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• W1963670229 startingPage "e1003972" @default.
• W1963670229 abstract "Molecular signaling networks are ubiquitous across life and likely evolved to allow organisms to sense and respond to environmental change in dynamic environments. Few examples exist regarding the dispensability of signaling networks, and it remains unclear whether they are an essential feature of a highly adapted biological system. Here, we show that signaling network function carries a fitness cost in yeast evolving in a constant environment. We performed whole-genome, whole-population Illumina sequencing on replicate evolution experiments and find the major theme of adaptive evolution in a constant environment is the disruption of signaling networks responsible for regulating the response to environmental perturbations. Over half of all identified mutations occurred in three major signaling networks that regulate growth control: glucose signaling, Ras/cAMP/PKA and HOG. This results in a loss of environmental sensitivity that is reproducible across experiments. However, adaptive clones show reduced viability under starvation conditions, demonstrating an evolutionary tradeoff. These mutations are beneficial in an environment with a constant and predictable nutrient supply, likely because they result in constitutive growth, but reduce fitness in an environment where nutrient supply is not constant. Our results are a clear example of the myopic nature of evolution: a loss of environmental sensitivity in a constant environment is adaptive in the short term, but maladaptive should the environment change." @default.
• W1963670229 created "2016-06-24" @default.
• W1963670229 creator A5016787543 @default.
• W1963670229 creator A5058333700 @default.
• W1963670229 date "2013-11-21" @default.
• W1963670229 modified "2023-10-13" @default.
• W1963670229 title "Whole Genome, Whole Population Sequencing Reveals That Loss of Signaling Networks Is the Major Adaptive Strategy in a Constant Environment" @default.
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• W1963670229 doi "https://doi.org/10.1371/journal.pgen.1003972" @default.
• W1963670229 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3836717" @default.
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• W1963670229 hasPublicationYear "2013" @default.
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