7K Papers found (0.015 seconds)

Jin I Lee et al. (2004) West Coast Worm Meeting "IDENTIFYING REGULATORS OF NEURONAL PLASTICITY IN THE OLFACTORY ADAPTATION BEHAVIOR OF C. ELEGANS"

Jin I Lee, Ty Swartzlander, Hyun U Kim, Noelle L'Etoile

[

West Coast Worm Meeting,

2004]

Animals adjust their behaviors in response to the ever-changing surrounding environment. In olfaction, sensitivity to odors is adjusted by the process of adaptation. The nematode C. elegans can not only sense numerous volatile attractive odors in its environment, but can also adapt to these odors. Two pairs of primary sensory neurons, the AWA and AWC, allow the worm to detect and respond to a wide variety of volatile compounds. In the AWC neurons, odor is detected by G-protein coupled receptors and transduced as a signal via cGMP-dependent mechanisms to generate chemotaxis movement towards the odor. Adaptation occurs by inhibiting chemotaxis signaling through the cGMP-dependent protein kinase EGL-4. The EGL-4 kinase is postulated to inhibit early events of chemotaxis signaling by inactivating a cGMP-gated channel in the AWC primary sensory neuron after 30 minutes of exposure to odor. This resulted in a transient short-term adaptation (L'Etoile et al, 2002). We show here that a stable and robust long-term adaptation coincided with the nuclear translocation of EGL-4. Both changes occur after the 60-80 minute time point after exposure to odor. We will also show that nuclear translocation is specific for odors sensed by AWC. In order to understand processes of behavior plasticity, we decided to look for molecules that may regulate the transition from short-term to long-term adaptation. To do this we utilized the nuclear translocation of a GFP-tagged EGL-4 as a read-out for long-term adaptation. We will show that an essential component of odor-sensation, the transmembrane guanylyl cyclase ODR-1, is also necessary for cytoplasmic localization of EGL-4. We have also screened for mutants that, upon odor exposure, are defective in both nuclear translocation of EGL-4 and adaptation to the odor. We have thus far isolated 4 out (Odor indUced Translocation defective) mutants, py1, py2, py3, and py4, and are in the process of mapping and cloning these mutants.

Jin I Lee et al. (2003) International Worm Meeting "Investigating regulators of the cGMP-dependent protein kinase EGL-4s nuclear translocation during long-term olfactory adaptation behavior"

Noelle D L'Etoile, Jin I Lee

[

International Worm Meeting,

2003]

Odorant adaptation is a complex process which involves a temporally-regulated modulation mechanism in response to sensory stimulus. For instance, it has been shown that a consensus cGMP-dependent protein kinase phosphorylation site within the cGMP-gated channel -subunit TAX-2 is necessary for short-term adaptation of the AWC olfactory neurons (L'Etoile et al, 2002). On the other hand, long-term adaptation likely involves nuclear translocation of EGL-4 that encodes a cGMP-dependent protein kinase: animals expressing a nuclear translocation signal-deleted form of EGL-4 (EGL-4[NLS])had defects in long-term adaptation (L'Etoile et al, 2002). We will also show that odor exposure induces both nuclear translocation of GFP-fused EGL-4 (GFP::EGL-4) that can be monitored visually as well as adaptation that can be monitored in a behavioral assay. Furthermore, we will show that GFP-tagged EGL-4(NLS) fails both to translocate to the nucleus in response to odor-exposure and to induce long-term adaptation. These results bolster our confidence that nuclear translocation of EGL-4 correlates well with adaptation and could be a useful cell biological marker for adaptation. We are also examining the correlation between subcellular localization of GFP::EGL-4 and behavioral adaptation in a variety of adaptation-defective mutants as well as in response to a variety of odorants. Though EGL-4 is known to have an indispensable role in both short- and long-term adaptation, the molecular events that separate these two functions are not yet clear. To investigate initial mechanisms of long-term adaptation and identify new components that may regulate nuclear localization of EGL-4, we plan to isolate mutants that fail to translocate GFP::EGL-4 to the nucleus in response to odor-exposure. Wild-type worms carrying the integrated (p)odr-1::GFP::EGL-4 construct will be mutagenized and a visual screen for animals that show a defect in transporting the GFP-fused EGL-4 protein to the nucleus of AWC neurons will be conducted. In addition, we will implement secondary behavioral screens to observe and classify EGL-4 nuclear translocation-defective mutants with respect to their behavioral defects. These screens should identify multiple categories of genes that may be involved in several aspects of adaptation including EGL-4 nuclear localization, chemotaxis, odor specificity, and novel genes important for adaptation and long-term adaptation processes. L'Etoile N.D. et al. (2002). The cyclic GMP dependent protein kinase EGL-4 regulates olfactory adaptation in C. elegans. Neuron 36:1079-1089.

