Caenorhabditis elegans PAQR-2 and IGLR-2 Protect against Glucose Toxicity by Modulating Membrane Lipid Composition
Fig 5
Model of membrane fluidity regulation by PAQR-2 and IGLR-2.
The model proposes that PAQR-2 and IGLR-2 act as sensors that are activated by low membrane fluidity and act on downstream effectors to restore fluidity by promoting changes in fatty acid metabolism, including promoting the activity of Δ9 desaturases. Cold or availability of glucose tend to decrease membrane fluidity, which explains the sensitivity phenotypes of the paqr-2 and iglr-2 mutants. The effect of low temperature on membrane fluidity is purely biophysical, while the effect of glucose is indirect and may be attributed to lipogenesis whereby glucose is converted into saturated fatty acids or to an effect on the dietary FA in the E. coli used as food source. In the presence of glucose the relative abundance of saturated fatty acids increases within the available pool, leading to an increase in membrane rigidity as phospholipid turnover occurs.