Chemosensory Neurons Research Articles

Neuroendocrine regulation of fat metabolism by autophagy gene atg-18 in C.elegans dauer larvae.

In environments with limited food and high population density, Caenorhabditis elegans larvae may enter the dauer stage, in which metabolism is shifted to fat accumulation to allow larvae to survive for months without food. Mutations in the insulin‐like receptor gene daf‐2 force C. elegans to constitutively form dauer larva at higher temperature. It has been reported that autophagy is required for fat accumulation in daf‐2 dauer larva. However, the mechanism underlying this process remains unknown. Here, we report that autophagy gene atg‐18 acts in a cell nonautonomous manner in neurons and intestinal cells to mediate the influence of daf‐2 signaling on fat metabolism. Moreover, ATG‐18 in chemosensory neurons plays a vital role in this metabolic process. Finally, we report that neuronal ATG‐18 functions through neurotransmitters to control fat storage in daf‐2 dauers, which suggests an essential role of autophagy in the neuroendocrine regulation of fat metabolism by insulin‐like signaling.

SUN-115 Role of Olfactory Marker Protein in High-Fat, Diet-Induced Obese Models

Obesity causes chronic diseases such as diabetes, hyperlipidemia, and stroke, which increase the mortality rate. Among the various studies on obesity, the role of the olfactory system to regulate energy homeostasis has been recently studied. Olfactory marker protein (OMP) is a cytoplasmic protein expressed primarily in mature chemosensory neurons in the main olfactory epithelium and involved in the olfactory receptor (OR)-mediated signal transduction cascade with olfactory canonical signaling components. Recently, the expression of OR-associated components including OMP has been observed in non-olfactory tissues where there are involved in monitoring extracellular ligands. In this study, we evaluated the role of OMP on development of obesity. We confirmed that non-olfactory OMP is expressed specifically in white adipose tissue, brown adipose tissue, and Liver of mice, as well as in 3T3-L1 cell line. To determine whether OMP mediates diet-induced obesity, we examined the influence of high-fat diet (HFD) on the wild type C57/BL6 mice and OMP knock-out (KO) mice. The amount of food intake was similar in both wild-type and mutants. Although there was no difference in normal chow diet fed mice, the KO mice gained less weight than wild-type mice in HFD condition. While there was no difference in lean body mass, fat mass was significantly reduced in OMP KO mice. In white adipose tissue (WAT), fat size of OMP KO mice was smaller than wild-type mice on both normal chow and HFD condition. The principal adipogenic transcription factor, PPARγ expression was significantly decreased in OMP KO mice, whereas UCP-1 and PGC-1α expression was increased than wild-type mice. Likewise, in brown adipose tissue (BAT), reduction of fat size was observed in OMP KO mice on HFD. Thermogenesis factor, UCP-1 and PGC-1α expression was up-regulated as well. In liver, it was confirmed that the formation of fatty liver due to the high fat diet was significantly reduced in the OMP KO mice. Taken together, our results suggest that loss of olfactory function increases beige localization of white fat, promotes thermogenesis through the expression of UCP-1 and PGC-1α in brown adipose tissue, and decreases the expression of lipogenesis related markers in liver tissue, resulting in decreased body fat and reduced diet-induced obesity.

