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The origin of mutational robustness—whether it is a directly evolved trait or a byproduct of evolutionary history—remains debatable (6).In either case, metabolic network analysis shows that the nonessentiality of enzymes and associated genes is largely due to the inactivity of the corresponding metabolic reactions under laboratory conditions (7–9).The response of the metabolic network to knockout perturbations is modeled using both model-independent analysis and the two most accepted phenomenological approaches, minimization of metabolic adjustment (MOMA) (17) and regulatory on/off minimization (ROOM) (18) () of the original organism with that of a modified organism in which the latent reactions have been disabled.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.
On the contrary, we predict that it more often shows improved growth in the suboptimal regime shortly after the perturbation. Each row indicates the difference in early postperturbation growth rate between the strains with and without latent pathways for the knockout perturbation indicated along the vertical axis, when: () the modified organism lacks the set of simultaneously nonessential latent reactions, which is the subset of such latent reactions that are not needed for optimal growth in any of the other 51 single-gene knockout mutants.
Here, we test this hypothesis computationally and find, surprisingly, that the availability of latent pathways consistently offers no growth advantage and tends, in fact, to inhibit growth after genetic perturbations.
This is shown to be true even for latent pathways with a known function in alternate conditions, thus extending the significance of this adverse effect beyond apparently nonessential genes.
The statistics are summarized in the left and center columns of Table 1 for MOMA and ROOM, respectively.
The set of transiently active (latent) reactions depends on the perturbation.