The study explores how Ubp3 regulates mitochondrial repression by controlling glycolytic flux and Pi allocation. Loss of Ubp3 leads to increased trehalose production, decreased glycolytic enzymes, and higher Pi levels, enhancing mitochondrial activity. The findings suggest a novel mechanism involving Pi budgeting as a crucial factor in glucose-mediated mitochondrial repression.
The research identifies Ubp3 as essential for maintaining high glycolytic flux despite abundant glucose, leading to rewired glucose metabolism with increased trehalose production. This metabolic shift increases Pi release from trehalose synthesis and decreases Pi consumption via reduced GAPDH levels. Consequently, there is an accumulation of intracellular Pi available for mitochondria.
Furthermore, the study demonstrates that altering Pi availability influences mitochondrial activity. Increasing internal Pi levels enhances respiration, while restricting mitochondrial Pi transport reduces basal oxygen consumption rate (OCR). The role of Mir1 as a major mitochondrial Pi transporter is highlighted in regulating mitochondrial activity under different conditions.
Overall, the research uncovers a conserved mechanism across diverse yeast strains where intracellular Pi budgeting plays a critical role in modulating glucose-mediated mitochondrial repression. The findings shed light on the intricate balance between cytosolic glycolysis and mitochondrial processes through Pi allocation.
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by Laxman,S., V... at www.biorxiv.org 12-30-2022
https://www.biorxiv.org/content/10.1101/2022.12.29.522272v4Deeper Inquiries