Mitochondria are the tiny cellular energy generators that produce the energy rich chemical ATP, which powers our every move. Mitochondria consume oxygen to pump protons out of the mitochondrial matrix, which generates an electrical gradient that ultimately drives ATP synthase to produce ATP. But not all protons contribute to ATP synthesis. Some leak back across the mitochondrial inner membrane, producing heat and providing protection from toxic reactive oxygen species. But proton leak is energetically costly, and when times are hard, most creatures reduce it to cut back their metabolic expenditure. Curious to know how ectothermic creatures cope in challenging conditions, Martin Jastroch and his colleagues Magdalene Trzcionka and Martin Klingenspor in Marburg, Germany and Kerry Withers in Toowoomba, Australia,decided to investigate how cane toad mitochondrial metabolism responds to cold and hunger ().
Travelling from Northern European to Withers' tropical Queensland laboratory, Trzcionka acclimated one group of toads at a comfortable 30°C while the other half was cooled to a chilly 10°C. Feeding half of the warm toads while starving the remaining animals, and dividing the cold toads in the same way (half fed, half starved), Trzcionka measured their metabolic rates after several days and found that the temperature had a dramatic effect. The warm acclimated toads' metabolic rates were four times the metabolic rates of the cold acclimated toads, while their diet (or lack of) had virtually no effect on the animals' metabolic rates. The cold toads had reduced their metabolic costs.
Next Trzcionka tested how the toads' mitochondria had responded to cold and starvation by measuring their mitochondrial proton leak rates. Jastroch admits that this was a particularly ambitious task. `These experiments are usually only undertaken by experienced scientists' explains Jastroch; let alone a student early in her career in a laboratory 16 000 km from her supervisor. But after months of preparation and with a reliable Skype connection for technical support from Jastroch, Trzcionka successful measured the mitochondrial proton leak rates from the toads' muscle and liver tissues. Adaptation to the cold and starvation had hardly affected proton leak in skeletal muscle at all. But it was a different matter in the liver. The cold acclimated amphibians had significantly reduced their proton leak rate in the liver, and when they added in the effects of starvation the team was surprised to see that the proton leak rate increased even though the amphibians had reduced their energy consumption by reducing the rate at which they pumped protons out of the mitochondrial matrix.
Curious to know how the toads regulated proton leakage, Trzcionka measured the levels of mitochondrial proteins known to participate in proton leak. However, none of the protein levels correlated with the protein leak levels,leaving Jastroch keen to find out which mechanisms regulate cane toad's mitochondrial proton leak when conditions are metabolically challenging.
