Activation of the carbohydrate response element binding protein (ChREBP) in response to anoxia in the turtle Trachemys scripta elegans

• The anoxia-responsive activation of the transcription factor ChREBP was studied in turtles.
• Liver showed a full activation of ChREBP in response to anoxia.
• The ChREBP target gene, LPK was also upregulated in response to anoxia.
• These results suggest that ChREBP might play a role in turtle liver in response to anoxia.

BackgroundChREBP (carbohydrate response element binding protein) is a glucose-responsive transcription factor that is known to be an important regulator of glycolytic and lipogenic genes in response to glucose. We hypothesized that activation of ChREBP could be relevant to anoxia survival by the anoxia-tolerant turtle, Trachemys scripta elegans.MethodsExpression of ChREBP in response to 5 and 20 h of anoxia was examined using RT-PCR and Western immunoblotting. In addition, subcellular localization and DNA-binding activity of ChREBP protein were assessed and transcript levels of liver pyruvate kinase (LPK), a downstream gene under ChREBP control were quantified using RT-PCR.ResultsChREBP was anoxia-responsive in kidney and liver, with transcript levels increasing by 1.2–1.8 fold in response to anoxia and protein levels increasing by 1.8–1.9 fold. Enhanced nuclear presence under anoxia was also observed in both tissues by 2.2–2.8 fold. A 4.2 fold increase in DNA binding activity of ChREBP was also observed in liver in response to 5 h of anoxia. In addition, transcript levels of LPK increased by 2.1 fold in response to 5 h of anoxia in the liver.ConclusionsThe results suggest that activation of ChREBP in response to anoxia might be a crucial factor for anoxia survival in turtle liver by contributing to elevated glycolytic flux in the initial phases of oxygen limitation.General significanceThis study provides the first demonstration of activation of ChREBP in response to anoxia in a natural model of anoxia tolerance, further improving our understanding of the molecular nature of anoxia tolerance.