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A pair of transporters controls mitochondrial Zn2+ levels to maintain mitochondrial homeostasis

By Tengfei Ma, Liyuan Zhao, Jie Zhang, Ruofeng Tang, Xin Wang, Nan Liu, Qian Zhang, Fengyang Wang, Meijiao Li, Qian Shan, Yang Yang, Qiuyuan Yin, Limei Yang, Qiwen Gan, Chonglin Yang

Posted 21 Jul 2021
bioRxiv DOI: 10.1101/2021.07.21.453180

Zn2+ is required for the activity of many mitochondrial proteins, which regulate mitochondrial dynamics, apoptosis and mitophagy. However, it is not understood how the proper mitochondrial Zn2+ level is achieved to maintain mitochondrial homeostasis. Using Caenorhabditis elegans, we reveal here that a pair of mitochondrion-localized transporters controls the mitochondrial level of Zn2+. We demonstrate that SLC-30A9/ZnT9 is a mitochondrial Zn2+ exporter. Loss of SLC-30A9 leads to mitochondrial Zn2+ accumulation, which damages mitochondria, impairs animal development and shortens the life span. We further identify SLC-25A25/SCaMC-2 as an important regulator of mitochondrial Zn2+ import. Loss of SLC-25A25 suppresses the abnormal mitochondrial Zn2+ accumulation and defective mitochondrial structure and functions caused by loss of SLC-30A9. Moreover, we reveal that the endoplasmic reticulum contains the Zn2+ pool from which mitochondrial Zn2+ is imported. These findings establish the molecular basis for controlling the correct mitochondrial Zn2+ levels for normal mitochondrial structure and functions.

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