The Influence of Chemesthesis on Taste Bud Signal Transduction

Chemesthesis, the general chemical sensitivity of the skin and mucus membranes in the oronasal cavities and being perceived as pungency, irritation or heat, impacts taste responsiveness. Previously, capsaicin‐mediated modulation of taste nerve responses was thought to be produced indirectly, via stimulation of peripheral sensory nerve terminals that have ability to release stored transmitters, e.g., calcitonin gene‐related peptide (CGRP) and substance P (SP), onto taste cells. this implies a role in gustatory signaling, by efferent signals from somatosensory neurons. The underlying assumption has been that neuropeptides exert their effects on taste transmitter secretion in taste buds of mice, a well‐accepted model for studying taste bud functions, as theoretically may relate to the processing of the gustatory information. We reported that applying CGRP elicited Type III cells to secrete serotonin (5‐HT), which reduced ATP secretion from Type II cells during the gustatory stimulation. The complex interplay between taste cells and chemosensory neurons, via transmitters, may play an important role during the processing of the complex stimuli involving both spicy and tasty components. Furthermore, to test this assumption, using a combination of Ca2+ imaging with cellular biosensors – genetically‐engineered Chinese Hamster Ovary (CHO) cells, transgenic mice expressing green fluorescent protein (GFP) in the specific taste cell type and immunostaining, we investigated the net effect of SP reduced taste‐evoked ATP secretion from mouse taste buds. Specifically, SP elicited phospholipase C (PLC) activation‐dependent intracellular Ca2+ transients in taste cells via neurokinin 1 (NK1) receptors, most likely on glutamate‐aspartate transporter (GLAST)‐expressing Type I cells. Recently, γ‐aminobutyric acid (GABA) as well as the associated synthetic enzyme have been identified in Type I cells. Consequently, Type I cells secrete GABA in respond to SP. Combined with the recent findings that GABA provides negative paracrine feedback onto Type II cells by activating GABAA and/or GABAB receptors and reducing taste‐evoked ATP secretion, our results showed that taste‐evoked ATP secretion from intact taste buds, which remain cell‐cell communication intact, was reduced when SP was co‐applied with taste stimuli in the bath medium. We conclude that SP plays a role as an inhibitory transmitter that shapes peripheral taste signals via GABAergic signaling during processing gustatory information in taste buds. This seemingly tangled complex represents a new concept of taste signaling and that neuropeptides released from afferent sensory terminals play a regulatory role in processing taste signals.Support or Funding InformationAAA FGAP (AAA‐3419) and SIUSOM Research Grants to AYH.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Endogenous siRNAs are required for a learned pathogen avoidance behavior in Caenorhabditis elegans

The nematode C. elegansis a premier model for the study of learning and exhibits a variety behavioral plasticity phenotypes. For example, worms that are infected by the pathogen Pseudomonas aeruginosa (PA14) early in life associate pathogen odors with infection, and learn to avoid the pathogen as adults when given a choice between PA14 and a nonpathogenic E. coli food source (OP50). This associative learning requires an increase in serotonin in the ADF chemosensory neurons, but the remaining molecular circuitry that allows learned pathogen avoidance is unknown. Based on the known role of small noncoding RNA molecules in regulating other behavioral responses in the worm, we have used a genetic approach to determine the involvement of endogenous small RNAs in pathogen avoidance behavior. Mutants that are defective in small RNA pathways were raised in an environment with both pathogenic PA14 and nonpathogenic OP50, and their pathogen avoidance behavior as adults was compared to that of wild‐type worms using a standard choice assay. For each genotype, we have completed at least three replicate choice assays of at least 71 worms each for the naïve and trained conditions. Briefly, the choice assay involves placing either trained or naïve worms in the center of a standard Nematode Growth Medium plate, and worms are allowed to choose between PA14 and OP50 food sources spotted on opposite sides of the plate. The number of worms found in the PA14 and OP50 spots is counted after an hour, and the proportion of worms on PA14 is compared between naïve and trained worms using a one‐tailed t‐test. As previously published, trained wild‐type worms (raised in the presence of pathogen) show increased avoidance of PA14 when compared with naïve worms (p=0.04369). Interestingly, mut‐7(pk204)animals, which lack a large class of small RNAs known as the endogenous siRNAs, show no change in pathogen avoidance when raised under naïve or trained conditions (p =0.86258), suggesting that endogenous siRNAs are required for learned pathogen avoidance. mut‐7is an upstream component of several functionally and genetically distinct endogenous siRNA pathways, including the 26G‐RNA and 21U RNA‐triggered pathways, the CSR‐1 pathway, and the WAGO pathway. To determine which of these pathways is specifically required for learned pathogen avoidance behavior, we are currently testing learning in mutants that disrupt individual pathways and will report on these results.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Hif-1 plays a role in hypoxia-induced gustatory plasticity of Caenorhabditis elegans

