation and microtubule formation in both the anterior and posterior touch receptor neurons. Our results indicate that neuronally enhanced feeding RNA interference screens complement traditional mutageneses by identifying additional nonviable genes needed for specific neuronal functions.

scholarly journals Comparing Caenorhabditis elegans gentle and harsh touch response behavior using a multiplexed hydraulic microfluidic device

2017 ◽  
Author(s):  
Patrick D. McClanahan ◽  
Joyce H. Xu ◽  
Christopher Fang-Yen
Keyword(s):  
Caenorhabditis Elegans ◽  
Microfluidic Device ◽  
Receptive Fields ◽  
The Body ◽  
Mechanical Stimuli ◽  
C Elegans ◽  
Response Characteristics ◽  
Touch Receptor Neurons ◽  
Touch Response ◽  
Receptor Neurons

AbstractThe roundworm Caenorhabditis elegans is an important model system for understanding the genetics and physiology of touch. Classical assays for C. elegans touch, which involve manually touching the animal with a probe and observing its response, are limited by their low throughput and qualitative nature. We developed a microfluidic device in which several dozen animals are subject to spatially localized mechanical stimuli with variable amplitude. The device contains 64 sinusoidal channels through which worms crawl, and hydraulic valves that deliver touch stimuli to the worms. We used this assay to characterize the behavioral responses to gentle touch stimuli and the less well studied harsh (nociceptive) touch stimuli. First, we measured the relative response thresholds of gentle and harsh touch. Next, we quantified differences in the receptive fields between wild type worms and a mutant with non-functioning posterior touch receptor neurons. We showed that under gentle touch the receptive field of the anterior touch receptor neurons extends into the posterior half of the body. Finally, we found that the behavioral response to gentle touch does not depend on the locomotion of the animal immediately prior to the stimulus, but does depend on the location of the previous touch. Responses to harsh touch, on the other hand, did not depend on either previous velocity or stimulus location. Differences in gentle and harsh touch response characteristics may reflect the different innervation of the respective mechanosensory cells. Our assay will facilitate studies of mechanosensation, sensory adaptation, and nociception.

Combinatorial control of touch receptor neuron expression in Caenorhabditis elegans

Development ◽  
1993 ◽  
Vol 119 (3) ◽  
pp. 773-783 ◽  
Author(s):  
S. Mitani ◽  
H. Du ◽  
D.H. Hall ◽  
M. Driscoll ◽  
M. Chalfie
Keyword(s):  
Caenorhabditis Elegans ◽  
Cell Types ◽  
Wild Type ◽  
Negative Regulators ◽  
C Elegans ◽  
Combinatorial Control ◽  
Touch Receptor Neurons ◽  
In The Wild ◽  
Receptor Neurons ◽  
Touch Receptor Neuron

Six touch receptor neurons with distinctive morphological features sense gentle touch in Caenorhabditis elegans. Previous studies have identified three genes (lin-32, unc-86 and mec-3) that regulate touch cell development. However, since other cell types also require these genes, we suspected that other genes help restrict the expression of touch cell characteristics to the six neurons seen in the wild type. To identify such genes, we have examined mutants defective in genes required for the development of other C. elegans cells for changes in the pattern of touch cell-specific features. Mutations in seven genes either reduce (lin-14) or increase (lin-4, egl-44, egl-46, sem-4, ced-3 and ced-4) the number of touch receptor-like cells. The combinatorial action of these genes, all of which are required for the production of many cell types, restrict the number of cells expressing touch receptor characteristics in wild-type animals by acting as positive and negative regulators and by removing cells by programmed cell death.

scholarly journals Regulated distribution of mitochondria in touch receptor neurons of C. elegans influences touch response

2020 ◽  
Author(s):  
Anjali Awasthi ◽  
Souvik Modi ◽  
Sneha Hegde ◽  
Anusheela Chatterjee ◽  
Sudip Mondal ◽  
...  
Keyword(s):  
Molecular Motors ◽  
Neuronal Function ◽  
Mitochondrial Density ◽  
Neuronal Process ◽  
C Elegans ◽  
Touch Receptor Neurons ◽  
Touch Response ◽  
Receptor Neurons ◽  
Touch Receptor Neuron

