期刊
PROTEIN & CELL
卷 13, 期 3, 页码 180-202出版社
OXFORD UNIV PRESS
DOI: 10.1007/s13238-021-00881-4
关键词
mitochondria; Zn2+ transporter; C; elegans; ER-mitochondrial contact; development
类别
资金
- National Science Foundation of China [91954204, 31730053]
- National Basic Research Program of China [2017YFA0503403]
- Yunnan Province Science and Technology Department [202001BB050077, 202105AB160003]
- Program of Yunnan Province Leading Talents in Science and Technology
Zn2+ is essential for the activity of many mitochondrial proteins, but how the proper mitochondrial Zn2+ level is maintained is not well understood. Two mitochondrion-localized transporters, SLC-30A9 and SLC-25A25, regulate mitochondrial Zn2+ levels. The endoplasmic reticulum serves as a source of Zn2+ for mitochondrial import.
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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