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Mitochondrial gene‐knockout (ρ0) cells: A versatile model for exploring the secrets of trans‐plasma membrane electron transport

Mitochondrial gene‐knockout (ρ0) cells: A versatile model for exploring the secrets of... Plasma membrane electron transport (tPMET) pathways have been identified in all living cells, and a wide variety of tools have been used to study these processes. In our laboratory we have used the cell‐impermeable tetrazolium dye WST‐1, together with the mitochondrial gene knockout ρ0) cell model, to investigate one of these pathways. We have shown that growth of HL60ρ0 cells is dependent on oxygen, and that these cells consume oxygen at the cell surface. Similarities in inhibition profiles between non‐mitochondrial oxygen consumption and WST‐1 reduction suggest that both systems share a common tPMET pathway. In support of this, oxygen was shown to compete with the intermediate electron acceptor that mediates WST‐1 reduction, for reducing electrons. The observation that tPMET activity is higher in ρ0 cells compared to their mitochondrially‐competent counterparts was shown to be the result of competition between the mitochondrial and plasma membrane electron transport systems for intracellular reducing equivalents. Elevated rates of dye reduction appear to be mediated through increased expression of the key components of tPMET, which include the cell surface NADH oxidase, CNOX. These findings have played a critical role in shaping our current understanding of the mechanisms of this particular pathway of tPMET. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png BioFactors Wiley

Mitochondrial gene‐knockout (ρ0) cells: A versatile model for exploring the secrets of trans‐plasma membrane electron transport

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References (25)

Publisher
Wiley
Copyright
Copyright © 2004 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0951-6433
eISSN
1872-8081
DOI
10.1002/biof.5520200404
Publisher site
See Article on Publisher Site

Abstract

Plasma membrane electron transport (tPMET) pathways have been identified in all living cells, and a wide variety of tools have been used to study these processes. In our laboratory we have used the cell‐impermeable tetrazolium dye WST‐1, together with the mitochondrial gene knockout ρ0) cell model, to investigate one of these pathways. We have shown that growth of HL60ρ0 cells is dependent on oxygen, and that these cells consume oxygen at the cell surface. Similarities in inhibition profiles between non‐mitochondrial oxygen consumption and WST‐1 reduction suggest that both systems share a common tPMET pathway. In support of this, oxygen was shown to compete with the intermediate electron acceptor that mediates WST‐1 reduction, for reducing electrons. The observation that tPMET activity is higher in ρ0 cells compared to their mitochondrially‐competent counterparts was shown to be the result of competition between the mitochondrial and plasma membrane electron transport systems for intracellular reducing equivalents. Elevated rates of dye reduction appear to be mediated through increased expression of the key components of tPMET, which include the cell surface NADH oxidase, CNOX. These findings have played a critical role in shaping our current understanding of the mechanisms of this particular pathway of tPMET.

Journal

BioFactorsWiley

Published: Jan 1, 2004

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