AbstractDensity of mitochondria and their localization at specific sub-cellular regions of the neurons is regulated by molecular motors, their adaptors and the cytoskeleton. However, the regulation of the mitochondrial density, the positioning of mitochondria along the neuronal process and the role of axonal mitochondria in neuronal function remain poorly understood. This study shows that the density of mitochondria in C. elegans touch receptor neuron processes remains constant through development. Simulations show that mitochondrial positioning along parts of the neuronal process that are devoid of synapses is regulated. Additionally, we also demonstrate that axonal mitochondria are necessary for maintaining touch responsiveness.

scholarly journals Characterization of Caenorhabditis elegans Homologs of the Down Syndrome Candidate Gene DYRK1A

Genetics ◽  
2003 ◽  
Vol 163 (2) ◽  
pp. 571-580 ◽  
Author(s):  
William B Raich ◽  
Celine Moorman ◽  
Clay O Lacefield ◽  
Jonah Lehrer ◽  
Dusan Bartsch ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Caenorhabditis Elegans ◽  
Trisomy 21 ◽  
Gene Dosage ◽  
Inducible Promoters ◽  
C Elegans ◽  
Dual Specificity ◽  
Specificity Protein

Abstract The pathology of trisomy 21/Down syndrome includes cognitive and memory deficits. Increased expression of the dual-specificity protein kinase DYRK1A kinase (DYRK1A) appears to play a significant role in the neuropathology of Down syndrome. To shed light on the cellular role of DYRK1A and related genes we identified three DYRK/minibrain-like genes in the genome sequence of Caenorhabditis elegans, termed mbk-1, mbk-2, and hpk-1. We found these genes to be widely expressed and to localize to distinct subcellular compartments. We isolated deletion alleles in all three genes and show that loss of mbk-1, the gene most closely related to DYRK1A, causes no obvious defects, while another gene, mbk-2, is essential for viability. The overexpression of DYRK1A in Down syndrome led us to examine the effects of overexpression of its C. elegans ortholog mbk-1. We found that animals containing additional copies of the mbk-1 gene display behavioral defects in chemotaxis toward volatile chemoattractants and that the extent of these defects correlates with mbk-1 gene dosage. Using tissue-specific and inducible promoters, we show that additional copies of mbk-1 can impair olfaction cell-autonomously in mature, fully differentiated neurons and that this impairment is reversible. Our results suggest that increased gene dosage of human DYRK1A in trisomy 21 may disrupt the function of fully differentiated neurons and that this disruption is reversible.

Potential role of protein stabilizers in amelioration of Parkinson's disease and associated effects in transgenic Caenorhabditis elegans model expressing alpha-synuclein

RSC Advances ◽  
2015 ◽  
Vol 5 (95) ◽  
pp. 77706-77715 ◽  
Author(s):  
Supinder Kaur ◽  
Aamir Nazir
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Caenorhabditis Elegans ◽  
Potential Role ◽  
Alpha Synuclein ◽  
C Elegans

Studies employing transgenicC. elegansmodel show that trehalose, a protein stabilizer, alleviates manifestations associated with Parkinson's diseaseviaits inherent activity and through induction of autophagic machinery.

scholarly journals Autophagosomes fuse to phagosomes and play important roles in the degradation of apoptotic cells in Caenorhabditis elegans

2021 ◽  
Author(s):  
Omar Pena-Ramos ◽  
Lucia Chiao ◽  
Xianghua Liu ◽  
Tianyou Yao ◽  
Henry He ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Small Gtpase ◽  
Apoptotic Cells ◽  
Phagosome Maturation ◽  
Double Membrane ◽  
C Elegans ◽  
Intracellular Organelles ◽  
Intracellular Vesicles ◽  
Cellular Components

