scholarly journals C. elegans Ciliated Sensory Neurons Release Extracellular Vesicles that Function in Animal Communication

2014 ◽  
Vol 24 (5) ◽  
pp. 519-525 ◽  
Author(s):  
Juan Wang ◽  
Malan Silva ◽  
Leonard A. Haas ◽  
Natalia S. Morsci ◽  
Ken C.Q. Nguyen ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Sensory Neurons ◽  
Animal Communication ◽  
C Elegans

scholarly journals Ectocytosis prevents accumulation of ciliary cargo in C. elegans sensory neurons

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Adria Razzauti ◽  
Patrick Laurent
Keyword(s):  
Caenorhabditis Elegans ◽  
Extracellular Vesicles ◽  
Sensory Neurons ◽  
Glial Cells ◽  
Cell Surfaces ◽  
C Elegans ◽  
Membrane Compartment ◽  
Safeguard Mechanism ◽  
Local Accumulation ◽  
Ciliated Neurons

Cilia are sensory organelles protruding from cell surfaces. Release of extracellular vesicles (EVs) from cilia was previously observed in mammals, Chlamydomonas, and in male Caenorhabditis elegans. Using the EV marker TSP-6 (an ortholog of mammalian CD9) and other ciliary receptors, we show that EVs are formed from ciliated sensory neurons in C. elegans hermaphrodites. Release of EVs is observed from two ciliary locations: the cilia tip and/or periciliary membrane compartment (PCMC). Outward budding of EVs from the cilia tip leads to their release into the environment. EVs’ budding from the PCMC is concomitantly phagocytosed by the associated glial cells. To maintain cilia composition, a tight regulation of cargo import and removal is achieved by the action of intra-flagellar transport (IFT). Unbalanced IFT due to cargo overexpression or mutations in the IFT machinery leads to local accumulation of ciliary proteins. Disposal of excess ciliary proteins via EVs reduces their local accumulation and exports them to the environment and/or to the glia associated to these ciliated neurons. We suggest that EV budding from cilia subcompartments acts as a safeguard mechanism to remove deleterious excess of ciliary material.

scholarly journals The G Protein regulators EGL-10 and EAT-16, the Giα GOA-1 and the Gqα EGL-30 modulate the response of the C. elegans ASH polymodal nociceptive sensory neurons to repellents

BMC Biology ◽  
2010 ◽  
Vol 8 (1) ◽  
pp. 138 ◽  
Author(s):  
Giovanni Esposito ◽  
Maria R Amoroso ◽  
Carmela Bergamasco ◽  
Elia Di Schiavi ◽  
Paolo Bazzicalupo
Keyword(s):  
G Protein ◽  
Sensory Neurons ◽  
C Elegans

scholarly journals Steroid hormones sulfatase inactivation extends lifespan and ameliorates age-related diseases

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Mercedes M. Pérez-Jiménez ◽  
José M. Monje-Moreno ◽  
Ana María Brokate-Llanos ◽  
Mónica Venegas-Calerón ◽  
Alicia Sánchez-García ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Caenorhabditis Elegans ◽  
Protein Aggregation ◽  
Steroid Hormones ◽  
Sensory Neurons ◽  
Environmental Cues ◽  
Steroid Sulfatase ◽  
Loss Of Function ◽  
C Elegans ◽  
Age Related

AbstractAging and fertility are two interconnected processes. From invertebrates to mammals, absence of the germline increases longevity. Here we show that loss of function of sul-2, the Caenorhabditis elegans steroid sulfatase (STS), raises the pool of sulfated steroid hormones, increases longevity and ameliorates protein aggregation diseases. This increased longevity requires factors involved in germline-mediated longevity (daf-16, daf-12, kri-1, tcer-1 and daf-36 genes) although sul-2 mutations do not affect fertility. Interestingly, sul-2 is only expressed in sensory neurons, suggesting a regulation of sulfated hormones state by environmental cues. Treatment with the specific STS inhibitor STX64, as well as with testosterone-derived sulfated hormones reproduces the longevity phenotype of sul-2 mutants. Remarkably, those treatments ameliorate protein aggregation diseases in C. elegans, and STX64 also Alzheimer’s disease in a mammalian model. These results open the possibility of reallocating steroid sulfatase inhibitors or derivates for the treatment of aging and aging related diseases.

scholarly journals Polymodal Functionality of C. elegans OLL Neurons in Mechanosensation and Thermosensation