Jin I Lee et al. (2005) International Worm Meeting "Odor-induced nuclear translocation of EGL-4 is required for the transition to long-term adaptation and is regulated by the receptor guanylyl cyclase ODR-1"

Jin I Lee, Noelle L'Etoile

[

International Worm Meeting,

2005]

Animals adjust their behaviors in response to the ever-changing surrounding environment. In olfaction, sensitivity to odors is adjusted by the process of adaptation. The nematode C. elegans can not only sense numerous volatile attractive odors in its environment, but can also adapt to these odors. Two pairs of primary sensory neurons, the AWA and AWC, allow the worm to detect and respond to a wide variety of volatile compounds. In the AWC neurons, odor is detected by G-protein coupled receptors and transduced as a signal via cGMP-dependent mechanisms to generate chemotaxis movement towards the odor. Adaptation occurs by inhibiting chemotaxis signaling through the cGMP-dependent protein kinase EGL-4. Adaptation, though robust, can be modulated by other environmental factors such as food and stress. The EGL-4 kinase is postulated to inhibit early events of chemotaxis signaling by attenuating the activity of a cGMP-gated channel in the AWC primary sensory neuron after 30 minutes of exposure to odor. This resulted in a transient short-term adaptation (L'Etoile et al, 2002). We show here that a stable and robust long-term adaptation coincided with the nuclear translocation of EGL-4. Both changes occurred after 60-80 minutes of odor exposure. We also show that nuclear translocation was specific for odors sensed by AWC and that this odor-induced nuclear translocation did not depend on synaptic activity. In order to understand processes that regulate the behavioral plasticity underlying olfactory adaptation, we decided to look for molecules that regulate the transition from short-term to long-term adaptation. To do this we utilized the nuclear translocation of a GFP-tagged EGL-4 as a read-out for long-term adaptation. Surprisingly, we found that mutations in an essential component of odor-sensation, the receptor guanylyl cyclase (RGC) ODR-1, showed constitutively nuclear EGL-4. Thus, ODR-1 may be necessary to keep EGL-4 in the cytoplasm. We found that the cyclase activity of ODR-1 was not required to keep EGL-4 in the cytoplasm. However, the extracellular receptor-like domain of ODR-1 might be important for allowing environmental factors to restrict odor-induced EGL-4 nuclear entry. Though other sensory neurons such as rods and vertebrate olfactory neurons express RGCs, no function has been ascribed to the receptor portion. C. elegans may be utilizing this extracellular domain to allow for a sensory neuron to integrate two inputs before allowing long lasting changes to ensue.

Jin I. Lee et al. (2006) East Asia C. elegans Meeting "To adapt or not to adapt, that is the odor question: How a receptor guanylyl cyclase may help worms to find food"

Jin I. Lee, Noelle D. L'Etoile

[

East Asia C. elegans Meeting,

2006]

Organisms must learn to ignore profitless odors and attend to odors that are associated with food, but the mechanism of how they can accomplish this is not yet understood. We show that in the absence of food C. elegans learns to ignore normally attractive odors that it encounters by sending the cGMP-dependent protein kinase EGL-4 into the nucleus of the sensory AWC neuron. This diminishes attraction to an AWC-sensed odor such as benzaldehyde for nearly three hours. Odors that the worm encounters while feeding, however, remain attractive. We show that the extracellular domain of a receptor guanylyl cylase, ODR-1, acts as a sensor for food and can prevent the EGL-4 from entering the nucleus in the presence of food and inhibit odor adaptation. This receptor provides C. elegans with the ability to focus on odors that are likely to predict food.

Lee C et al. (2017) Bio Protoc "Single-molecule RNA Fluorescence in situ Hybridization (smFISH) in Caenorhabditis elegans."

Sorensen EB, Lee C, Seidel HS, Lynch TR, Crittenden SL, Kimble J

[

Bio Protoc,

2017]

Single-molecule RNA fluorescence in situ hybridization (smFISH) is a technique to visualize individual RNA molecules using multiple fluorescently-labeled oligonucleotide probes specific to the target RNA ( Raj et al., 2008 ; Lee et al., 2016a ). We adapted this technique to visualize RNAs in the C. elegans whole adult worm or its germline, which enabled simultaneous recording of nascent transcripts at active transcription sites and mature mRNAs in the cytoplasm ( Lee et al., 2013 and 2016b). Here we describe each step of the smFISH procedure, reagents, and microscope settings optimized for C. elegans extruded gonads.

Jin YS et al. (1994) Worm Breeder's Gazette "unc-25 Encodes a C. elegans Glutamic Acid Decarboxylase (GAD)"

Horvitz HR, Jin YS

[

Worm Breeder's Gazette,

1994]

unc-25 encodes a C elegans glutamic acid decarboxylase (GAD) Yishi Jin and Bob Horvitz, HHMI, Dept. Biology, Mrr, Cambridge, MA 02139, USA

Miranda MC et al. (2024) MicroPubl Biol "Investigating the effects of antipsychotic drugs as a treatment for improving the activity of the unc-33 /Dpysl2 gene in C. elegans."

