Mitotic ER-mitochondria contact enhances mitochondrial Ca2+ influx to promote cell division

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 CA²⁺ influx events and ATP production during Mitosis. While both events promote ATP production during Mitosis, the second event, the CA²⁺ influx surge, is substantial. To facilitate this CA²⁺ influx surge, the lamin B receptor (LBR) organizes a mitosis-specific endoplasmic reticulum (ER)-mitochondrial contact site (ERMCS), creating a rapid CA²⁺ transport pathway. LBR acts as a tether, connecting the ER CA²⁺ release channel IP₃R with the mitochondrial VDAC2. Depletion of LBR disrupts the CA²⁺ 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.