Mitochondria declines with age in many species, but just why this happens is not very well understood. Max Planck Institute for Biology of Ageing designed this study to investigate how mitochondrial function is diminished with age and to examine factors that may prevent this process. The scientists found that communication between mitochondria and other parts of cells plays a key role in the process.
Caenorhabditis elegans were used as the model for aging in this study as over half of the genes in this animal are similar to those found in humans, and their mitochondria also declines with age. The nuclear protein NFYB-1 that switches on/off genes affecting mitochondrial activity was found itself to decline during aging; mutant animals lacking this protein had mitochondria that did not function as well and they had shorter lifespans.
NFYB-1 was discovered to steer the activity of mitochondria through the lysosome, which is where basic molecules are broken down and recycled as nutrients; feeding the NFYB-1 mutant worms cardiolipin was observed to restore mitochondrial function and animal health.
“We think the lysosome talks with the mitochondria through special fats called cardiolipins and ceramides, which are essential to mitochondrial activity,” says Max Planck Director, Adam Antebi.
Ceramides and cardiolipins are essential to human mitochondria, findings may mean that human health and aging might be improved by gaining a better understanding of how such molecules facilitate communication between the different parts of the cell.
