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

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.

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The C. elegans septin genes, unc-59 and unc-61, are required for normal postembryonic cytokineses and morphogenesis but have no essential function in embryogenesis

Journal of Cell Science ◽

10.1242/jcs.113.21.3825 ◽

2000 ◽

Vol 113 (21) ◽

pp. 3825-3837 ◽

Cited By ~ 4

Author(s):

T.Q. Nguyen ◽

H. Sawa ◽

H. Okano ◽

J.G. White

Keyword(s):

Caenorhabditis Elegans ◽

Embryonic Development ◽

Sensory Neurons ◽

Leading Edge ◽

The Other ◽

Male Tail ◽

Genomic Database ◽

C Elegans ◽

Essential Function ◽

Normal Embryonic Development

Septins have been shown to play important roles in cytokinesis in diverse organisms ranging from yeast to mammals. In this study, we show that both the unc-59 and unc-61 loci encode Caenorhabditis elegans septins. Genomic database searches indicate that unc-59 and unc-61 are probably the only septin genes in the C. elegans genome. UNC-59 and UNC-61 localize to the leading edge of cleavage furrows and eventually reside at the midbody. Analysis of unc-59 and unc-61 mutants revealed that each septin requires the presence of the other for localization to the cytokinetic furrow. Surprisingly, unc-59 and unc-61 mutants generally have normal embryonic development; however, defects were observed in post-embryonic development affecting the morphogenesis of the vulva, male tail, gonad, and sensory neurons. These defects can be at least partially attributed to failures in post-embryonic cytokineses although our data also suggest other possible roles for septins. unc-59 and unc-61 double mutants show similar defects to each of the single mutants.

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Regulatory changes in two chemoreceptor genes contribute to a Caenorhabditis elegans QTL for foraging behavior

eLife ◽

10.7554/elife.21454 ◽

2016 ◽

Vol 5 ◽

Cited By ~ 39

Author(s):

Joshua S Greene ◽

May Dobosiewicz ◽

Rebecca A Butcher ◽

Patrick T McGrath ◽

Cornelia I Bargmann

Keyword(s):

Caenorhabditis Elegans ◽

Foraging Behavior ◽

Sensory Neurons ◽

Exploratory Behavior ◽

Adaptive Variation ◽

C Elegans ◽

Regulatory Changes ◽

Naturally Occurring ◽

Genome Wide ◽

Natural Isolates

Natural isolates of C. elegans differ in their sensitivity to pheromones that inhibit exploratory behavior. Previous studies identified a QTL for pheromone sensitivity that includes alternative alleles of srx-43, a chemoreceptor that inhibits exploration through its activity in ASI sensory neurons. Here we show that the QTL is multigenic and includes alternative alleles of srx-44, a second chemoreceptor gene that modifies pheromone sensitivity. srx-44 either promotes or inhibits exploration depending on its expression in the ASJ or ADL sensory neurons, respectively. Naturally occurring pheromone insensitivity results in part from previously described changes in srx-43 expression levels, and in part from increased srx-44 expression in ASJ, which antagonizes ASI and ADL. Antagonism between the sensory neurons results in cellular epistasis that is reflected in their transcription of insulin genes that regulate exploration. These results and genome-wide evidence suggest that chemoreceptor genes may be preferred sites of adaptive variation in C. elegans.

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Regulation of Satiety Quiescence by Neuropeptide Signaling in Caenorhabditis elegans

Frontiers in Neuroscience ◽

10.3389/fnins.2021.678590 ◽

2021 ◽

Vol 15 ◽

Author(s):

Mei Makino ◽

Enkhjin Ulzii ◽

Riku Shirasaki ◽

Jeongho Kim ◽

Young-Jai You

Keyword(s):

Caenorhabditis Elegans ◽

Sensory Neurons ◽

Significant Role ◽

Sleep Cycle ◽

Over Expression ◽

C Elegans ◽

Feeding Cycle ◽

Cgmp Signaling ◽

Key Aspects ◽

Tgfβ Pathway

Sleep and metabolism are interconnected homeostatic states; the sleep cycle can be entrained by the feeding cycle, and perturbation of the sleep often results in dysregulation in metabolism. However, the neuro-molecular mechanism by which metabolism regulates sleep is not fully understood. We investigated how metabolism and feeding regulate sleep using satiety quiescence behavior as a readout in Caenorhabditis elegans, which shares certain key aspects of postprandial sleep in mammals. From an RNA interference-based screen of two neuropeptide families, RFamide-related peptides (FLPs) and insulin-like peptides (INSs), we identified flp-11, known to regulate other types of sleep-like behaviors in C. elegans, as a gene that plays the most significant role in satiety quiescence. A mutation in flp-11 significantly reduces quiescence, whereas over-expression of the gene enhances it. A genetic analysis shows that FLP-11 acts upstream of the cGMP signaling but downstream of the TGFβ pathway, suggesting that TGFβ released from a pair of head sensory neurons (ASI) activates FLP-11 in an interneuron (RIS). Then, cGMP signaling acting in downstream of RIS neurons induces satiety quiescence. Among the 28 INSs genes screened, ins-1, known to play a significant role in starvation-associated behavior working in AIA is inhibitory to satiety quiescence. Our study suggests that specific combinations of neuropeptides are released, and their signals are integrated in order for an animal to gauge its metabolic state and to control satiety quiescence, a feeding-induced sleep-like state in C. elegans.

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

eLife ◽

10.7554/elife.67670 ◽

2021 ◽

Vol 10 ◽

Cited By ~ 2

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.

