Perturbation of mitochondrial Ca2+ homeostasis activates cross-compartmental proteostatic response in Arabidopsis

作者：Xiaoyan Zhang, Chongyang Ma, Xinyue Bao, Shenyu Zhang, Omar Zayed, Zhengjing Zhang, Kai Tang, Shaojun Xie, Yunsheng Wang, Dayong Zhang, Huawei Xu, Huifang Jia, X Wang, Qianyan Lei, Xiaocui Wang, J H Zhang, Savithramma P. Dinesh‐Kumar, Chun-Peng Song, Jian-Kang Zhu, Xiaohong Zhu · 发表于：Stress Biology · 年份：2026 · DOI：10.1007/s44154-026-00314-4 · 研究领域：Endoplasmic Reticulum Stress and Disease、Mitochondrial Function and Pathology、Photosynthetic Processes and Mechanisms

Abstract 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 2+ ( mt Ca 2+ ) homeostasis is fundamental to mitochondrial function; yet, how mitochondrial Ca 2+ ( mt Ca 2+ ) homeostasis modulates nuclear gene expression to establish and maintain cellular homeostasis remains unclear. Here, we first characterize the critical role of the mitochondrial Ca 2+ uniporter (MCU) in control of mt Ca 2+ uptake and maintaining mt Ca 2+ homeostasis in planta. Using gain-of-function and sextuple MCU knockdown mutants, we then analyzed the effects of impaired MCU-controlled mt Ca 2+ homeostasis (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-controlled mt Ca 2+ homeostasis plays a pivotal role in sustaining mitochondrial and cytosolic proteosta...