Fusion, fission, and transport control asymmetric inheritance of mitochondria and protein aggregates
| Autor: | Matthias Weiss, Stefan Böckler, Ralf J. Braun, Nadine Hock, Till Klecker, Madita Wolter, Benedikt Westermann, Xenia Chelius |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Saccharomyces cerevisiae Proteins Time Factors Genotype Cell division Myosin Type V Saccharomyces cerevisiae Biology Mitochondrion DNA Mitochondrial Mitochondrial Dynamics Article Protein Aggregates 03 medical and health sciences 0302 clinical medicine Gene Expression Regulation Fungal Myosin Computer Simulation DNA Fungal Research Articles Mitochondrial transport Microscopy Video Myosin Heavy Chains Biological Transport Cell Biology Mitochondria Cell biology Cytosol Phenotype 030104 developmental biology mitochondrial fusion Cytoplasm Mutation Mitochondrial fission Cell Division 030217 neurology & neurosurgery |
| Zdroj: | The Journal of Cell Biology |
| ISSN: | 1540-8140 0021-9525 |
| DOI: | 10.1083/jcb.201611197 |
| Popis: | Asymmetric inheritance of cell organelles determines the fate of daughter cells. Böckler et al. use yeast as a model to demonstrate that the dynamics of mitochondrial fusion, fission, and transport determine partitioning of mitochondria and cytosolic protein aggregates, which is critical for rejuvenation of daughter cells. Partitioning of cell organelles and cytoplasmic components determines the fate of daughter cells upon asymmetric division. We studied the role of mitochondria in this process using budding yeast as a model. Anterograde mitochondrial transport is mediated by the myosin motor, Myo2. A genetic screen revealed an unexpected interaction of MYO2 and genes required for mitochondrial fusion. Genetic analyses, live-cell microscopy, and simulations in silico showed that fused mitochondria become critical for inheritance and transport across the bud neck in myo2 mutants. Similarly, fused mitochondria are essential for retention in the mother when bud-directed transport is enforced. Inheritance of a less than critical mitochondrial quantity causes a severe decline of replicative life span of daughter cells. Myo2-dependent mitochondrial distribution also is critical for the capture of heat stress–induced cytosolic protein aggregates and their retention in the mother cell. Together, these data suggest that coordination of mitochondrial transport, fusion, and fission is critical for asymmetric division and rejuvenation of daughter cells. |
| Databáze: | OpenAIRE |
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