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<p>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<sup>2+</sup> (<sub>mt</sub>Ca<sup>2+</sup>) homeostasis is fundamental to mitochondrial function; yet, how mitochondrial Ca<sup>2+</sup> (<sub>mt</sub>Ca<sup>2+</sup>) homeostasis modulates nuclear gene expression to establish and maintain cellular homeostasis remains unclear. Here, we first characterize the critical role of the mitochondrial Ca<sup>2+</sup> uniporter (MCU) in control of <sub>mt</sub>Ca<sup>2+</sup> uptake and maintaining <sub>mt</sub>Ca<sup>2+</sup> homeostasis <i>in planta.</i> Using gain-of-function and sextuple MCU knockdown mutants, we then analyzed the effects of impaired MCU-controlled <sub>mt</sub>Ca<sup>2+</sup> 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 <sub>mt</sub>Ca<sup>2+</sup> homeostasis plays a pivotal role in sustaining mitochondrial and cytosolic proteostasis through an interconnected organelle quality control system, which ultimately determines cell growth and fitness.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月28日

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  • Xiaoyan Zhang,
  • Chongyang Ma,
  • Xinyue Bao,
  • Shenyu Zhang,
  • Omar Zayed,
  • Zhengjing Zhang,
  • Kai Tang,
  • Shaojun Xie,
  • Yunsheng Wang,
  • Dayong Zhang,
  • Huawei Xu,
  • Huifang Jia,
  • Xinying Wang,
  • Qianyan Lei,
  • Xiaocui Wang,
  • Junli Zhang,
  • Savithramma P. Dinesh-Kumar,
  • Chun-Peng Song,
  • Jian-Kang Zhu,
  • Xiaohong Zhu

摘要

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 Ca2+ (mtCa2+) homeostasis is fundamental to mitochondrial function; yet, how mitochondrial Ca2+ (mtCa2+) homeostasis modulates nuclear gene expression to establish and maintain cellular homeostasis remains unclear. Here, we first characterize the critical role of the mitochondrial Ca2+ uniporter (MCU) in control of mtCa2+ uptake and maintaining mtCa2+ homeostasis in planta. Using gain-of-function and sextuple MCU knockdown mutants, we then analyzed the effects of impaired MCU-controlled mtCa2+ 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 mtCa2+ homeostasis plays a pivotal role in sustaining mitochondrial and cytosolic proteostasis through an interconnected organelle quality control system, which ultimately determines cell growth and fitness.