To refer to this page use:
|Abstract:||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.|
|Citation:||Heimbucher, Thomas, Hog, Julian, Gupta, Piyush, Murphy, Coleen T. (2020). PQM-1 controls hypoxic survival via regulation of lipid metabolism. Nature communications, 11 (1), 4627 - 4627. doi:10.1038/s41467-020-18369-w|
|Pages:||4627 - 4627|
|Type of Material:||Journal Article|
|Journal/Proceeding Title:||Nature Communications|
|Version:||Final published version. This is an open access article.|
Items in OAR@Princeton are protected by copyright, with all rights reserved, unless otherwise indicated.