Miranda MC, Hyde J, Holgado A, Salazar K, Bell B

[

MicroPubl Biol,

2024]

Prenatal stress is hypothesized to contribute to the development of schizophrenia. Lee and colleagues determined that prenatal stress in rats decreases levels of Dpysl2, which is found to be inactivated in schizophrenic patients. UNC-33 , the homolog to Dpysl2 in C. elegans , is important for axonal outgrowth and synapse formation. Herein, we study the effects of antipsychotic drugs on developing C.elegans exposed to stress through high temperatures. Results indicate that the unc-33 promoter was not impacted by antipsychotic drug treatment, but the lifespan was decreased.

Souza ACR et al. (2018) Genes (Basel) "Pathogenesis of the Candida parapsilosis Complex in the Model Host Caenorhabditis elegans."

Colombo AL, Fuchs BB, Jayamani E, Mylonakis E, Souza ACR, Alves VS

[

Genes (Basel),

2018]

Caenorhabditiselegans is a valuable tool as an infection model toward the study of Candida species. In this work, we endeavored to develop a C. elegans-Candidaparapsilosis infection model by using the fungi as a food source. Three species of the C. parapsilosis complex (C.parapsilosis (sensustricto), Candidaorthopsilosis and Candidametapsilosis) caused infection resulting in C. elegans killing. All three strains that comprised the complex significantly diminished the nematode lifespan, indicating the virulence of the pathogens against the host. The infection process included invasion of the intestine and vulva which resulted in organ protrusion and hyphae formation. Importantly, hyphae formation at the vulva opening was not previously reported in C. elegans-Candida infections. Fungal infected worms in the liquid assay were susceptible to fluconazole and caspofungin and could be found to mount an immune response mediated through increased expression of cnc-4, cnc-7, and fipr-22/23. Overall, the C. elegans-C. parapsilosis infection model can be used to model C. parapsilosis host-pathogen interactions.

Vigneshwari, Loganathan et al. (2019) International Worm Meeting "Effect of altering gravity on TGF-beta signaling during organogenesis and innate immunity in the model animal C. elegans."

Vigneshwari, Loganathan, Higashitani, Atsushi, Lee, Jin I.

[

International Worm Meeting,

2019]

C. elegans has been used as a successful model system to study the pathogenesis of Gram-positive, Gram-negative pathogens and fungal pathogens. In the recent years, C. elegans is widely used to study the effect of space flight conditions on susceptibility to pathogenic microbes, organogenesis and so on using simulated microgravity in a clinostat. C. elegans responds to pathogens through an array of immune signaling pathways. When compared to other model organisms, C. elegans genetic amenability and availability of mutants and ability to survive in space conditions helps to study the immune responsive pathways during pathogenic infections. TGF-beta/DBL-1 signaling in C. elegans plays a primary role in body length, organogenesis of male tail structures and the innate immune system. Previous spaceflight studies showed that the body length was decreased in microgravity, as well as expression of dbl-1. On this backdrop, our study is focused on the effect of hypergravity, simulated microgravity and space microgravity on the regulation of DBL-1-mediated male tail sensory ray formation and DBL-1-mediated innate immune response against bacterial pathogens. We expect that exposure of C. elegans to microgravity or hypergravity conditions may affect its behavior, brood size, body length, intestinal colonization of pathogens and innate immune responsive pathways

Fourie R et al. (2021) Front Cell Infect Microbiol "Candida albicans SET3 Plays a Role in Early Biofilm Formation, Interaction With Pseudomonas aeruginosa and Virulence in Caenorhabditis elegans."

Sebolai O, Fourie R, Albertyn J, Pohl CH, Gcilitshana O

[

Front Cell Infect Microbiol,

2021]

The yeast Candida albicans exhibits multiple morphologies dependent on environmental cues. Candida albicans biofilms are frequently polymicrobial, enabling interspecies interaction through proximity and contact. The interaction between C. albicans and the bacterium, Pseudomonas aeruginosa, is antagonistic in vitro, with P. aeruginosa repressing the yeast-to-hyphal switch in C. albicans. Previous transcriptional analysis of C. albicans in polymicrobial biofilms with P. aeruginosa revealed upregulation of genes involved in regulation of morphology and biofilm formation, including SET3, a component of the Set3/Hos2 histone deacetylase complex (Set3C). This prompted the question regarding the involvement of SET3 in the interaction between C. albicans and P. aeruginosa, both in vitro and in vivo. We found that SET3 may influence early biofilm formation by C. albicans and the interaction between C. albicans and P. aeruginosa. In addition, although deletion of SET3 did not alter the morphology of C. albicans in the presence of P. aeruginosa, it did cause a reduction in virulence in a Caenorhabditis elegans infection model, even in the presence of P. aeruginosa.

load 10 more results