Mitochondrial damage is considered to be an important contribution to degenerative aging. Here researchers find stem cells performing a preferential assignment of cellular components during cell division, giving one of the daughter cells more of the components likely to be damaged - such as older mitochondria. This differential assignment of damage during replication has been seen in bacteria as well; it is clearly a very ancient aspect of cellular biology.
While interesting, there may or may not be any near term practical application for the treatment of aging resulting from a better understanding of how cells are determining which mitochondria to assign to which daughter cell. A more direct path such as mitochondrial repair or replacement may be a more efficient towards medical intervention in the aging process given the present state of technology and knowledge:
During division, stem cells distinguish between old and young mitochondria and allocate them disproportionately between daughter cells. As a result, the daughter cell destined to remain a stem cell receives predominantly young mitochondria, while the cell meant to differentiate into another cell type carries with it a higher compliment of the aged organelles. This asymmetric apportioning of cellular contents may represent a mechanism through which stem cells prevent the accumulation of damage in their lineage over time.
Among the hallmarks of stem cells is so-called asymmetric cell division. Unlike their ordinary cellular counterparts, which divide symmetrically to create two cells with identical fates, stem cell division can produce one daughter cell that will remain a stem cell and another bound for further differentiation into another cell type. Scientists have observed that non-mammalian organisms are able to apportion damaged components asymmetrically during cell division, but it was unclear whether mammalian stem cells could behave similarly.
To track the destinations of subcellular components during cell division, the researchers tagged the components - including lysosomes, mitochondria, Golgi apparatus, ribosomes, and chromatin - with a fluorescent protein that glows when hit by a pulse of ultraviolet light. By tracing the movements of the glowing organelles, the researchers were able to demonstrate that while normal epithelial cells distributed all of the tagged components symmetrically to daughter cells, stem cells localized their older mitochondria distinctly and passed on the lion's share of them to the daughter cells headed for differentiation. The researchers ultimately found that the number of older mitochondria in those cells was roughly six times that in daughter cells whose fate was to remain as stem cells.
Further, they discovered that chemically disrupting the cells' inherent mitochondrial quality-control mechanisms prevented asymmetric apportioning of young and old mitochondria and caused the loss of stem-like characteristics. Taken together, these results indicate that this disproportionate allocation of aged mitochondria during stem cell division is essential for maintaining stemness in the next generation. "While we do not know how stem cells recognize the age of their mitochondria, forced symmetric apportioning of aged mitochondria resulted in loss of stemness in all of the daughter cells. This suggests that the age-selective apportioning of old and potentially damaged organelles may be a way to fight stem cell exhaustion and aging."