Background: Hypoxia-inducible factor 1 (HIF-1) is a key transcription factor in the detection of low oxygen levels, inducing expression of genes involved in mediating the response to hypoxia to maintain cellular oxygen homeostasis. Caenorhabditis elegans is a soil nematode that has evolved specialized chemosensory neurons that detect changes in oxygen levels and guide its behaviour and responses to food. The role of the hif-1 gene in modifying chemosensory behaviour in response to chemical hypoxia however remains unclear. Furthermore, the role of epigenetic modifiers in mediating this behavioural response to hypoxia is unclear.Aims: Our study addresses two questions (a) Do hypoxia-mimetics modify worm behaviour and (b) Are these behaviours modulated by HIF-dependent expression of epigenetic regulators?Material and methods: This study used established behavioural paradigms in hif-1 mutant strains of C. elegans, to study responses to chemical hypoxia.Results: We show that exposure to the hypoxia-mimetic, sodium sulphite, changes the gustatory responses, chemotaxis, gustatory plasticity and associative conditioning behaviour. Longer-term exposure to hypoxia changes the behavioural response of wild type C. elegans, mediated by the HIF pathway. Epigenetic modifiers, lithium chloride and valproic acid, further modulate these behavioural responses.

The role of PHOX2B-derived astrocytes in chemosensory control of breathing and sleep homeostasis.

The embryonic PHOX2B-progenitor domain generates neuronal and glial cells which together are involved in chemosensory control of breathing and sleep homeostasis. Ablating PHOX2B-derived astrocytes significantly contributes to secondary hypoxic respiratory depression as well as abnormalities in sleep homeostasis. PHOX2B-derived astrocyte ablation results in axonal pathologies in the retrotrapezoid nucleus. We identify in mice a population of ∼800 retrotrapezoid nucleus (RTN) astrocytes derived from PHOX2B-positive, OLIG3-negative progenitor cells, that interact with PHOX2B-expressing RTN chemosensory neurons. PHOX2B-derived astrocyte ablation during early life results in adult-onset O2 chemoreflex deficiency. These animals also display changes in sleep homeostasis, including fragmented sleep and disturbances in delta power after sleep deprivation, all without observable changes in anxiety or social behaviours. Ultrastructural evaluation of the RTN demonstrates that PHOX2B-derived astrocyte ablation results in features characteristic of degenerative neuro-axonal dystrophy, including abnormally dilated axon terminals and increased amounts of synapses containing autophagic vacuoles/phagosomes. We conclude that PHOX2B-derived astrocytes are necessary for maintaining a functional O2 chemosensory reflex in the adult, modulate sleep homeostasis, and are key regulators of synaptic integrity in the RTN region, which is necessary for the chemosensory control of breathing. These data also highlight how defects in embryonic development may manifest as neurodegenerative pathology in an adult.

Parallel Multimodal Circuits Control an Innate Foraging Behavior

Foraging strategies emerge from genetically encoded programs that are similar across animal species. Here, we examine circuits that control a conserved foraging state, local search behavior after food removal, in Caenorhabditis elegans. We show that local search is triggered by two parallel groups of chemosensory and mechanosensory glutamatergic neurons that detect food-related cues. Each group of sensory neurons suppresses distinct integrating neurons through a G protein-coupled metabotropic glutamate receptor, MGL-1, to release local search. The chemosensory and mechanosensory modules are separate and redundant; glutamate release from either module can drive the full behavior. A transition from local search to global search over several minutes after food removal is associated with two changes in circuit function. First, the spontaneous activity of sensory neurons falls. Second, the motor pattern generator for local search becomes less responsive to sensory input. This multimodal, distributed short-term food memory provides robust control of an innate behavior.

Cold acclimation via the KQT-2 potassium channel is modulated by oxygen in Caenorhabditis elegans.

Adaptive responses to external temperatures are essential for survival in changing environments. We show here that environmental oxygen concentration affects cold acclimation in Caenorhabditis elegans and that this response is regulated by a KCNQ-type potassium channel, KQT-2. Depending on culture conditions, kqt-2 mutants showed supranormal cold acclimation, caused by abnormal thermosensation in ADL chemosensory neurons. ADL neurons are responsive to temperature via transient receptor potential channels-OSM-9, OCR-2, and OCR-1-with OCR-1 negatively regulating ADL function. Similarly, KQT-2 and KQT-3 regulate ADL activity, with KQT-2 positively regulating ADL function. Abnormal cold acclimation and acute temperature responses of ADL neurons in kqt-2 mutants were suppressed by an oxygen-receptor mutation in URX coelomic sensory neurons, which are electrically connected to ADL via RMG interneurons. Likewise, low oxygen suppressed supranormal kqt-2 cold acclimation. These data thus demonstrate a simple neuronal circuit integrating two different sensory modalities, temperature and oxygen, that determines cold acclimation.

