Abstract
Genome-scale 13C-flux analysis in Saccharomyces cerevisiae revealed that the apparent dispensability of knockout mutants with metabolic function can be explained by gene inactivity under a particular condition, by network redundancy through duplicated genes or by alternative pathways.
Highlights
Quantification of intracellular metabolite fluxes by 13C-tracer experiments is maturing into a routine higher-throughput analysis
Identification of flexible reactions in yeast metabolism To identify all potentially flexible reactions in yeast glucose metabolism that were active under a given condition, we used the recently reconciled metabolic network model iLL672 with 1,038 reactions that represent 745 biochemically distinct reactions (L Kuepfer, U Sauer and LM Blank, unpublished work), which was based on the genomescale S. cerevisiae model iFF708 [3]
As fluxes in the peripheral reactions were typically below 0.1% of the glucose uptake rate, we focused on the 51 geneencoded flexible reactions that catalyzed a flux of at least 0.1%
Summary
Quantification of intracellular metabolite fluxes by 13C-tracer experiments is maturing into a routine higher-throughput analysis. The availability of annotated genomes and accumulated biochemical evidence for individual enzymes triggered the reconstruction of stoichiometric reaction models for network-based pathway analysis [1,2]. For many microbes, such network models are available at the genome scale, providing a largely comprehensive metabolic skeleton by interconnecting all known reactions in a given organism [3,4]. Network properties such as optimal performance, flexibility to cope with ever-changing environmental conditions, and Genome Biology 2005, 6:R49. That flux quantification in hundreds of null mutants under a particular condition is feasible in principle, the question arises of which mutants should be analyzed
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