scholarly journals Hierarchical sparse coding in the sensory system of Caenorhabditis elegans

2015 ◽  
Vol 112 (4) ◽  
pp. 1185-1189 ◽  
Author(s):  
Alon Zaslaver ◽  
Idan Liani ◽  
Oshrat Shtangel ◽  
Shira Ginzburg ◽  
Lisa Yee ◽  
...  

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.

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Mercedes M. Pérez-Jiménez ◽  
José M. Monje-Moreno ◽  
Ana María Brokate-Llanos ◽  
Mónica Venegas-Calerón ◽  
Alicia Sánchez-García ◽  
...  

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.


Author(s):  
Ramiro Lorenzo ◽  
Michiho Onizuka ◽  
Matthieu Defrance ◽  
Patrick Laurent

Abstract Single-cell RNA-sequencing (scRNA-seq) of the Caenorhabditis elegans nervous system offers the unique opportunity to obtain a partial expression profile for each neuron within a known connectome. Building on recent scRNA-seq data and on a molecular atlas describing the expression pattern of ∼800 genes at the single cell resolution, we designed an iterative clustering analysis aiming to match each cell-cluster to the ∼100 anatomically defined neuron classes of C. elegans. This heuristic approach successfully assigned 97 of the 118 neuron classes to a cluster. Sixty two clusters were assigned to a single neuron class and 15 clusters grouped neuron classes sharing close molecular signatures. Pseudotime analysis revealed a maturation process occurring in some neurons (e.g. PDA) during the L2 stage. Based on the molecular profiles of all identified neurons, we predicted cell fate regulators and experimentally validated unc-86 for the normal differentiation of RMG neurons. Furthermore, we observed that different classes of genes functionally diversify sensory neurons, interneurons and motorneurons. Finally, we designed 15 new neuron class-specific promoters validated in vivo. Amongst them, 10 represent the only specific promoter reported to this day, expanding the list of neurons amenable to genetic manipulations.


Lab on a Chip ◽  
2017 ◽  
Vol 17 (10) ◽  
pp. 1725-1731 ◽  
Author(s):  
Wei Zhou ◽  
Jingjing Wang ◽  
Kaiyue Wang ◽  
Bin Huang ◽  
Lili Niu ◽  
...  

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


Author(s):  
Chrisitian O. Pritz ◽  
Eyal Itskovits ◽  
Eduard Bokman ◽  
Rotem Ruach ◽  
Vladimir Gritsenko ◽  
...  

SummaryA major goal in neuroscience is to elucidate the principles by which memories are stored in a neural network. Here, we have systematically studied how the four types of associative memories (short- and long-term memories, each formed using positive and negative associations) are encoded within the compact neural network of C. elegans worms. Interestingly, short-term, but not long-term, memories are evident in the sensory system. Long-term memories are relegated to inner layers of the network, allowing the sensory system to resume innate functionality. Furthermore, a small set of sensory neurons is allocated for coding short-term memories, a design that can increase memory capacity and limit non-innate behavioral responses. Notably, individual sensory neurons may code for the conditioned stimulus or the experience valence. Interneurons integrate these information to modulate animal behavior upon memory reactivation. This comprehensive study reveals basic principles by which memories are encoded within a neural network, and highlights the central roles of sensory neurons in memory formation.


2000 ◽  
Vol 113 (21) ◽  
pp. 3825-3837 ◽  
Author(s):  
T.Q. Nguyen ◽  
H. Sawa ◽  
H. Okano ◽  
J.G. White

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.