Repression of an activity-dependent autocrine insulin signal is required for sensory neuron development in C. elegans.

Nervous system development is instructed by genetic programs and refined by distinct mechanisms that couple neural activity to gene expression. How these processes are integrated remains poorly understood. Here, we report that the regulated release of insulin-like peptides (ILPs) during development of the Caenorhabditis elegans nervous system accomplishes such an integration. We find that the p38 MAP kinase PMK-3, which is required for the differentiation of chemosensory BAG neurons, limits an ILP signal that represses expression of a BAG neuron fate. ILPs are released from BAGs themselves in an activity-dependent manner during development, indicating that ILPs constitute an autocrine signal that regulates the differentiation of BAG neurons. Expression of a specialized neuronal fate is, therefore, coordinately regulated by a genetic program that sets levels of ILP expression during development, and by neural activity, which regulates ILP release. Autocrine signals of this kind might have general and conserved functions as integrators of deterministic genetic programs with activity-dependent mechanisms during neurodevelopment.

Lineage context switches the function of a C. elegans Pax6 homolog in determining a neuronal fate.

The sensory nervous system of C. elegans comprises cells with varied molecular and functional characteristics, and is, therefore, a powerful model for understanding mechanisms that generate neuronal diversity. We report here that VAB-3, a C. elegans homolog of the homeodomain-containing protein Pax6, has opposing functions in regulating expression of a specific chemosensory fate. A homeodomain-only short isoform of VAB-3 is expressed in BAG chemosensory neurons, where it promotes gene expression and cell function. In other cells, a long isoform of VAB-3, comprising a Paired homology domain and a homeodomain, represses expression of ETS-5, a transcription factor required for expression of BAG fate. Repression of ets-5 requires the Eyes Absent homolog EYA-1 and the Six-class homeodomain protein CEH-32. We determined sequences that mediate high-affinity binding of ETS-5, VAB-3 and CEH-32. The ets-5 locus is enriched for ETS-5-binding sites but lacks sequences that bind VAB-3 and CEH-32, suggesting that these factors do not directly repress ets-5 expression. We propose that a promoter-selection system together with lineage-specific expression of accessory factors allows VAB-3/Pax6 to either promote or repress expression of specific cell fates in a context-dependent manner. This article has an associated 'The people behind the papers' interview.

Gene expression profiling of the olfactory tissues of sex-separated and sex-combined female and male mice

Olfactory experience can alter the molecular and cellular composition of chemosensory neurons within the olfactory sensory epithelia of mice. We sought to investigate the scope of cellular and molecular changes within a mouse’s olfactory system as a function of its exposure to complex and salient sets of odors: those emitted from members of the opposite sex. We housed mice either separated from members of the opposite sex (sex-separated) or together with members of the opposite sex (sex-combined) until six months of age, resulting in the generation of four cohorts of mice. From each mouse, the main olfactory epithelium (MOE), vomeronasal organ (VNO), and olfactory bulb (OB) were removed and RNA-extracted. A total of 36 RNA samples, representing three biological replicates per sex/condition/tissue combination, were analyzed for integrity and used to prepare RNA-seq libraries, which were subsequently analyzed via qPCR for the presence of tissue- or sex-specific markers. Libraries were paired-end sequenced to a depth of ~20 million fragments per replicate and the data were analyzed using the Tuxedo suite.

