5 Papers found (0.134 seconds)

Pradhan, Sreeparna et al. (2019) International Worm Meeting "Environmental programming of adult foraging behavior."

Hendricks, Michael, Quilez, Sabrina Rita, Homer, Kai, Pradhan, Sreeparna

[

International Worm Meeting,

2019]

Animals tune their foraging strategies by using past experience to estimate current resource availability and distribution. Previous studies have reported plasticity in foraging strategies in C. elegans over short time scales over a few hours in response to environmental fluctuations. Genetic variation between different wild isolates are also known to affect foraging decisions, with the lab wild-type N2 strain being the least exploratory and the wild HW CB4856 strain being the most exploratory. We explored whether foraging behavior can be tuned over the time scale of the lifetime of an individual. Stressful environmental conditions like scarcity of food in early larval stages directly affect C. elegans development inducing entry into the dauer developmental arrest phase. We examined adult foraging strategies in post-dauer animals of different genetic backgrounds. Our results show that HW post-dauers have permanently reduced adult foraging behavior, but this long-term plasticity is absent in the lab adapted N2 strain. We also observed changes in the temporal pattern of food search in HW post-dauers, coupled with a high propensity of reversals and turns. We then investigated the neural correlates of this permanent change in behavior, and simultaneously imaged calcium transients in AVA, AIB and RIM which form a local interneuron circuit controlling reversal output. Our results indicate that post-dauer HWs have higher dynamic activity in this circuit in both presence and absence of food cues. We next examined known polymorphisms between the N2 and HW strains to determine the genetic basis of between-strain differences in long-term plasticity. Our work shows that adult foraging behaviour is tuned by developmental experience and involves altering the dynamics of a core navigation circuit, and this plasticity is dependent on the genetic background and life history of the strain.

Hong M et al. (2008) Biochem Biophys Res Commun "The anesthetic action of ethanol analyzed by genetics in Caenorhabditis elegans."

Lee J, Choi MK, Hong M

[

Biochem Biophys Res Commun,

2008]

Acute exposure to ethanol causes paralysis at high concentrations in the nematode Caenorhabditis elegans. We set out to elucidate the mechanism of the anesthetic action of ethanol by genetic approaches. We identified nine mutations that conferred reduced sensitivity to ethanol after chemical, irradiation, or transposon insertion mutagenesis. Of these nine, we further characterized five mutations that defined four genes, jud-1-jud-4. Analysis of the phenotypes of the animals heterozygous for two unlinked genes revealed that jud-1 and jud-3 act synergistically in a gene dose-dependent manner. We cloned jud-4 and found that it encodes a protein with limited homology to human Homer proteins. jud-4 was expressed in the hypodermis and vulva muscles, suggesting that this gene acts in tissues directly exposed to the external environment. Characterization of the other mutations identified in this study will facilitate the elucidation of the molecular mechanism for the anesthetic action of ethanol.

Choi M et al. (2010) Neuronal Development, Synaptic Function and Behavior, Madison, WI "PTR-6, a C. elegans Patched related gene, regulates the anesthetic effect of ethanol"

Lee J, Choi M, Hong M

[

Neuronal Development, Synaptic Function and Behavior, Madison, WI,

2010]

Acute exposure to ethanol causes paralysis at high concentrations in the nematode Caenorhabditis elegans. We set out to elucidate the mechanism of the anesthetic action of ethanol by genetic approaches. We identified nine mutations that conferred reduced sensitivity to ethanol after chemical, irradiation, or transposon insertion mutagenesis. In the previous study, molecular nature of the mutant made by transposon insertion, jud-4, was identified. jud-4 encodes a C. elegans homolog of Homer proteins, which are important for synaptic protein localization in other organisms. jud-4 was expressed in the hypodermis and vulva muscles, suggesting that this gene acts in tissues directly exposed to the external environment. In this study, we wanted to characterize other mutations affecting ethanol sensitivity. Among them, jud-1 mutations, most strong mutants, were identified by SNP mapping and whole-genome sequencing. We found that jud-1 encodes a C. elegans homolog of PATCHED-related receptor, PTR-6. PTR-6 has an SSD (Sterol-sensing domain) and a PATCHED family motif which has an essential role for hedgehog signal transduction. Although hedgehog signaling is not fully conserved in C. elegans, it has been reported that homologs of core components in the hedgehog pathway have many biological significance. Detailed analysis of ptr-6 should elucidate a novel mechanism for the anesthetic effect of ethanol.

