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- W3183314754 abstract "Abstract Zn 2+ 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 Zn 2+ 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 Zn 2+ . We demonstrate that SLC-30A9/ZnT9 is a mitochondrial Zn 2+ exporter. Loss of SLC-30A9 leads to mitochondrial Zn 2+ 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 Zn 2+ import. Loss of SLC-25A25 suppresses the abnormal mitochondrial Zn 2+ accumulation and defective mitochondrial structure and functions caused by loss of SLC-30A9. Moreover, we reveal that the endoplasmic reticulum contains the Zn 2+ pool from which mitochondrial Zn 2+ is imported. These findings establish the molecular basis for controlling the correct mitochondrial Zn 2+ levels for normal mitochondrial structure and functions. Summary Zn 2+ is a trace ion essential for the function of many mitochondrial proteins. It is not known how mitochondrial Zn 2+ levels are regulated. Ma at al. identify transporters that mediate mitochondrial Zn 2+ export and import to maintain mitochondrial homeostasis." @default.
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- W3183314754 date "2021-07-21" @default.
- W3183314754 modified "2023-10-17" @default.
- W3183314754 title "A pair of transporters controls mitochondrial Zn2+ levels to maintain mitochondrial homeostasis" @default.
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- W3183314754 doi "https://doi.org/10.1101/2021.07.21.453180" @default.
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