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described that the transcription factor involved in the regulation of CIT2 expression in yeast is a heterodimeric complex of Rtg1p and Rtg3p proteins (Retrograde regulation protein 1 and 3). One of the first descriptions of mitochondrial retrograde signaling was made in the yeast Saccromyces cerevisiae, where the genes RTG1 and RTG2 were found to regulate the expression of the nuclear gene citrate synthase ( CIT2) in response to alteration of mitochondrial function. 1).įull size image Mitochondrial retrograde response Hence, different pathways are involved in regulating mito-nuclear communication (Fig. It can be triggered by several stressors such as misfolded proteins, inhibition of the ETC, mitochondrial depolarization, nutrient deprivation and/or redox imbalances. This mito-nuclear communication-also termed mitochondrial retrograde signaling or mitohormesis-is an evolutionary conserved process. Therefore, to ensure homeostasis, mitochondria have developed several mechanisms to sense and respond to stress via nuclear communication. Additionally, mitochondria also need to cope with oxidative stress. While mitochondria have their own genome, the vast majority of mitochondrial proteins are encoded in the nucleus and therefore require import to maintain mitochondrial function. Thus, mitochondria have their own genome (mtDNA) in the matrix, which is surrounded by the inner (IMM) and outer mitochondrial membrane (OMM). Mitochondria are organelles of bacterial ancestry. Regulation of mitochondrial quality control at the molecular level Our discussion is not intended to be exhaustive, for instance, for in-depth discussion of the cellular response to ROS, NAD + (nicotinamide adenine dinucleotide) and calcium signaling, the reader is referred to recent, comprehensive reviews. Due to the complexity and diversity of these pathways we have divided them into two broad areas: regulation at the molecular level (focusing on mitochondrial-to-nuclear communication) and regulation at the organelle level (including mitochondrial dynamics and mitophagy). In this review, we will discuss key mechanisms of mitochondrial quality control pathways. Īlterations in mitochondrial quality control responses have been described in several mitochondrial diseases such as neurodegenerative diseases (Parkinson’s, Alzheimer’s and Huntington’s disease), cardiomyopathies, ocular diseases and cancer, highlighting the importance of an adequate balance of these pathways for maintaining homeostasis. However, in the face of persistent damage, another homeostatic mechanism is to remove damaged mitochondria through a process called mitophagy. Hence, when cells are challenged, mitochondria can maintain function through a second line of defense, by altering their mitochondrial dynamics. Besides these stresses, mitochondria also face external ones such as mechanical stress, infection and environmental stress (e.g., hypoxia). Mitochondria can adapt to these by retrograde signaling to the nucleus leading to the transcriptional upregulation of stress response proteins. For instance, mitochondria can sense internal stresses such as misfolded proteins, mitochondrial DNA (mtDNA) mutations, metabolic or oxidative stress. These mechanisms react differently depending on the nature or intensity of the stress that mitochondria face. To maintain function, cells have evolved various processes that sense and respond to defective mitochondrial activity. Mitochondria are implicated in an expanding array of biological processes including redox balance, calcium homeostasis, energy production, metabolism and cell death.