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The Circuit for Chemotaxis and Exploratory Behavior in Caenorhabditis Elegans

Handbook of Brain Microcircuits ◽

10.1093/med/9780190636111.003.0031 ◽

2017 ◽

pp. 369-376

Author(s):

Cornelia I. Bargmann

Keyword(s):

Nervous System ◽

Caenorhabditis Elegans ◽

Sensory Neurons ◽

Motor Neurons ◽

Neuromuscular Junctions ◽

Wiring Diagram ◽

C Elegans ◽

Section Electron ◽

Adult Hermaphrodite ◽

Electrophysiological Characterization

A wiring diagram of the Caenorhabditis elegans nervous system was constructed from serial-section electron micrographs 30 years ago. This wiring diagram divides the 302 neurons in the nervous system of the adult hermaphrodite into three overall classes: sensory neurons, motor neurons that form neuromuscular junctions, and interneurons that connect sensory neurons with motor neurons. Most sensory neurons and interneurons belong to bilaterally symmetric pairs with similar connections and morphologies, while motor neurons belong to larger classes. The C. elegans nervous system presents an exceptional situation in which neuroanatomical connections are extremely well defined and reproducible among animals. These detailed anatomical studies and a parallel genetic attack have increasingly been joined by functional and electrophysiological characterization.

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Hierarchical sparse coding in the sensory system of Caenorhabditis elegans

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1423656112 ◽

2015 ◽

Vol 112 (4) ◽

pp. 1185-1189 ◽

Cited By ~ 57

Author(s):

Alon Zaslaver ◽

Idan Liani ◽

Oshrat Shtangel ◽

Shira Ginzburg ◽

Lisa Yee ◽

...

Keyword(s):

Caenorhabditis Elegans ◽

Sensory Neurons ◽

Single Neuron ◽

Sensory System ◽

Complex Environment ◽

C Elegans ◽

Calcium Indicator ◽

Functional Map ◽

Chemical Stimuli ◽

Encoding Strategy

Animals with compact sensory systems face an encoding problem where a small number of sensory neurons are required to encode information about its surrounding complex environment. Using Caenorhabditis elegans worms as a model, we ask how chemical stimuli are encoded by a small and highly connected sensory system. We first generated a comprehensive library of transgenic worms where each animal expresses a genetically encoded calcium indicator in individual sensory neurons. This library includes the vast majority of the sensory system in C. elegans. Imaging from individual sensory neurons while subjecting the worms to various stimuli allowed us to compile a comprehensive functional map of the sensory system at single neuron resolution. The functional map reveals that despite the dense wiring, chemosensory neurons represent the environment using sparse codes. Moreover, although anatomically closely connected, chemo- and mechano-sensory neurons are functionally segregated. In addition, the code is hierarchical, where few neurons participate in encoding multiple cues, whereas other sensory neurons are stimulus specific. This encoding strategy may have evolved to mitigate the constraints of a compact sensory system.

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The ETS-5 transcription factor regulates activity states in Caenorhabditis elegans by controlling satiety

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1610673114 ◽

2017 ◽

Vol 114 (9) ◽

pp. E1651-E1658 ◽

Cited By ~ 19

Author(s):

Vaida Juozaityte ◽

David Pladevall-Morera ◽

Agnieszka Podolska ◽

Steffen Nørgaard ◽

Brent Neumann ◽

...

Keyword(s):

Transcription Factor ◽

Caenorhabditis Elegans ◽

Sensory Neurons ◽

Animal Behavior ◽

Major Influence ◽

Behavioral State ◽

C Elegans ◽

State Switching ◽

Control Food ◽

Fat Stores

Animal behavior is shaped through interplay among genes, the environment, and previous experience. As in mammals, satiety signals induce quiescence in Caenorhabditis elegans. Here we report that the C. elegans transcription factor ETS-5, an ortholog of mammalian FEV/Pet1, controls satiety-induced quiescence. Nutritional status has a major influence on C. elegans behavior. When foraging, food availability controls behavioral state switching between active (roaming) and sedentary (dwelling) states; however, when provided with high-quality food, C. elegans become sated and enter quiescence. We show that ETS-5 acts to promote roaming and inhibit quiescence by setting the internal “satiety quotient” through fat regulation. Acting from the ASG and BAG sensory neurons, we show that ETS-5 functions in a complex network with serotonergic and neuropeptide signaling pathways to control food-regulated behavioral state switching. Taken together, our results identify a neuronal mechanism for controlling intestinal fat stores and organismal behavioral states in C. elegans, and establish a paradigm for the elucidation of obesity-relevant mechanisms.

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Characterization of RF Sputtered ZnO Piezoelectric Films Using Transmission Electron Microscope

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100114050 ◽

1975 ◽

Vol 33 ◽

pp. 86-87

Author(s):

Kemining W. Yeh ◽

Richard S. Muller ◽

Wei-Kuo Wu ◽

Jack Washburn

Keyword(s):

Integrated Circuit ◽

Acoustic Waves ◽

New Technology ◽

Surface Acoustic Waves ◽

Electromechanical Properties ◽

Leading Role ◽

Saw Devices ◽

Transmission Electron ◽

High Degree

Considerable and continuing interest has been shown in the thin film transducer fabrication for surface acoustic waves (SAW) in the past few years. Due to the high degree of miniaturization, compatibility with silicon integrated circuit technology, simplicity and ease of design, this new technology has played an important role in the design of new devices for communications and signal processing. Among the commonly used piezoelectric thin films, ZnO generally yields superior electromechanical properties and is expected to play a leading role in the development of SAW devices.

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