AI Article Synopsis
- Cells can get used to cold temperatures by changing their fats and making their membranes more flexible.
- Scientists found a big protein called LPD-3 in tiny worms (C. elegans) that helps move fats around inside the cells to help them survive cold better.
- When LPD-3 doesn't work right, the worms can't handle the cold as well, and this problem is similar in other animals, including fish and humans.
Article Abstract
Cells adapt to cold by increasing levels of unsaturated phospholipids and membrane fluidity through conserved homeostatic mechanisms. Here we report an exceptionally large and evolutionarily conserved protein LPD-3 in C. elegans that mediates lipid trafficking to confer cold resilience. We identify lpd-3 mutants in a mutagenesis screen for genetic suppressors of the lipid desaturase FAT-7. LPD-3 bridges the endoplasmic reticulum (ER) and plasma membranes (PM), forming a structurally predicted hydrophobic tunnel for lipid trafficking. lpd-3 mutants exhibit abnormal phospholipid distribution, diminished FAT-7 abundance, organismic vulnerability to cold, and are rescued by Lecithin comprising unsaturated phospholipids. Deficient lpd-3 homologues in Zebrafish and mammalian cells cause defects similar to those observed in C. elegans. As mutations in BLTP1, the human orthologue of lpd-3, cause Alkuraya-Kucinskas syndrome, LPD-3 family proteins may serve as evolutionarily conserved highway bridges critical for ER-associated non-vesicular lipid trafficking and resilience to cold stress in eukaryotic cells.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9649747 | PMC |
| http://dx.doi.org/10.1038/s41467-022-34450-y | DOI Listing |
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