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1), reflecting regulatory changes that locally reroute fluxes in the short-term metabolic response to the perturbation (21, 22).If the perturbation is nonlethal, the perturbed organisms will undergo adaptive evolution—adopting beneficial mutations over longer timescales (23, 24) to achieve a new optimal growth state, which can be predicted by FBA (18, 25). The dashed lines indicate the possible behavior for a modified strain in which the original latent pathways have been removed: The postperturbation growth rate may decrease (red), remain the same (green), or increase (blue), and a smaller number of new latent pathways may be created.
We consider glucose minimal medium and gene knockouts that necessarily change the original metabolic flux distribution but that nonetheless are compatible with nonzero growth according to FBA.
There are 52 enzyme-coding genes associated with 97 metabolic reactions in the reconstructed network that satisfy this condition.
We systematically predict the impact of latent pathway activation on growth rate following perturbations caused by the knockouts of each of these genes.
A recent groundbreaking study has shown, however, that a large fraction of reactions not active under standard laboratory conditions become transiently active after a genetic or environmental perturbation (12, 13). The prevailing interpretation has been that the transient activation of such latent pathways facilitates adaptation to new conditions, thereby attributing function to genes that have been classified as dispensable for the lack of phenotype in steady-state experiments.
This is naturally formulated as the hypothesis that latent pathways have a positive impact on postperturbation growth (cellular reproduction), which is a measure of competitive advantage with a strong empirical basis (1–3, 10, 11, 13).