@article{3974,
  keywords = {Stress, Physiological, Trans-Activators, Animals, Larva, Transcription, Genetic, Caenorhabditis elegans, Signal Transduction, Mutation, Gene Expression Regulation, Embryo, Mammalian, Caenorhabditis elegans Proteins, Insulin, Lipid Metabolism, Oxygen Consumption, Hypoxia, Glycogen, Survival Analysis, Vitellogenins},
  author = {Thomas Heimbucher and Julian Hog and Piyush Gupta and Coleen Murphy},
  title = {PQM-1 controls hypoxic survival via regulation of lipid metabolism.},
  abstract = { <p>Animals have evolved responses to low oxygen conditions to ensure their survival. Here, we have identified the C. elegans zinc finger transcription factor PQM-1 as a regulator of the hypoxic stress response. PQM-1 is required for the longevity of insulin signaling mutants, but surprisingly, loss of PQM-1 increases survival under hypoxic conditions. PQM-1 functions as a metabolic regulator by controlling oxygen consumption rates, suppressing hypoxic glycogen levels, and inhibiting the expression of the sorbitol dehydrogenase-1 SODH-1, a crucial sugar metabolism enzyme. PQM-1 promotes hypoxic fat metabolism by maintaining the expression of the stearoyl-CoA desaturase FAT-7, an oxygen consuming, rate-limiting enzyme in fatty acid biosynthesis. PQM-1 activity positively regulates fat transport to developing oocytes through vitellogenins under hypoxic conditions, thereby increasing survival rates of arrested progeny during hypoxia. Thus, while pqm-1 mutants increase survival of mothers, ultimately this loss is detrimental to progeny survival. Our data support a model in which PQM-1 controls a trade-off between lipid metabolic activity in the mother and her progeny to promote the survival of the species under hypoxic conditions.</p> },
  year = {2020},
  journal = {Nat Commun},
  volume = {11},
  pages = {4627},
  month = {2020 Oct 02},
  issn = {2041-1723},
  doi = {10.1038/s41467-020-18369-w},
  language = {eng},
}