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SLC-30A9 is required for Zn
- Source :
- Proc Natl Acad Sci U S A
- Publication Year :
- 2021
-
Abstract
- The trace element zinc is essential for many aspects of physiology. The mitochondrion is a major Zn(2+) store, and excessive mitochondrial Zn(2+) is linked to neurodegeneration. How mitochondria maintain their Zn(2+) homeostasis is unknown. Here, we find that the SLC-30A9 transporter localizes on mitochondria and is required for export of Zn(2+) from mitochondria in both Caenorhabditis elegans and human cells. Loss of slc-30a9 leads to elevated Zn(2+) levels in mitochondria, a severely swollen mitochondrial matrix in many tissues, compromised mitochondrial metabolic function, reductive stress, and induction of the mitochondrial stress response. SLC-30A9 is also essential for organismal fertility and sperm activation in C. elegans, during which Zn(2+) exits from mitochondria and acts as an activation signal. In slc-30a9–deficient neurons, misshapen mitochondria show reduced distribution in axons and dendrites, providing a potential mechanism for the Birk–Landau–Perez cerebrorenal syndrome where an SLC30A9 mutation was found.
- Subjects :
- Male
Membrane Potential, Mitochondrial
Cell Cycle Proteins
Dendrites
Biological Sciences
Spermatozoa
Axons
Mitochondria
Gene Knockout Techniques
Zinc
Mutation
Animals
Homeostasis
Humans
Female
Caenorhabditis elegans
Caenorhabditis elegans Proteins
Cation Transport Proteins
HeLa Cells
Transcription Factors
Subjects
Details
- ISSN :
- 10916490
- Volume :
- 118
- Issue :
- 35
- Database :
- OpenAIRE
- Journal :
- Proceedings of the National Academy of Sciences of the United States of America
- Accession number :
- edsair.pmid..........eddd612a2375882d85f46245a51af5bd