Xiao L et al. (2020) Rejuvenation Res "The Traditional Formula Kai-Xin-San Alleviates Polyglutamine-Mediated Neurotoxicity by Modulating Proteostasis Network in Caenorhabditis elegans."

Tian J, Huang Z, Xiao L, Zhou L, Yang F, Wang Q, Zhang J, Jin N, Li H

[

Rejuvenation Res,

2020]

The inherited polyglutamine (polyQ) expansion diseases are characterized by progressive accumulation of aggregation-prone polyQ proteins, which may provoke proteostasis imbalance and result in significant neurotoxicity. Using polyQ transgenic Caenorhabditis elegans models, we find that Kai-Xin-San (KXS), a well-known herbal formula traditionally used to treat mental disorders in China, can alleviate polyQ-mediated neuronal death and associated chemosensory deficiency. Intriguingly, KXS does not reduce polyQ aggregation in vitro as demonstrated by Thioflavin-T test, but does inhibit polyQ aggregation in C. elegans models, indicating an indirect aggregation-inhibitory mechanism. Further investigation reveals that KXS can modulate two key arms of the protein quality control system, that is, heat shock response and autophagy, to clear polyQ aggregates, but has little effect on proteasome activity. In addition, KXS is able to reduce oxidative stress, which is involved in proteostasis and neurodegeneration, but has no effect on life span or dietary restriction response. To examine potential interaction of the four component herbs of KXS, a dissection strategy was used to study the effects of differential herbal combinations in C. elegans polyQ models. While the four herbs do contribute additively to KXS function, Panax ginseng is found to be the most effective constituent. Taken together, these findings not only demonstrate the neuroprotective ability of KXS but also suggest its potential as a proteostasis regulator in protein aggregation disorders and provide an insight into the mechanism studies of traditionally used complex prescriptions and their rationality.

Hidehito KUROYANAGI et al. (2001) International C. elegans Meeting "Characterization of Candidate Genes for Postsynaptic Proteins in C. elegans Nervous System."

Shigeo OKABE, Hidehito KUROYANAGI

[

International C. elegans Meeting,

2001]

GFP-labeling of synaptic vesicles using SNB-1::GFP enabled visualization of presynaptic specializations in living worms [Nonet, ML, J. Neuroscience Methods 89: 33-40, 1999]. These worms have been proved to be powerful tools for isolation and description of mutants in which the synapse formation is affected. On the other hand, studies using a GFP-labeled glutamate receptor subunit, GLR-1, revealed that the neurotransmitter receptor is targeted to postysynaptic structures and that the targeting depends on PDZ proteins such as LIN-10 [Rongo, C. et al., Cell 94: 751-759, 1998]. In order to obtain genetic tools to study further the formation of pre- and postsynaptic structures during development as well as the mechanisms of targeting postsynaptic proteins to synapses, we are searching for a panneuronal postsynaptic marker protein in C. elegans . We amplified cDNA fragments of homologous genes of postsynaptic proteins recently identified in mammalian postsynaptic structures. The proteins whose putative homologues we are studying are: Drosophila Discs Large and mammalian PSD-95/SAP90 family proteins; S-SCAM/SLIPR/MAGI family, proteins associating with various kinds of receptor proteins; MAGUIN, a scaffolding protein interacting with PSD-95 and S-SCAM; synamon/shank, proteins coupling NMDAR/PSD-95 complex and mGluR/Homer complex; CRIPT, comprising complex with PSD-95 and tubulin. Sequencing of the cDNA fragments revealed genomic structures and complete amino acid sequences. Domain structures are well conserved between worm and mammals for these genes. We are now studying the expression pattern of these genes using GFP reporter constructs. We are also analyzing the subcellular localization of these proteins in neurons by expressing GFP-fusion proteins.