2021 ◽  
Author(s):  
Yuedan Fan ◽  
Wenjuan Zou ◽  
Jia Liu ◽  
Umar Al-Sheikh ◽  
Hankui Cheng ◽  
...  
Keyword(s):  
Glutamate Receptor ◽  
Sensory Neurons ◽  
Molecular Mechanisms ◽  
Temperature Sensitive ◽  
Cold Sensation ◽  
Cold Response ◽  
C Elegans ◽  
Sensory Modalities ◽  
A Cell ◽  
Bona Fide

AbstractSensory modalities are important for survival but the molecular mechanisms remain challenging due to the polymodal functionality of sensory neurons. Here, we report the C. elegans outer labial lateral (OLL) sensilla sensory neurons respond to touch and cold. Mechanosensation of OLL neurons resulted in cell-autonomous mechanically-evoked Ca2+ transients and rapidly-adapting mechanoreceptor currents with a very short latency. Mechanotransduction of OLL neurons might be carried by a novel Na+ conductance channel, which is insensitive to amiloride. The bona fide mechano-gated Na+-selective degenerin/epithelial Na+ channels, TRP-4, TMC, and Piezo proteins are not involved in this mechanosensation. Interestingly, OLL neurons also mediated cold but not warm responses in a cell-autonomous manner. We further showed that the cold response of OLL neurons is not mediated by the cold receptor TRPA-1 or the temperature-sensitive glutamate receptor GLR-3. Thus, we propose the polymodal functionality of OLL neurons in mechanosensation and cold sensation.

scholarly journals A RasGRP, C. elegans RGEF-1b, Couples External Stimuli to Behavior by Activating LET-60 (Ras) in Sensory Neurons

Neuron ◽  
2011 ◽  
Vol 70 (1) ◽  
pp. 51-65 ◽  
Author(s):  
Lu Chen ◽  
Ya Fu ◽  
Min Ren ◽  
Bing Xiao ◽  
Charles S. Rubin
Keyword(s):  
Sensory Neurons ◽  
C Elegans ◽  
External Stimuli

Serotonergic neuron ADF modulates avoidance behaviors by inhibiting sensory neurons in C. elegans

2018 ◽  
Vol 471 (2) ◽  
pp. 357-363 ◽  
Author(s):  
Jiajie Shao ◽  
Xiaoyan Zhang ◽  
Hankui Cheng ◽  
Xiaomin Yue ◽  
Wenjuan Zou ◽  
...  
Keyword(s):  
Sensory Neurons ◽  
Serotonergic Neuron ◽  
C Elegans ◽  
Avoidance Behaviors

scholarly journals Knockout of glial channel ACD-1 exacerbates sensory deficits in a C. elegans mutant by regulating calcium levels of sensory neurons

2012 ◽  
Vol 107 (1) ◽  
pp. 148-158 ◽  
Author(s):  
Ying Wang ◽  
Giulia D'Urso ◽  
Laura Bianchi
Keyword(s):  
Sensory Neurons ◽  
Neuronal Excitability ◽  
Sensory Deficits ◽  
C Elegans ◽  
Hypomorphic Allele ◽  
Low Concentrations ◽  
Wide Range ◽  
Gated Channel ◽  
Intracellular Ca

Degenerin/epithelial Na+ channels (DEG/ENaCs) are voltage-independent Na+ or Na+/Ca2+ channels expressed in many tissues and are needed for a wide range of physiological functions, including sensory perception and transepithelial Na+ transport. In the nervous system, DEG/ENaCs are expressed in both neurons and glia. However, the role of glial vs. neuronal DEG/ENaCs remains unclear. We recently reported the characterization of a novel DEG/ENaC in Caenorhabditis elegans that we named ACD-1. ACD-1 is expressed in glial amphid sheath cells. The glial ACD-1, together with the neuronal DEG/ENaC DEG-1, is necessary for acid avoidance and attraction to lysine. We report presently that knockout of acd-1 in glia exacerbates sensory deficits caused by another mutant: the hypomorphic allele of the cGMP-gated channel subunit tax-2. Furthermore, sensory deficits caused by mutations in Gi protein odr-3 and guanylate cyclase daf-11, which regulate the activity of TAX-2/TAX-4 channels, are worsened by knockout of acd-1. We also show that sensory neurons of acd-1 tax-2(p694) double mutants fail to undergo changes in intracellular Ca2+ when animals are exposed to low concentrations of attractant. Finally, we show that exogenous expression of TRPV1 in sensory neurons and exposure to capsaicin rescue sensory deficits of acd-1 tax-2(p694) mutants, suggesting that sensory deficits of these mutants are bypassed by increasing neuronal excitability. Our data suggest a role of glial DEG/ENaC channel ACD-1 in supporting neuronal activity.

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