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TOR 复合物控制 ATP 水平以调节 中的肌动蛋白细胞骨架动态。

The TOR complex controls ATP levels to regulate actin cytoskeleton dynamics in .

机构信息

Key Laboratory of Cell Proliferation and Regulation Biology of Ministry of Education, College of Life Science, Beijing Normal University, Beijing 100875, China.

Martin-Luther-University Halle-Wittenberg, Institute of Plant Physiology, 06120 Halle (Saale), Germany.

出版信息

Proc Natl Acad Sci U S A. 2022 Sep 20;119(38):e2122969119. doi: 10.1073/pnas.2122969119. Epub 2022 Sep 12.

DOI:10.1073/pnas.2122969119
PMID:36095209
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9499549/
Abstract

Energy is essential for all cellular functions in a living organism. How cells coordinate their physiological processes with energy status and availability is thus an important question. The turnover of actin cytoskeleton between its monomeric and filamentous forms is a major energy drain in eukaryotic cells. However, how actin dynamics are regulated by ATP levels remain largely unknown in plant cells. Here, we observed that seedlings with impaired functions of target of rapamycin complex 1 (TORC1), either by mutation of the key component, , or inhibition of TOR activity by specific inhibitors, displayed reduced sensitivity to actin cytoskeleton disruptors compared to their controls. Consistently, actin filament dynamics, but not organization, were suppressed in TORC1-impaired cells. Subcellular localization analysis and quantification of ATP concentration demonstrated that RAPTOR1B localized at cytoplasm and mitochondria and that ATP levels were significantly reduced in TORC1-impaired plants. Further pharmacologic experiments showed that the inhibition of mitochondrial functions led to phenotypes mimicking those observed in mutants at the level of both plant growth and actin dynamics. Exogenous feeding of adenine could partially restore ATP levels and actin dynamics in TORC1-deficient plants. Thus, these data support an important role for TORC1 in coordinating ATP homeostasis and actin dynamics in plant cells.

摘要

能量对于生物体的所有细胞功能都是必不可少的。因此,细胞如何将其生理过程与能量状态和可用性协调起来是一个重要的问题。真核细胞中肌动蛋白细胞骨架从单体到丝状形式的转化是一个主要的能量消耗过程。然而,在植物细胞中,ATP 水平如何调节肌动蛋白动力学在很大程度上仍不清楚。在这里,我们观察到,与对照相比,雷帕霉素靶蛋白复合物 1(TORC1)功能受损的幼苗,无论是通过关键成分突变,还是通过特异性抑制剂抑制 TOR 活性,对肌动蛋白细胞骨架破坏剂的敏感性降低。一致的是,在 TORC1 受损的细胞中,肌动蛋白丝动力学受到抑制,而肌动蛋白丝的组织不受影响。亚细胞定位分析和 ATP 浓度的定量表明,RAPTOR1B 定位于细胞质和线粒体,并且 TORC1 受损的植物中 ATP 水平显著降低。进一步的药理实验表明,线粒体功能的抑制导致了与突变体在植物生长和肌动蛋白动力学水平上观察到的表型相似的表型。外源性添加腺嘌呤可部分恢复 TORC1 缺陷植物中的 ATP 水平和肌动蛋白动力学。因此,这些数据支持 TORC1 在协调植物细胞中 ATP 动态平衡和肌动蛋白动力学方面的重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3516/9499549/fdd5eec04fed/pnas.2122969119fig06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3516/9499549/86d16337b0f0/pnas.2122969119fig01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3516/9499549/283c2e9360e1/pnas.2122969119fig02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3516/9499549/5af4e3f12587/pnas.2122969119fig03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3516/9499549/d0c1fb2b4b12/pnas.2122969119fig04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3516/9499549/7ef3261ae3aa/pnas.2122969119fig05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3516/9499549/fdd5eec04fed/pnas.2122969119fig06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3516/9499549/86d16337b0f0/pnas.2122969119fig01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3516/9499549/283c2e9360e1/pnas.2122969119fig02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3516/9499549/5af4e3f12587/pnas.2122969119fig03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3516/9499549/d0c1fb2b4b12/pnas.2122969119fig04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3516/9499549/7ef3261ae3aa/pnas.2122969119fig05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3516/9499549/fdd5eec04fed/pnas.2122969119fig06.jpg

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