Lemieux 2018 MiP2018

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Helene Lemieux
Plasticity of a critical regulator of energy production under hypothermia, the phosphorylation system.

Link: MiP2018

Lemieux H (2018)

Event: MiP2018

COST Action MitoEAGLE

The world climate is changing and life is facing an evolving thermal environment. Mitochondrial oxidative phosphorylation (OXPHOS) is critical to ensure sufficient cellular energy production, and is strongly influenced by temperature. The thermally-induced variations in specific steps and in regulation of the OXPHOS process is complex and still not well understood. The phosphorylation system is an important player as the control exerted by this system change drastically between species [1] and with temperature [2]. Previous studies in mammals indicated that in hypothermic conditions, the NADH-linked mitochondrial matrix dehydrogenase [3] and the phosphorylation system [2], rather than the electron transfer complexes, exert the primary control on the OXPHOS process. In order to be able to test the plasticity of the regulating steps under hypothermia, the experiment needs to be performed on an ectotherm animal model.

The planarian Dugesia tigrina was used to study the thermal sensitivity of OXPHOS and the adjustment of specific steps following thermal acclimation. When temperature decreases, the maximal OXPHOS capacity relied more on the Succinate-Pathway, while the NADH-Pathway is strongly compromised. Furthermore, as previously observed in the mouse heart [2], the limitation of OXPHOS by the phosphorylation system increased while temperature decreased in the planarian model. The animals were then acclimated for four weeks at 5°C (compared to 22°C), in order to see if the NADH-Pathway and the phosphorylation system are able to adapt and increase their capacity while facing thermal challenge. Low temperature acclimation resulted in increased contribution of the NADH-Pathway and decreased in limitation of OXPHOS by the phosphorylation system. These adjustment occurred only at a low assay temperature (10°C), and not at an assay temperature of 20°C. Our results indicated that the acclimation specifically targets the limiting steps under hypothermic conditions, the NADH-Pathway and the phosphorylation system capacities.

This opens new perspectives on evolutionary temperature adaptation, suggesting a key neglected target in the control of energy transformation and survival at low temperatures, the phosphorylation system. The specific part of the phosphorylation system responsible for the limitation at low temperature and for the adjustment following thermal acclimation still remains to be identified.


Bioblast editor: Plangger M, Kandolf G O2k-Network Lab: CA Edmonton Lemieux H


Labels: MiParea: Respiration, Comparative MiP;environmental MiP 

Stress:Temperature  Organism: Other invertebrates 

Preparation: Intact organism 


Coupling state: OXPHOS  Pathway: N, S  HRR: Oxygraph-2k 


Affiliations

Fac Saint-Jean, Univ Alberta, Edmonton, AB, Canada. - helene.lemieux@ualberta.ca

References

  1. Lemieux H, Warren B (2012) An animal model to study human muscular diseases involving mitochondrial oxidative phosphorylation. J Bioenerg Biomembr 44:503-12.
  2. Lemieux H, Blier PU, Gnaiger E (2017) Remodeling pathway control of oxidative phosphorylation by temperature in the heart. Sci Rep 7:1-13.
  3. Lemieux H, Tardif JC, Blier PU (2010) Thermal sensitivity of oxidative phosphorylation in rat heart mitochondria: Does pyruvate dehydrogenase dictate the response to temperature? J Therm Biol 35:105-11.