Perturbation of mitochondrial Cahomeostasis activates cross-compartmental proteostatic response in Arabidopsis

Source: PubMed Central Open Access, NCBI / U.S. National Library of Medicine

Cross-compartment communication is critical for maintaining cellular homeostasis, which is essential for cell function and survival under stressful conditions. However, the cellular cues that trigger interorganellar communication remain poorly understood. Mitochondrial Ca(Ca) homeostasis is fundamental to mitochondrial function; yet, how mitochondrial Ca(Ca) homeostasis modulates nuclear gene expression to establish and maintain cellular homeostasis remains unclear. Here, we first characterize the critical role of the mitochondrial Cauniporter (MCU) in control ofCauptake and maintainingCahomeostasisUsing gain-of-function and sextuple MCU knockdown mutants, we then analyzed the effects of impaired MCU-controlledCahomeostasis (iMUCH). We find that iMUCH elicits an interorganellar transcription program that activates multiple compartment-specific unfolded protein responses (UPRs) and genes critical for mitochondrial and cytosolic proteostasis. Additionally, iMUCH induces a post-transcriptional program that selectively represses the synthesis of ribosomes and RNA modification proteins. Furthermore, eukaryotic initiation factor α (eIFα and its phosphorylation likely serve as a protective mechanism under long-term mitochondrial proteotoxic stress induced by iMUCH. Collectively, the data demonstrate that MCU-controlledCahomeostasis plays a pivotal role in sustaining mitochondrial and cytosolic proteostasis through an interconnected organelle quality control system, which ultimately