The evolution and adaptation of the living organisms is attributed, in part, to the duplication and divergence of genetic modules. While the fitness effect of single-gene manipulations (either knock-out or over-expression) is studied in many bacterial systems, the effect of specific perturbations to the transcription regulatory network was not addressed before this study.
E. coli, the model organism of choice, has a well studied hierarchical transcription network in which a few master regulators (e.g. CRP, FNR, IHF, Fis...) affect half of the genome (including other transcription factors) either directly or indirectly. The authors set out to randomly modify this network through introducing new regulatory nodes. For example, in the figure below (taken from the original paper), they have artificially put CRP under the control of CsgD. GFP is used as a reporter to measure the expression level of each artificial operon.
Using the same set-up, they have constructed 598 such artificial operons with different transcription and sigma factors. Following the construction of this library, they show that these re-wired operons are generally tolerated and some of them actually do better than the wild-type network in certain conditions.These observations suggest that the transcription network may be re-wired through evolution for higher adaptation without changes in the underlying genes. In other words, all the functions are already there in the cell, it's just the question of activation/deactivation at the right moment.
Although utterly simple in concept, this paper makes a very vivid point regarding the evolutionary strategies. For example, I'm trying to use this very concept to engineer an E. coli strain with a higher ethanol tolerance compared to wild-type.
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