Abstract
Mitochondrion maintains important cellular functions, such as energy production, cell-cycle regulation, signal transduction, oxidative stress responses, calcium transferring and apoptosis. Mitochondria are highly dynamic organelles that constantly undergo fission and fusion processes to shape mitochondria and coordinate with different cellular states. Disrupting mitochondrial dynamics would affect tumorigenesis, neurodegeneration and abnormal aging. However, little is known about the relationship between senescence and mitochondrial dynamics. In this study, we applied the replicative aging model of yeast to examine the mitochondrial dynamics and bioenergetics in cellular senescence. We found that the mitochondrial morphology turns into fragmented and major mitochondrial fission proteins’ levels are elevated in senescent cells. Moreover, the changes of mtDNA copy number, mitochondrial membrane potential, reactive oxygen species (ROS) production and oxygen consumption were found in the senescent cells. Furthermore, the proteomics analysis showed that the expressions of proteins involved in stress response were changed in senescent cells. All these findings strongly suggested that the shift of mitochondrial dynamics is accompanied with the changes of mitochondrial activities and closely associated with cellular senescence. Our results indicated that a compensative signaling network existed to strengthen the mitochondrial-related cellular activities during cellular senescence.