A novel sex difference in Drosophila contact chemosensory neurons unveiled using single cell labeling

Among the sensory modalities involved in controlling mating behavior in Drosophila melanogaster, contact sex pheromones play a primary role. The key receptor neurons for contact sex pheromones are located on the forelegs, which are activated in males upon touching the female abdomen during tapping events in courtship actions. A fruitless (fru)-positive (fru [+]) male-pheromone sensing cell (M-cell) and a fru [+] female-pheromone sensing cell (F-cell) are paired in a sensory bristle on the legs, and some fru [+] chemoreceptor axons project across the midline in the thoracic neuromere in males but not in females. However, the receptor cells that form sexually dimorphic axon terminals in the thoracic ganglia remain unknown. By generating labeled single-cell clones, we show that only a specific subset of fru [+] chemosensory neurons have axons that cross the midline in males. We further demonstrate that there exist two male-specific bristles, each harboring two chemosensory neurons; neither of which exhibits midline crossing, a masculine characteristic. This study reveals hitherto unrecognized sex differences in chemosensory neurons, imposing us to reinvestigate the pheromone input pathways that impinge on the central courtship circuit.

Insect Pheromone Receptors - Key Elements in Sensing Intraspecific Chemical Signals.

Pheromones are chemicals that serve intraspecific communication. In animals, the ability to detect and discriminate pheromones in a complex chemical environment substantially contributes to the survival of the species. Insects widely use pheromones to attract mating partners, to alarm conspecifics or to mark paths to rich food sources. The various functional roles of pheromones for insects are reflected by the chemical diversity of pheromonal compounds. The precise detection of the relevant intraspecific signals is accomplished by specialized chemosensory neurons housed in hair-like sensilla located on the surface of body appendages. Current data indicate that the extraordinary sensitivity and selectivity of the pheromone-responsive neurons (PRNs) is largely based on specific pheromone receptors (PRs) residing in their ciliary membrane. Besides these key elements, proper ligand-induced responses of PR-expressing neurons appear to generally require a putative co-receptor, the so-called “sensory neuron membrane protein 1” (SNMP1). Regarding the PR-mediated chemo-electrical signal transduction processes in insect PRNs, ionotropic as well as metabotropic mechanisms may be involved. In this review, we summarize and discuss current knowledge on the peripheral detection of pheromones in the olfactory system of insects with a focus on PRs and their specific role in the recognition and transduction of volatile intraspecific chemical signals.

Mutations in the guanylate cyclase gcy-28 neuronally dissociate naïve attraction and memory retrieval.

The molecules and mechanisms that are involved in the acquisition, storage, and retrieval of memories in many organisms are unclear. To investigate these processes, we use the nematode worm Caenorhabditis elegans, which is attracted naïvely to the odorant benzaldehyde but learns to avoid it after paired exposure with starvation. Mutations in the receptor-like guanylate cyclase GCY-28 have previously been thought to result in a behavioral switch in the primary chemosensory neuron AWCON , from an attractive state to an aversive (already-learned) state. Here, we offer a different interpretation and show that GCY-28 functions in distinct neurons to modulate two independent processes: naïve attraction to AWCON -sensed odors in the AWCON neuron, and associative learning of benzaldehyde and starvation in the AIA interneurons. Consequently, mutants that lack gcy-28 do not approach AWCON -sensed odors and cannot associate benzaldehyde with starvation. We further show that this learning deficit lies in memory retrieval, not in its acquisition or storage, and that GCY-28 is required in AIA for sensory integration only when both AWC neurons (ON and OFF) are activated by chemical stimuli. Our results reveal a novel role of GCY-28 in the retrieval of associative memories and may have wide implications for the neural machineries of learning and memory in general.

Neuropeptide Signaling Regulates Pheromone-Mediated Gene Expression of a Chemoreceptor Gene in C. elegans.

Animals need to be able to alter their developmental and behavioral programs in response to changing environmental conditions. This developmental and behavioral plasticity is mainly mediated by changes in gene expression. The knowledge of the mechanisms by which environmental signals are transduced and integrated to modulate changes in sensory gene expression is limited. Exposure to ascaroside pheromone has been reported to alter the expression of a subset of putative G protein-coupled chemosensory receptor genes in the ASI chemosensory neurons of C. elegans (Kim et al., 2009; Nolan et al., 2002; Peckol et al., 1999). Here we show that ascaroside pheromone reversibly represses expression of the str-3 chemoreceptor gene in the ASI neurons. Repression of str-3 expression can be initiated only at the L1 stage, but expression is restored upon removal of ascarosides at any developmental stage. Pheromone receptors including SRBC-64/66 and SRG-36/37 are required for str-3 repression. Moreover, pheromone-mediated str-3 repression is mediated by FLP-18 neuropeptide signaling via the NPR-1 neuropeptide receptor. These results suggest that environmental signals regulate chemosensory gene expression together with internal neuropeptide signals which, in turn, modulate behavior.

