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Factors That Affect The Cell Of Mitochondrial Proteins And Enzymes Of Electron Transport Chain

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The mitochondrion is an organelle which originated from the endosymbiosis of eubacteria and, as a result, contains its own genome which encodes for essential mitochondrial transcriptional machinery proteins and subunits of electron transport chain (ETC) complexes [1, 2]. However, the vast majority of mitochondrial proteins are encoded for by the nucleus [3]. As a result, these two organelles must be able to communicate in order to coordinate protein synthesis and maintain mitochondrial homeostasis [4]. This communication is also particularly important in the cells response to stress. Mitochondria are deemed ‘endogenous stress detectors’ as they can sense stresses induced by high reactive oxygen species (ROS) levels and oxidative stress, membrane depolarisation, cellular energy levels, and an accumulation of unfolded proteins [5]. Therefore, in response to stress, this mitochondrial-to-nuclear communication is essential to bring about a change in nuclear gene expression, which will relieve the stress and protect the cell from damage. This commonly occurs through the activation of specific retrograde stress response pathways from mitochondria to the nucleus, which combat the stress and allow mitochondria to regain homeostasis [6, 7].
It is important that we understand these retrograde stress responses, as many of these pathways have been implicated in lifespan regulation in model organisms [8]. For example, dysregulation of two well characterised stress response pathways, the

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