Published in

Cell Press, Cell Metabolism, 4(9), p. 309-310, 2009

DOI: 10.1016/j.cmet.2009.03.007

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The worm profits from undercharging

Journal article published in 2009 by Ian Stansfield, Christopher G. Proud ORCID
This paper was not found in any repository, but could be made available legally by the author.
This paper was not found in any repository, but could be made available legally by the author.

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Abstract

Protein synthesis is a fundamentally important cellular process, being both a key stage in gene expression and a requirement for cell growth and proliferation. Protein synthesis also places heavy demands upon the cell: it consumes a high proportion of cellular energy and also requires machinery to ensure proteins are correctly folded into their functional 3D structures. Oxidative metabolism is the most effective way to provide cells with these resources. There are several situations of major clinical importance where restricted oxygen supply (hypoxia) leads to serious adverse consequences—examples include stroke and heart attacks (myocardial infarction). The interior of solid tumors may also be hypoxic. In their recent study, Anderson et al. (2009) conducted a screen for mutations that would confer resistance to hypoxia using the genetically tractable nematode worm, C. elegans. They discovered that a mutation in the gene rrt-1, which encodes an arginyl-tRNA synthetase, allows worms to resist hypoxia-induced death.