Damage control
Certain proteins involved in Parkinson’s disease help dispose of damaged mitochondria in living organisms.
Parkinson’s disease is a brain disorder where certain nerve cells slowly die, and the symptoms gradually worsen over time. While the risk of developing the condition increases with age, in certain patients the illness is caused by defects in two proteins, PINK1 and parkin.
PINK1 and parkin help to manage mitochondria, the compartments in our cells that create molecules that serve as the energy currency for nearly all biological processes. When mitochondria get damaged, they release harmful substances that can kill their host cell. To prevent this, PINK1 and parkin can start a process known as mitophagy, which allows the cell to safely dispose of these dangerous mitochondria.
Yet, mitophagy that is triggered by PINK1 and parkin has only been observed in cells grown in the laboratory; there is very little direct evidence that it also takes place in living organisms. If this mechanism does not happen in animals, then it is probably not relevant to Parkinson’s disease.
Here, Cornelissen et al. genetically engineered fruit flies that carry a fluorescent marker which helps to track when and where damaged mitochondria are destroyed by a cell. The experiments revealed that mitophagy took place in muscles and in brain tissues. As the animals grew older, mitophagy became more frequent. However, this increase in mitophagy was not seen in insects that did not have PINK1 and parkin. These results showed that the role of PINK1 and parkin in mitophagy is not restricted to cells grown artificially.
The fruit flies designed by Cornelissen et al. will be useful to investigate how PINK1 and parkin keep cells healthy by disposing of harmful mitochondria in living organisms. Ultimately, this may help to develop treatments that slow down the development of Parkinson’s disease.
To find out more
Read the eLife research paper on which this eLife digest is based:
