PQM-1 controls hypoxic survival via regulation of lipid metabolism

Thomas Heimbucher (), Julian Hog, Piyush Gupta and Coleen T. Murphy ()
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Thomas Heimbucher: Princeton University
Julian Hog: University of Freiburg
Piyush Gupta: University of Freiburg
Coleen T. Murphy: Princeton University

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: 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.

Date: 2020
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DOI: 10.1038/s41467-020-18369-w

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