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| Main Authors: | , , , , , , |
|---|---|
| Format: | Artículo científico |
| Language: | en |
| Published: |
bioRxiv : the preprint server for biology
2025
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| Online Access: | https://pubmed.ncbi.nlm.nih.gov/41332531/ |
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Table of Contents:
- OSM-11 modulates salinity-stress tolerance in . Zhang, Pengchi Xue, Beining Xie, Yusu Li, Kunlin Yang, Hanwen Sun, Peiqi Zhang, Liusuo Most terrestrial animals exhibit narrow salinity tolerance compared to their marine counterparts. Previous studies identified (which encodes a Notch co-ligand) mutations as a driver of hyper-saline tolerance in , but mechanistic insights remained unclear. This study employs RNA sequencing and CRISPR/Cas-9 genome editing to demonstrate that mutations enhance salinity stress resistance through upregulation of fatty acid metabolism () and cytochrome P450 pathways (), while suppressing calcium signaling. Furthermore, we demonstrated that mutation impairs salinity-stress tolerance by activating ferroptosis and mitophagy, accompanied by down-regulated oxidative phosphorylation and up-regulated autophagic pathways. Morphological observations show that mitochondrial fragmentation contributes to wild-type nematode mortality under high salinity, while enlarged lipid droplets in wild-types correlate with reduced β-oxidation gene expression (), whose knockout disrupts tolerance in mutants. These findings unravel the multi-pathway regulatory network of -mediated salinity tolerance, providing mechanistic insights for developing protective strategies against environmental salinity stressors impacting animal survival.