Sensory Interaction Between Attractant Diacetyl and Repellent 2‐<scp>N</scp>onanone in the Nematode <i>Caenorhabditis elegans</i>

Matsuura, Tetsuya; Izumi, Junichi; Hioki, Mamoru; Nagaya, Hiroki; Kobayashi, Yasuaki

doi:10.1002/jez.1795

Cited by 8 publications

(4 citation statements)

References 32 publications

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“…IFT mutations decrease sensory responses in most ciliated sensory neurons (Inglis et al, 2007), but AWA had robust calcium responses across a range of odor concentrations in che-2, che-3 and osm-6 mutants (Figure 4a,b), and only mild defects in diacetyl chemotaxis at the concentrations at which AWA is required (Bargmann et al, 1993; Matsuura et al, 2013; Figure S3). All of the IFT mutants had abnormal AWA cilia, in agreement with previous studies (Figure 4c, S3 and data not shown).…”

Section: Resultsmentioning

confidence: 99%

A Circuit for Gradient Climbing in C. elegans Chemotaxis

Larsch¹,

Flavell²,

Liu³

et al. 2015

Cell Reports

134

195

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Animals have a remarkable ability to track dynamic sensory information. For example, the nematode Caenorhabditis elegans can locate a diacetyl odor source across a 100,000-fold concentration range. Here, we relate neuronal properties, circuit implementation, and behavioral strategies underlying this robust navigation. Diacetyl responses in AWA olfactory neurons are concentration- and history-dependent; AWA integrates over time at low odor concentrations, but as concentrations rise it desensitizes rapidly through a process requiring cilia transport. After desensitization, AWA retains sensitivity to small odor increases. The downstream AIA interneuron amplifies weak odor inputs and desensitizes further, resulting in a stereotyped response to odor increases over three orders of magnitude. The AWA-AIA circuit drives asymmetric behavioral responses to odor increases that facilitate gradient climbing. The adaptation-based circuit motif embodied by AWA and AIA shares computational properties with bacterial chemotaxis and the vertebrate retina, each providing a solution for maintaining sensitivity across a dynamic range.

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Section: Resultsmentioning

confidence: 99%

A Circuit for Gradient Climbing in C. elegans Chemotaxis

Larsch¹,

Flavell²,

Liu³

et al. 2015

Cell Reports

134

195

View full text Add to dashboard Cite

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“…Staged young adults (obtained by growing the progeny of bleached gravid adults) (Porta‐de‐la‐Riva et al, 2012) were used for chemotaxis assays (Figure 2a, b). Attraction to diacetyl and avoidance to SDS were assessed in quadrant assays, as described (Matsuura et al, 2013). Briefly, a 10‐cm‐diameter tissue culture dish containing 0.001 M CaCl 2 , 0.001 M MgSO 4 , 0.2 M KH 2 PO 4 buffer, 0.5 mg/ml cholesterol and agar was divided into four quadrants.…”

Section: Methodsmentioning

confidence: 99%

Neuronal membrane glycoprotein (nmgp‐1) gene deficiency affects chemosensation‐related behaviors, dauer exit and egg‐laying in Caenorhabditis elegans

Fernández

Cutraro

Adams

et al. 2021

Journal of Neurochemistry

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The nervous system monitors the environment to maintain homeostasis, which can be affected by stressful conditions. Using mammalian models of chronic stress, we previously observed altered brain levels of GPM6A, a protein involved in neuronal morphology. However, GPM6A's role in systemic stress responses remains unresolved. The nematode Caenorhabditis elegans expresses a GPM6A ortholog, the neuronal membrane glycoprotein 1 (NMGP‐1). Because of the shared features between nematode and mammalian nervous systems and the vast genetic tools available in C. elegans, we used the worm to elucidate the role of GPM6A in the stress response. We first identified nmgp‐1 expression in different amphid and phasmid neurons. To understand the nmgp‐1 role, we characterized the behavior of nmgp‐1(RNAi) animals and two nmgp‐1 mutant alleles. Compared to control animals, mutant and RNAi‐treated worms exhibited increased recovery time from the stress‐resistant dauer stage, altered SDS chemosensation and reduced egg‐laying rate resulting in egg retention (bag‐of‐worms phenotype). Silencing of nmgp‐1 expression induced morphological abnormalities in the ASJ sensory neurons, partly responsible for dauer exit. These results indicate that nmgp‐1 is required for neuronal morphology and for behaviors associated with chemosensation. Finally, we propose nmgp‐1 mutants as a tool to screen drugs for human nervous system pathologies.

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“…Wild-type N2 C. elegans (strain N2) was obtained from the Caenorhabditis Genetics 91 Centre, University of Minnesota, Minneapolis, USA, and was cultured on Nematode Growth Medium. Chemosensory assays were performed as described by [ 29 ] with some minor modifications.…”

Section: Methodsmentioning

confidence: 99%

Assessment and Validation of Globodera pallida as a Novel In Vivo Model for Studying Alzheimer’s Disease

Althobaiti

Menaa

Albalawi

et al. 2021

Cells

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Background: Whole transgenic or non-transgenic organism model systems allow the screening of pharmacological compounds for protective actions in Alzheimer’s disease (AD). Aim: In this study, a plant parasitic nematode, Globodera pallida, which assimilates intact peptides from the external environment, was investigated as a new potential non-transgenic model system of AD. Methods: Fresh second-stage juveniles of G. pallida were used to measure their chemosensory, perform immunocytochemistry on their neurological structures, evaluate their survival rate, measure reactive oxygen species, and determine total oxidized glutathione to reduced glutathione ratio (GSSG/GSH) levels, before and after treatment with 100 µM of various amyloid beta (Aβ) peptides (1–40, 1–42, 17–42, 17–40, 1–28, or 1–16). Wild-type N2 C. elegans (strain N2) was cultured on Nematode Growth Medium and directly used, as control, for chemosensory assays. Results: We demonstrated that: (i) G. pallida (unlike Caenorhabditis elegans) assimilates amyloid-β (Aβ) peptides which co-localise with its neurological structures; (ii) pre-treatment with various Aβ isoforms (1–40, 1–42, 17–42, 17–40, 1–28, or 1–16) impairs G. pallida’s chemotaxis to differing extents; (iii) Aβ peptides reduced survival, increased the production of ROS, and increased GSSG/GSH levels in this model; (iv) this unique model can distinguish differences between different treatment concentrations, durations, and modalities, displaying good sensitivity; (v) clinically approved neuroprotective agents were effective in protecting G. pallida from Aβ (1–42) exposure. Taken together, the data indicate that G. pallida is an interesting in vivo model with strong potential for discovery of novel bioactive compounds with anti-AD activity.

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Sensory Interaction Between Attractant Diacetyl and Repellent 2‐Nonanone in the Nematode Caenorhabditis elegans

Cited by 8 publications

References 32 publications

A Circuit for Gradient Climbing in C. elegans Chemotaxis

A Circuit for Gradient Climbing in C. elegans Chemotaxis

Neuronal membrane glycoprotein (nmgp‐1) gene deficiency affects chemosensation‐related behaviors, dauer exit and egg‐laying in Caenorhabditis elegans

Assessment and Validation of Globodera pallida as a Novel In Vivo Model for Studying Alzheimer’s Disease

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