Moisoi 2018 MiP2018a
Moisoi N (2018)
Mitochondrial dysfunction and DNA damage accumulation are recognised hallmarks of age related diseases. Mitochondrial dysfunction initiates protective signalling mechanisms coordinated at nuclear level particularly by modulating transcription of stress signalling factors. In turn, the cellular response to DNA lesions comprises a series of interconnected complex protective pathways, which require the energetic and metabolic support of the mitochondria. Here I will discuss how mitochondria-nucleus communication operates in physiologically relevant stress conditions to protect against neurodegeneration. Thus in mammalian cells and Drosophila subjected to both mitochondrial and genotoxic stress, mitochondrial activity slows down while maintaining the DNA integrity takes priority. Depending on the site of the initiating stress, mitochondria or the nucleus can take the lead in stress response initiation - ‘talks first’. In most situations the nucleus and its integrity appear to be a priority - ‘talks louder’. These communication phenomena have a protective role against neurodegenerative processes.
Labels: MiParea: nDNA;cell genetics Pathology: Aging;senescence, Neurodegenerative
Organism: Other mammals, Drosophila
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