Food perception without ingestion leads to metabolic changes and irreversible developmental arrest in C. elegans

BackgroundDevelopmental physiology is very sensitive to nutrient availability. For instance, in the nematode Caenorhabditis elegans, newly hatched L1-stage larvae require food to initiate postembryonic development. In addition, larvae arrested in the dauer diapause, a non-feeding state of developmental arrest that occurs during the L3 stage, initiate recovery when exposed to food. Despite the essential role of food in C. elegans development, the contribution of food perception versus ingestion on physiology has not been delineated.ResultsWe used a pharmacological approach to uncouple the effects of food (bacteria) perception and ingestion in C. elegans. Perception was not sufficient to promote postembryonic development in L1-stage larvae. However, L1 larvae exposed to food without ingestion failed to develop upon return to normal culture conditions, instead displaying an irreversible arrest phenotype. Inhibition of gene expression during perception rescued subsequent development, demonstrating that the response to perception without feeding is deleterious. Perception altered DAF-16/FOXO subcellular localization, reflecting activation of insulin/IGF signaling (IIS). The insulin-like peptide daf-28 was specifically required, suggesting perception in chemosensory neurons, where it is expressed, regulates peptide synthesis and possibly secretion. However, genetic manipulation of IIS did not modify the irreversible arrest phenotype caused by food perception, revealing that wild-type function of the IIS pathway is not required to produce this phenotype and that other pathways affected by perception of food in the absence of its ingestion are likely to be involved. Gene expression and Nile red staining showed that food perception could alter lipid metabolism and storage. We found that starved larvae sense environmental polypeptides, with similar molecular and developmental effects as perception of bacteria. Environmental polypeptides also promoted recovery from dauer diapause, suggesting that perception of polypeptides plays an important role in the life history of free-living nematodes.ConclusionsWe conclude that actual ingestion of food is required to initiate postembryonic development in C. elegans. We also conclude that polypeptides are perceived as a food-associated cue in this and likely other animals, initiating a signaling and gene regulatory cascade that alters metabolism in anticipation of feeding and development, but that this response is detrimental if feeding does not occur.

A natural variant and engineered mutation in a GPCR promote DEET resistance in C. elegans.

DEET (N,N-diethyl-meta-toluamide) is a synthetic chemical identified by the US Department of Agriculture in 1946 in a screen for repellents to protect soldiers from mosquito-borne diseases1,2. Since its discovery, DEET has become the world's most widely used arthropod repellent and is effective against invertebrates separated by millions of years of evolution-including biting flies3, honeybees4, ticks5, and land leeches3. In insects, DEET acts on the olfactory system5-12 and requires the olfactory receptor co-receptor Orco7,9-12, but exactly how it works remains controversial13. Here we show that the nematode Caenorhabditis elegans is sensitive to DEET and use this genetically tractable animal to study the mechanism of action of this chemical. We found that DEET is not a volatile repellent, but instead interferes selectively with chemotaxis to a variety of attractant and repellent molecules. In a forward genetic screen for DEET-resistant worms, we identified a gene that encodes a single Gprotein-coupled receptor, str-217, which is expressed in a single pair of chemosensory neurons that are responsive to DEET, called ADL neurons. Mis-expression of str-217 in another chemosensory neuron conferred responses to DEET. Engineered str-217 mutants, and a wild isolate of C. elegans that carries a str-217 deletion, are resistant to DEET. We found that DEET can interfere with behaviour by inducing an increase in average pause length during locomotion, and show that this increase in pausing requires both str-217 and ADL neurons. Finally, we demonstrated that ADL neurons are activated by DEET and that optogenetic activation of ADL neurons increased average pause length. This is consistent with the 'confusant' hypothesis, which proposes that DEET is not a simple repellent but that it instead modulates multiple olfactory pathways to scramble behavioural responses10,11. Our results suggest a consistent motif in the effectiveness of DEET across widely divergent taxa: an effect on multiple chemosensory neurons that disrupts the pairing between odorant stimulus and behavioural response.

