The Ministry of Education Key Laboratory of Cell Proliferation and Differentiation, College of Life Sciences, Peking University, Beijing 100871, China.
The Ministry of Education Key Laboratory of Cell Proliferation and Differentiation, College of Life Sciences, Peking University, Beijing 100871, China; The Academy for Cell and Life Health, Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming 650500, China.
Cell Rep. 2024 Oct 22;43(10):114794. doi: 10.1016/j.celrep.2024.114794. Epub 2024 Sep 28.
Cell division is tightly regulated and requires an expanded energy supply. However, how this energy is generated remains unclear. Here, we establish a correlation between two mitochondrial Ca influx events and ATP production during mitosis. While both events promote ATP production during mitosis, the second event, the Ca influx surge, is substantial. To facilitate this Ca influx surge, the lamin B receptor (LBR) organizes a mitosis-specific endoplasmic reticulum (ER)-mitochondrial contact site (ERMCS), creating a rapid Ca transport pathway. LBR acts as a tether, connecting the ER Ca release channel IPR with the mitochondrial VDAC2. Depletion of LBR disrupts the Ca influx surge, reduces ATP production, and postpones the metaphase-anaphase transition and subsequent cell division. These findings provide insight into the mechanisms underlying mitotic energy production and supply required for cell proliferation.
细胞分裂受到严格调控，需要扩展的能量供应。然而，这种能量是如何产生的仍然不清楚。在这里，我们建立了两个线粒体钙内流事件与有丝分裂期间 ATP 产生之间的相关性。虽然这两个事件都促进了有丝分裂期间的 ATP 产生，但第二个事件，钙内流激增，是巨大的。为了促进这种钙内流激增，核纤层蛋白 B 受体 (LBR) 组织了一个有丝分裂特异性内质网 (ER)-线粒体接触位点 (ERMCS)，创建了一个快速的钙运输途径。LBR 作为一个系绳，连接内质网 Ca 释放通道 IPR 与线粒体 VDAC2。LBR 的耗竭会破坏钙内流激增，减少 ATP 的产生，并推迟中期-后期转变和随后的细胞分裂。这些发现为有丝分裂能量产生的机制以及细胞增殖所需的能量供应提供了深入了解。
