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 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 Luqin-like RYamide peptides regulate food-evoked responses in C. elegans

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Hayao Ohno ◽  
Morikatsu Yoshida ◽  
Takahiro Sato ◽  
Johji Kato ◽  
Mikiya Miyazato ◽  
...  
Keyword(s):  
Critical Role ◽  
Egg Laying ◽  
Serotonergic Neuron ◽  
Pacemaker Neurons ◽  
C Elegans ◽  
Peptide Signaling ◽  
Multiple Organs ◽  
Locomotory Behavior ◽  
Control Food ◽  
And Control

Peptide signaling controls many processes involving coordinated actions of multiple organs, such as hormone-mediated appetite regulation. However, the extent to which the mode of action of peptide signaling is conserved in different animals is largely unknown, because many peptides and receptors remain orphan and many undiscovered peptides still exist. Here, we identify two novel Caenorhabditis elegans neuropeptides, LURY-1-1 and LURY-1-2, as endogenous ligands for the neuropeptide receptor-22 (NPR-22). Both peptides derive from the same precursor that is orthologous to invertebrate luqin/arginine-tyrosine-NH2 (RYamide) proneuropeptides. LURY-1 peptides are secreted from two classes of pharyngeal neurons and control food-related processes: feeding, lifespan, egg-laying, and locomotory behavior. We propose that LURY-1 peptides transmit food signals to NPR-22 expressed in feeding pacemaker neurons and a serotonergic neuron. Our results identified a critical role for luqin-like RYamides in feeding-related processes and suggested that peptide-mediated negative feedback is important for satiety regulation in C. elegans.

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

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.

Ultrasound neuro-modulation chip: activation of sensory neurons in Caenorhabditis elegans by surface acoustic waves

Lab on a Chip ◽  
2017 ◽  
Vol 17 (10) ◽  
pp. 1725-1731 ◽  
Author(s):  
Wei Zhou ◽  
Jingjing Wang ◽  
Kaiyue Wang ◽  
Bin Huang ◽  
Lili Niu ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Sensory Neurons ◽  
Acoustic Waves ◽  
Surface Acoustic Waves ◽  
C Elegans

We demonstrate an ultrasound neuro-modulation chip capable of activating neurons of the C. elegans directly.

scholarly journals Sensory Neurons Arouse C. elegans Locomotion via Both Glutamate and Neuropeptide Release

PLoS Genetics ◽  
2015 ◽  
Vol 11 (7) ◽  
pp. e1005359 ◽  
Author(s):  
Seungwon Choi ◽  
Kelsey P. Taylor ◽  
Marios Chatzigeorgiou ◽  
Zhitao Hu ◽  
William R. Schafer ◽  
...  
Keyword(s):  
Sensory Neurons ◽  
C Elegans ◽  
Neuropeptide Release

scholarly journals Centriolar remodeling underlies basal body maturation during ciliogenesis in Caenorhabditis elegans

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Inna V Nechipurenko ◽  
Cristina Berciu ◽  
Piali Sengupta ◽  
Daniela Nicastro
Keyword(s):  
Electron Microscopy ◽  
High Resolution ◽  
Sensory Neurons ◽  
Basal Body ◽  
Three Dimensional ◽  
C Elegans ◽  
Mother Centriole ◽  
Section Electron ◽  
Serial Section Electron Microscopy ◽  
Section Electron Microscopy

The primary cilium is nucleated by the mother centriole-derived basal body (BB) via as yet poorly characterized mechanisms. BBs have been reported to degenerate following ciliogenesis in the C. elegans embryo, although neither BB architecture nor early ciliogenesis steps have been described in this organism. In a previous study (Doroquez et al., 2014), we described the three-dimensional morphologies of sensory neuron cilia in adult C. elegans hermaphrodites at high resolution. Here, we use serial section electron microscopy and tomography of staged C. elegans embryos to demonstrate that BBs remodel to support ciliogenesis in a subset of sensory neurons. We show that centriolar singlet microtubules are converted into BB doublets which subsequently grow asynchronously to template the ciliary axoneme, visualize degeneration of the centriole core, and define the developmental stage at which the transition zone is established. Our work provides a framework for future investigations into the mechanisms underlying BB remodeling.

Sign in / Sign up

Export Citation Format

Share Document