Genetics ◽  
2009 ◽  
Vol 183 (3) ◽  
pp. 917-927 ◽  
Author(s):  
Claire Bénard ◽  
Nartono Tjoe ◽  
Thomas Boulin ◽  
Janine Recio ◽  
Oliver Hobert

Vertebrate and invertebrate genomes contain scores of small secreted or transmembrane proteins with two immunoglobulin (Ig) domains. Many of them are expressed in the nervous system, yet their function is not well understood. We analyze here knockout alleles of all eight members of a family of small secreted or transmembrane Ig domain proteins, encoded by the Caenorhabditis elegans zig (“zwei Ig Domänen”) genes. Most of these family members display the unusual feature of being coexpressed in a single neuron, PVT, whose axon is located along the ventral midline of C. elegans. One of these genes, zig-4, has previously been found to be required for maintaining axon position postembryonically in the ventral nerve cord of C. elegans. We show here that loss of zig-3 function results in similar postdevelopmental axon maintenance defects. The maintenance function of both zig-3 and zig-4 serves to counteract mechanical forces that push axons around, as well as various intrinsic attractive forces between axons that cause axon displacement if zig genes like zig-3 or zig-4 are deleted. Even though zig-3 is expressed only in a limited number of neurons, including PVT, transgenic rescue experiments show that zig-3 can function irrespective of which cell or tissue type it is expressed in. Double mutant analysis shows that zig-3 and zig-4 act together to affect axon maintenance, yet they are not functionally interchangeable. Both genes also act together with other, previously described axon maintenance factors, such as the Ig domain proteins DIG-1 and SAX-7, the C. elegans ortholog of the human L1 protein. Our studies shed further light on the use of dedicated factors to maintain nervous system architecture and corroborate the complexity of the mechanisms involved.


2015 ◽  
Vol 113 (8) ◽  
pp. E1082-E1088 ◽  
Author(s):  
Vivek Venkatachalam ◽  
Ni Ji ◽  
Xian Wang ◽  
Christopher Clark ◽  
James Kameron Mitchell ◽  
...  

We present an imaging system for pan-neuronal recording in crawling Caenorhabditis elegans. A spinning disk confocal microscope, modified for automated tracking of the C. elegans head ganglia, simultaneously records the activity and position of ∼80 neurons that coexpress cytoplasmic calcium indicator GCaMP6s and nuclear localized red fluorescent protein at 10 volumes per second. We developed a behavioral analysis algorithm that maps the movements of the head ganglia to the animal’s posture and locomotion. Image registration and analysis software automatically assigns an index to each nucleus and calculates the corresponding calcium signal. Neurons with highly stereotyped positions can be associated with unique indexes and subsequently identified using an atlas of the worm nervous system. To test our system, we analyzed the brainwide activity patterns of moving worms subjected to thermosensory inputs. We demonstrate that our setup is able to uncover representations of sensory input and motor output of individual neurons from brainwide dynamics. Our imaging setup and analysis pipeline should facilitate mapping circuits for sensory to motor transformation in transparent behaving animals such as C. elegans and Drosophila larva.


2017 ◽  
Author(s):  
Wataru Aoki ◽  
Hidenori Matsukura ◽  
Yuji Yamauchi ◽  
Haruki Yokoyama ◽  
Koichi Hasegawa ◽  
...  

ABSTRACTEven in Caenorhabditis elegans, which has only 302 neurons, relationships between behaviors and neural networks are not easily elucidated. In this study, we proposed a novel cellomics approach enabling high-throughput and comprehensive exploration of the functions of a single neuron or a subset of neurons in a complex neural network on a particular behavior. To realize this, we combined optogenetics and Brainbow technologies. Using these technologies, we established a C. elegans library where opsin is labeled in a randomized pattern. Behavioral analysis on this library under light illumination enabled high-throughput annotation of neurons affecting target behaviors. We applied this approach to the egg-laying behavior of C. elegans and succeeded in high-throughput confirmation that hermaphrodite-specific neurons play an important role in the egg-laying behavior. This cellomics approach will lead to the accumulation of neurophysiological and behavioral data of the C. elegans neural network, which is necessary for constructing neuroanatomically grounded models of behavior.


eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Joshua S Greene ◽  
May Dobosiewicz ◽  
Rebecca A Butcher ◽  
Patrick T McGrath ◽  
Cornelia I Bargmann

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.


2021 ◽  
Vol 15 ◽  
Author(s):  
Mei Makino ◽  
Enkhjin Ulzii ◽  
Riku Shirasaki ◽  
Jeongho Kim ◽  
Young-Jai You

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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