Mitochondria-ER contact sites expand during mitosis
Fang Yu,
Raphael Courjaret,
Lama Assaf,
Asha Elmi,
Ayat Hammad,
Melanie Fisher,
Mark Terasaki,
Khaled Machaca
Affiliations
Fang Yu
Calcium Signaling Group, Research Department, Weill Cornell Medicine Qatar, Education City, Qatar Foundation, Doha, Qatar; Department of Physiology and Biophysics, Weill Cornell Medicine, New York, NY, USA
Raphael Courjaret
Calcium Signaling Group, Research Department, Weill Cornell Medicine Qatar, Education City, Qatar Foundation, Doha, Qatar; Department of Physiology and Biophysics, Weill Cornell Medicine, New York, NY, USA
Lama Assaf
Calcium Signaling Group, Research Department, Weill Cornell Medicine Qatar, Education City, Qatar Foundation, Doha, Qatar; College of Health and Life Science, Hamad bin Khalifa University, Doha, Qatar
Asha Elmi
Calcium Signaling Group, Research Department, Weill Cornell Medicine Qatar, Education City, Qatar Foundation, Doha, Qatar; College of Health and Life Science, Hamad bin Khalifa University, Doha, Qatar
Ayat Hammad
Calcium Signaling Group, Research Department, Weill Cornell Medicine Qatar, Education City, Qatar Foundation, Doha, Qatar; College of Health and Life Science, Hamad bin Khalifa University, Doha, Qatar
Melanie Fisher
Department of Cell Biology, UConn Health, 263 Farmington Ave, Farmington, CT 06030, USA
Mark Terasaki
Department of Cell Biology, UConn Health, 263 Farmington Ave, Farmington, CT 06030, USA
Khaled Machaca
Calcium Signaling Group, Research Department, Weill Cornell Medicine Qatar, Education City, Qatar Foundation, Doha, Qatar; Department of Physiology and Biophysics, Weill Cornell Medicine, New York, NY, USA; Corresponding author
Summary: Mitochondria-ER contact sites (MERCS) are involved in energy homeostasis, redox and Ca2+ signaling, and inflammation. MERCS are heavily studied; however, little is known about their regulation during mitosis. Here, we show that MERCS expand during mitosis in three cell types using various approaches, including transmission electron microscopy, serial EM coupled to 3D reconstruction, and a split GFP MERCS marker. We further show enhanced Ca2+ transfer between the ER and mitochondria using either direct Ca2+ measurements or by quantifying the activity of Ca2+-dependent mitochondrial dehydrogenases. Collectively, our results support a lengthening of MERCS in mitosis that is associated with improved Ca2+ coupling between the two organelles. This augmented Ca2+ coupling could be important to support the increased energy needs of the cell during mitosis.
