Emr1 regulates the number of foci of the endoplasmic reticulum-mitochondria encounter structure complex

Faiz Rasul, Fan Zheng, Fenfen Dong, Jiajia He, Ling Liu, Wenyue Liu, Javairia Yousuf Cheema, Wenfan Wei () and Chuanhai Fu ()
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Faiz Rasul: University of Science and Technology of China
Fan Zheng: University of Science and Technology of China
Fenfen Dong: University of Science and Technology of China
Jiajia He: University of Science and Technology of China
Ling Liu: University of Science and Technology of China
Wenyue Liu: University of Science and Technology of China
Javairia Yousuf Cheema: University of Science and Technology of China
Wenfan Wei: University of Science and Technology of China
Chuanhai Fu: University of Science and Technology of China

Nature Communications, 2021, vol. 12, issue 1, 1-14

Abstract: Abstract The endoplasmic reticulum-mitochondria encounter structure (ERMES) complex creates contact sites between the endoplasmic reticulum and mitochondria, playing crucial roles in interorganelle communication, mitochondrial fission, mtDNA inheritance, lipid transfer, and autophagy. The mechanism regulating the number of ERMES foci within the cell remains unclear. Here, we demonstrate that the mitochondrial membrane protein Emr1 contributes to regulating the number of ERMES foci. We show that the absence of Emr1 significantly decreases the number of ERMES foci. Moreover, we find that Emr1 interacts with the ERMES core component Mdm12 and colocalizes with Mdm12 on mitochondria. Similar to ERMES mutant cells, cells lacking Emr1 display defective mitochondrial morphology and impaired mitochondrial segregation, which can be rescued by an artificial tether capable of linking the endoplasmic reticulum and mitochondria. We further demonstrate that the cytoplasmic region of Emr1 is required for regulating the number of ERMES foci. This work thus reveals a crucial regulatory protein necessary for ERMES functions and provides mechanistic insights into understanding the dynamic regulation of endoplasmic reticulum-mitochondria communication.

Date: 2021
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DOI: 10.1038/s41467-020-20866-x

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