期刊
MOLECULAR SYSTEMS BIOLOGY
卷 14, 期 9, 页码 -出版社
WILEY
DOI: 10.15252/msb.20178102
关键词
constrained evolution; epistasis; gene regulatory networks; regulatory mechanisms; synthetic circuits
资金
- Swiss National Science Foundation [PZ00P3-148235, 31003A_175608, 31003A_146137]
- ERC [739874]
- EpiphysX RTD grant from SystemsX.ch
- University Priority Research Program in Evolutionary Biology at the University of Zurich
- Wellcome Trust UK New Investigator Award [WT102944]
- Volkswagen Foundation
- Spanish Ministry of Economy, Industry and Competitiveness (MINECO) [BFU2010-16428]
- European Union's Horizon 2020 research and innovation program [670555]
- European Union Seventh Framework Program (FP7/2007-2013) [601062]
- Spanish Ministry of Economy, Industry and Competitiveness Centro de Excelencia Severo Ochoa 2013-2017 [SEV-2012-0208]
- Cerca Programme/Generalitat de Catalunya
- Swiss National Science Foundation (SNF) [31003A_175608, PZ00P3_148235] Funding Source: Swiss National Science Foundation (SNF)
- European Research Council (ERC) [670555, 739874] Funding Source: European Research Council (ERC)
Phenotypic variation is the raw material of adaptive Darwinian evolution. The phenotypic variation found in organismal development is biased towards certain phenotypes, but the molecular mechanisms behind such biases are still poorly understood. Gene regulatory networks have been proposed as one cause of constrained phenotypic variation. However, most pertinent evidence is theoretical rather than experimental. Here, we study evolutionary biases in two synthetic gene regulatory circuits expressed in Escherichia coli that produce a gene expression stripe-a pivotal pattern in embryonic development. The two parental circuits produce the same phenotype, but create it through different regulatory mechanisms. We show that mutations cause distinct novel phenotypes in the two networks and use a combination of experimental measurements, mathematical modelling and DNA sequencing to understand why mutations bring forth only some but not other novel gene expression phenotypes. Our results reveal that the regulatory mechanisms of networks restrict the possible phenotypic variation upon mutation. Consequently, seemingly equivalent networks can indeed be distinct in how they constrain the outcome of further evolution.
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