landerer.bib

@article{zanger2013,
author = {Zanger, UM and Schwab, M},
title = {Cytochrome P450 enzymes in drug metabolism: Regulation of gene expression, enzyme activities, and impact of genetic variation},
journal = {Pharmacology \& Therapeutics},
volume = {138},
pages = {103-141},
year = {2013},
}

@article{brown1997,
author = {Brown, L and Elliot, T},
title = {Mutations That Increase Expression of the rpoS Gene and Decrease Its Dependence on hfq Function in Salmonella typhimurium},
journal = {J. Bacteriol.},
volume = {179},
number = {3},
pages = {656-662},
year = {1997},
}

@article{allison2012,
author = {Allison, SD},
title = {A trait-based approach for modelling microbial litter decomposition},
journal = {Ecology Letters},
volume = {15},
pages = {1058-1070},
year = {2012},
}

@article{allison2017,
author = {Allison, SD and Goulden, ML},
title = {Consequences of drought tolerance traits for microbial decompositionin the DEMENT model},
journal = {Soil Biology \& Biochemistry},
volume = {107},
pages = {104-113},
year = {2017},
}

@article{Goldsmith2009,
abstract = {Phenotypic mutations (errors occurring during protein synthesis) are orders of magnitude more frequent than genetic mutations. Consequently, the sequences of individual protein molecules transcribed and translated from the same gene can differ. To test the effects of such mutations, we established a bacterial system in which an antibiotic resistance gene (TEM-1 $\beta$-lactamase) was transcribed by either a high-fidelity RNA polymerase or its error-prone mutant. This setup enabled the analysis of individual mRNA transcripts that were synthesized under normal or error-prone conditions. We found that an increase of ≈20-fold in the frequency of transcription errors promoted the evolution of higher TEM-1 expression levels and of more stable enzyme variants. The stabilized variants exhibited a distinct advantage under error-prone transcription, although under normal transcription they conferred resistance similar to wild-type TEM-1. They did so, primarily, by increasing TEM-1's tolerance to destabilizing deleterious mutations that arise from transcriptional errors. The stabilized TEM-1 variants also showed increased tolerance to genetic mutations. Thus, although phenotypic mutations are not individually subjected to inheritance and natural selection, as are genetic mutations, they collectively exert a direct and immediate effect on protein fitness. They may therefore play a role in shaping protein traits such as expression levels, stability, and tolerance to genetic mutations.},
archivePrefix = {arXiv},
arxivId = {arXiv:1408.1149},
author = {Goldsmith, Moshe and Tawfik, Dan S},
doi = {https://doi.org/10.1073/pnas.0809506106},
eprint = {arXiv:1408.1149},
file = {:home/clandere/paper/Goldsmith, Tawfik - Unknown - Potential role of phenotypic mutations in the evolution of protein expression and stability.pdf:pdf},
journal = {Proceedings of the National Academy of Sciences},
number = {15},
pages = {6197--6202},
title = {{Potential role of phenotypic mutations in the evolution of protein expression and stability}},
url = {www.pnas.orgcgidoi10.1073pnas.0809506106},
volume = {106},
year = {2009}
}