Membrane Proteins Mediating Reception and Transduction in Chemosensory Neurons in Mosquitoes.

Mosquitoes use chemical cues to modulate important behaviors such as feeding, mating, and egg laying. The primary chemosensory organs comprising the paired antennae, maxillary palps and labial palps are adorned with porous sensilla that house primary sensory neurons. Dendrites of these neurons provide an interface between the chemical environment and higher order neuronal processing. Diverse proteins located on outer membranes interact with chemicals, ions, and soluble proteins outside the cell and within the lumen of sensilla. Here, we review the repertoire of chemosensory receptors and other membrane proteins involved in transduction and discuss the outlook for their functional characterization. We also provide a brief overview of select ion channels, their role in mammalian taste, and potential involvement in mosquito taste. These chemosensory proteins represent targets for the disruption of harmful biting behavior and disease transmission by mosquito vectors.

Structural organization of the olfactory organ in an amphihaline migratory fish Hilsa, Tenualosa ilisha.

The histological as well as ultramicroscopic structures of olfactory system of an amphihaline migratory fish hilsa Tenualosa ilisha, were studied. The sexually matured riverine fish were collected from a common breeding habitat-the Hooghly, a tributary of river Ganga, West Bengal, India. This study revealed that the riverine hilsa has larger olfactory bulb compared to marine hilsa with the olfactory lobes well exposed through nostrils. The olfactory lamellae (OL) are 40-45 in number and posses three distinct layers of sensory cells across each lamellae, namely, outer receptor cells (RC), middle sensory cells, and inner basal cells (BC). Besides the above arrangement, the sensory part of olfactory epithelium (OE) also bears rich microvillous cells exposed to the surface of the OE. The sensory and non-sensory surfaces on OL are distinguishable, with clear dendritic cells on sensory epithelium and solitary chemosensory cells on non sensory OE. Abundance of both types of cells in the OE is an indication of its chemoattraction ability towards molecules of amino acid origin. The feature of having abundant, dense, and large dendritic knobs on the surface of OE describes resemblance to the typical morphology of the chemosensory septal organs neuron. The expression of four G protein subunits, like Gαs/olf, Gαq, Gαo, and Gαi-3 in OE indicate that its olfaction is a functional attributes of two olfactory systems, namely main olfactory system and Vomaronasal Olfactory System. Expression of ACIII and PLCβ2 in OE further confirms two signaling pathways involved in odorant reception in hilsa. RESEARCH HIGHLIGHTS: The olfactory bulb in the amphihaline migratory fish hilsa is big in size, with 40-45 lamellae. Its sensory areas showed multilayered cellular features with prominent sensory as well as microvillous cells, whereas non-sensory area possesses solitary chemosensory cells. The expression of four G protein subunits, Gαs/olf, Gαq, Gαo, and Gαi-3 in olfactory epithelium indicates that its olfaction is a functional attributes of two olfactory systems, namely main olfactory system and vomaronasal olfactory system.

Endoribonuclease ENDU-2 regulates multiple traits including cold tolerance via cell autonomous and nonautonomous controls in Caenorhabditis elegans

Environmental temperature acclimation is essential to animal survival, yet thermoregulation mechanisms remain poorly understood. We demonstrate cold tolerance in Caenorhabditis elegans as regulated by paired ADL chemosensory neurons via Ca2+-dependent endoribonuclease (EndoU) ENDU-2. Loss of ENDU-2 function results in life span, brood size, and synaptic remodeling abnormalities in addition to enhanced cold tolerance. Enzymatic ENDU-2 defects localized in the ADL and certain muscle cells led to increased cold tolerance in endu-2 mutants. Ca2+ imaging revealed ADL neurons were responsive to temperature stimuli through transient receptor potential (TRP) channels, concluding that ADL function requires ENDU-2 action in both cell-autonomous and cell-nonautonomous mechanisms. ENDU-2 is involved in caspase expression, which is central to cold tolerance and synaptic remodeling in dorsal nerve cord. We therefore conclude that ENDU-2 regulates cell type-dependent, cell-autonomous, and cell-nonautonomous cold tolerance.