Abstract：
Mitochondrial function is essential for plant growth, but the mechanisms involved in adjusting growth and metabolism to changes in mitochondrial energy production are not fully understood. We studied plants with reduced expression of CYTC-1, one of two genes encoding the respiratory chain component cytochrome c (CYTc) in Arabidopsis, to understand how mitochondria communicate their status to coordinate metabolism and growth. Plants with CYTc deficiency show decreased mitochondrial membrane potential and lower ATP content, even when carbon sources are present. They also exhibit higher free amino acid content, induced autophagy, and increased resistance to nutritional stress caused by prolonged darkness, similar to plants with triggered starvation signals. CYTc deficiency affects target of rapamycin (TOR)-pathway activation, reducing S6 kinase (S6K) and RPS6A phosphorylation, as well as total S6K protein levels due to increased protein degradation via proteasome and autophagy. TOR overexpression restores growth and other parameters affected in cytc-1 mutants, even if mitochondrial membrane potential and ATP levels remain low. We propose that CYTc-deficient plants coordinate their metabolism and energy availability by reducing TOR-pathway activation as a preventive signal to adjust growth in anticipation of energy exhaustion, thus providing a mechanism by which changes in mitochondrial activity are transduced to the rest of the cell.
摘要：
线粒体功能对植物生长至关重要,但是调节生长和代谢以适应线粒体能量产生变化的机制尚不完全清楚。我们研究了CYTC-1表达降低的植物，CYTC-1是拟南芥中编码呼吸链成分细胞色素c（CYTc）的两个基因之一，了解线粒体如何传达其状态以协调新陈代谢和生长。CYTc缺乏的植物表现出降低的线粒体膜电位和较低的ATP含量,即使存在碳源。它们还表现出更高的游离氨基酸含量，诱导自噬，对长期黑暗造成的营养压力的抵抗力增强，类似于具有触发饥饿信号的植物。CYTc缺乏影响雷帕霉素靶蛋白(TOR)通路激活,减少S6激酶（S6K）和RPS6A磷酸化，以及由于蛋白酶体和自噬导致的蛋白质降解增加的总S6K蛋白质水平。TOR过表达可恢复cytc-1突变体的生长和其他受影响的参数，即使线粒体膜电位和ATP水平仍然很低。我们建议CYTc缺乏的植物通过减少TOR途径激活作为预防信号来调节生长以预期能量耗尽来协调其代谢和能量可用性。从而提供了一种机制，通过该机制，线粒体活性的变化被转导到细胞的其余部分。
