Conditional knockdown of hMRS2 results in loss of mitochondrial Mg(2+) uptake and cell death.

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Citation

Piskacek M, Zotova L, Zsurka G, Schweyen RJ

Conditional knockdown of hMRS2 results in loss of mitochondrial Mg(2+) uptake and cell death.

J Cell Mol Med. 2009 Apr;13(4):693-700. doi: 10.1111/j.1582-4934.2008.00328.x. Epub 2008 Mar 31.

PubMed ID
18384665 [ View in PubMed
]
Abstract

The human gene MRS2L encodes a mitochondrial protein distantly related to CorA Mg(2+) transport proteins. Constitutive shRNA-mediated knockdown of hMRS2 in human HEK-293 cell line was found here to cause death. To further study its role in Mg(2+) transport, we have established stable cell lines with conditionally expressing shRNAs directed against hMRS2L. The cells expressing shRNA for several generations exhibited lower steady-state levels of free mitochondrial Mg(2+) ([Mg(2+)](m)) and reduced capacity of mitochondrial Mg(2+) uptake than control cells. Long-term expression of shRNAs resulted in loss of mitochondrial respiratory complex I, decreased mitochondrial membrane potential and cell death. We conclude that hMrs2 is the major transport protein for Mg (+) uptake into mitochondria and that expression of hMrs2 is essential for the maintenance of respiratory complex I and cell viability.

DrugBank Data that Cites this Article

Polypeptides
NameUniProt ID
Magnesium transporter MRS2 homolog, mitochondrialQ9HD23Details