Mitotic ER-mitochondria contact enhances mitochondrial Ca2+ influx to promote cell division
Zhao Gan, Mingkang Jia, Shicong Zhu, He Ren, Guopeng Wang, Guangwei Xin, Mengjie Sun, Xiangyang Wang, Qiaoyu Lin, Jiang Qing, Chuanmao Zhang
Abstract
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 2+ influx events and ATP production during mitosis. While both events promote ATP production during mitosis, the second event, the Ca 2+ influx surge, is substantial. To facilitate this Ca 2+ influx surge, the lamin B receptor (LBR) organizes a mitosis-specific endoplasmic reticulum (ER)-mitochondrial contact site (ERMCS), creating a rapid Ca 2+ transport pathway. LBR acts as a tether, connecting the ER Ca 2+ release channel IP 3 R with the mitochondrial VDAC2. Depletion of LBR disrupts the Ca 2+ 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.