Perturbation of mitochondrial Ca2+ homeostasis activates cross-compartmental proteostatic response in Arabidopsis - PubMed
2 hours ago
- #Proteostasis
- #Interorganellar signaling
- #Mitochondrial Ca2+ homeostasis
- Cross-compartment communication is crucial for cellular homeostasis under stress.
- Mitochondrial Ca2+ (mtCa2+) homeostasis is key for mitochondrial function and nuclear gene expression modulation.
- The mitochondrial Ca2+ uniporter (MCU) controls mtCa2+ uptake and homeostasis in Arabidopsis.
- Impaired MCU-controlled mtCa2+ homeostasis (iMUCH) triggers interorganellar transcription activating unfolded protein responses (UPRs) across compartments.
- iMUCH also induces a post-transcriptional program repressing ribosome synthesis and RNA modification proteins.
- Eukaryotic initiation factor α (eIFα) phosphorylation may protect against long-term mitochondrial proteotoxic stress from iMUCH.
- MCU-controlled mtCa2+ homeostasis sustains mitochondrial and cytosolic proteostasis via an organelle quality control system, affecting cell growth and fitness.