Mitochondria are essential organelles responsible for producing cellular energy and contributing to metabolism. Dysfunctions of mitochondria, particularly the aggregation of mitochondrial proteins, have been implicated in neurodegenerative disorders. Therefore, it is crucial to understand the biosynthesis, regulation, and quality control mechanisms of mitochondria to advance potential future treatments. In this first part of the thesis, we identify an integrated mitochondrial-associated quality control mechanism in Saccharomyces cerevisiae that helps maintain cellular homeostasis in response to the overexpression of nuclear-encoded mitochondrial MMF1 mRNA. We demonstrate that ribosome pausing on MMF1 mRNA, along with the involvement of Not4 and Caf130, subunits of the Ccr4-Not complex, are necessary for this integrated quality control mechanism. In the second part of the thesis we explore the interplay between the Ccr4-Not complex and the RNA-binding protein Puf3, which finely regulates the expression of mitochondrial mRNAs. This interplay adds an additional layer of regulation to ensure precise control of mitochondrial gene expression.