Autophagosomes are double-membrane intracellular vesicles that degrade protein aggregates, intracellular organelles, and other cellular components. In the nematode Caenorhabditis elegans, 113 somatic cells undergo apoptosis during embryogenesis and are engulfed and degraded by their neighboring cells. We discovered a novel role of autophagosomes in facilitating the degradation of apoptotic cells in C. elegans embryos using a real-time imaging technique. Specifically, double-membrane autophagosomes in engulfing cells are recruited to the surfaces of phagosomes containing apoptotic cells and subsequently fuse to phagosomes, allowing the inner membrane to enter the phagosomal lumen. Mutants defective in the production of autophagosomes display significant delays in the degradation of apoptotic cells, demonstrating the important contribution of autophagosomes to this process. The signaling pathway led by the phagocytic receptor CED-1, CED-1s adaptor CED-6, and the large GTPase dynamin (DYN-1) promote the recruitment of autophagosomes to phagosomes. Moreover, the subsequent fusion of autophagosomes with phagosomes requires the functions of the small GTPase RAB-7 and the HOPS complex. Our findings reveal that, unlike the single-membrane, LC3- associated phagocytosis (LAP) vesicles reported for mammalian phagocytes, canonical autophagosomes function in the clearance of C. elegans apoptotic cells. These findings add autophagosomes to the collection of intracellular organelles that contribute to phagosome maturation, identify novel crosstalk between the autophagy and phagosome maturation pathways, and discover the upstream factors that initiate this crosstalk.

scholarly journals Distinct roles for innexin gap junctions and hemichannels in mechanosensation

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Denise S Walker ◽  
William R Schafer
Keyword(s):  
Blood Pressure ◽  
Heterologous Expression ◽  
Pain Perception ◽  
Mechanosensory Transduction ◽  
Wide Range ◽  
Touch Receptor Neurons ◽  
Touch Sensitivity ◽  
Range Of Functions ◽  
Receptor Neurons ◽  
And Control

Mechanosensation is central to a wide range of functions, including tactile and pain perception, hearing, proprioception, and control of blood pressure, but identifying the molecules underlying mechanotransduction has proved challenging. In Caenorhabditis elegans, the avoidance response to gentle body touch is mediated by six touch receptor neurons (TRNs), and is dependent on MEC-4, a DEG/ENaC channel. We show that hemichannels containing the innexin protein UNC-7 are also essential for gentle touch in the TRNs, as well as harsh touch in both the TRNs and the PVD nociceptors. UNC-7 and MEC-4 do not colocalize, suggesting that their roles in mechanosensory transduction are independent. Heterologous expression of unc-7 in touch-insensitive chemosensory neurons confers ectopic touch sensitivity, indicating a specific role for UNC-7 hemichannels in mechanosensation. The unc-7 touch defect can be rescued by the homologous mouse gene Panx1 gene, thus, innexin/pannexin proteins may play broadly conserved roles in neuronal mechanotransduction.

Mechanoreceptors and touch

2019 ◽  
pp. 76-98
Author(s):  
Gordon L. Fain
Keyword(s):  
Caenorhabditis Elegans ◽  
Molecular Biology ◽  
Stretch Receptor ◽  
Sensory Transduction ◽  
Merkel Cells ◽  
Anatomy And Physiology ◽  
Crayfish Stretch Receptor ◽  
Touch Sensitivity ◽  
Round Worm ◽  
Touch Sensation

“Mechanoreceptors and touch” is the fifth chapter of the book Sensory Transduction and describes general mechanisms of touch sensitivity in animals. It begins with a review of mechanoreception in the single-celled protozoan Paramecium and transduction of touch in the round worm Caenorhabditis elegans. A thorough treatment is next given of the crayfish stretch receptor and insect mechanoreceptors, including a description of NOMPC channels in Drosophila. The chapter then reviews the anatomy and physiology of mechanoreceptors and touch in mammals, both in glabrous and hairy skin. It concludes with recent discoveries of the molecular biology and physiology of Merkel cells, known to be responsible for much of mammalian touch sensation.

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