Summary of project PR002531
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR002531. The data can be accessed directly via it's Project DOI: 10.21228/M8GR97 This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
| Project ID: | PR002531 |
| Project DOI: | doi: 10.21228/M8GR97 |
| Project Title: | Soma to neuron communication links stress adaptation to stress avoidance behavior |
| Project Summary: | In multicellular organisms, signaling from the nervous system to the peripheral tissues can activate physiological responses to stress. Here, we show that inter-tissue stress communication can also function in reverse, i.e. from the peripheral tissue to the nervous system. osm-8 mutants, which activate the osmotic stress response in the C. elegans skin, also exhibit defective osmotic avoidance behavior, which is regulated by the ASH neuronal avoidance circuit. osm-8 osmotic avoidance behavior is completely suppressed by mutation of the Patched/NPC1 homolog ptr-23. The function of osm-8 and ptr-23 in the hypodermal epithelial cells is both necessary and sufficient for directing neuronal osmotic avoidance behavior. Endogenously tagged alleles of osm-8 and ptr-23 co-localize exclusively in the hypodermal lysosomes. Unbiased lipidomic analysis shows that osm-8 leads to a ptr-23-dependent elevation of the lysosome specific lipid bis(monoacylglycero)phosphate (BMP) and expansion of the pool of hypodermal lysosomes. Just as genetic activation of the osmotic stress response by loss of osm-8 in the hypodermis causes an Osm phenotype, acute physiological exposure to osmotic stress also confers a reversible Osm phenotype. Behavioral plasticity requires glycerol production, as mutations in the glycerol biosynthetic enzymes gpdh-1 and gpdh-2 are defective in acquired Osm behavior. While the osm-8 induced Osm behavior requires ptr-23, physiologically induced Osm behavior does not. Instead, both genetic and physiologically induced Osm phenotypes require the unusual non-neuronal lysosomal V-ATPase subunit vha-5, which is also critical for organismal osmotic stress survival. Together, these data reveal that genetic or physiological activation of stress signaling from the skin elicits lysosome-associated signals that modulate the function of a sensory neuron circuit. Such ‘body-brain’ interoceptive communication may allow organisms to better match neuronal decision-making with organismal physiological state. |
| Institute: | University of Pittsburgh |
| Department: | Pediatrics and Cell Biology |
| Laboratory: | Lamitina Lab |
| Last Name: | Lamitina |
| First Name: | Todd |
| Address: | Childrens Hospital of Pittsburgh |
| Email: | stl52@pitt.edu |
| Phone: | 267-439-0330 |
| Funding Source: | NIH R01GM135577; NIH S10OD023402 |
Summary of all studies in project PR002531
| Study ID | Study Title | Species | Institute | Analysis(* : Contains Untargted data) | Release Date | Version | Samples | Download(* : Contains raw data) |
|---|---|---|---|---|---|---|---|---|
| ST004039 | Soma to neuron communication links stress adaptation to stress avoidance behavior | Caenorhabditis elegans | University of Pittsburgh | MS | 2025-07-31 | 1 | 18 | Uploaded data (1.1G)* |
