Cell Reports (Oct 2024)

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

  • Gan Zhao,
  • Mingkang Jia,
  • Shicong Zhu,
  • He Ren,
  • Guopeng Wang,
  • Guangwei Xin,
  • Mengjie Sun,
  • Xiangyang Wang,
  • Qiaoyu Lin,
  • Qing Jiang,
  • Chuanmao Zhang

Journal volume & issue
Vol. 43, no. 10
p. 114794

Abstract

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Summary: 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.

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