Whole-genome resequencing of Escherichia coli K-12 MG1655 undergoing short-term laboratory evolution in lactate minimal media reveals flexible selection of adaptive mutations

Authors

Tom M. Conrad, University of California - San Diego
Andrew R. Royce, University of California - San Diego
M. Kenyon Applebee, University of California - San Diego
Christian L. Barrett, University of California - San Diego
Bin Xie, Virginia Commonwealth University
Yuan Gao, Virginia Commonwealth University
Bernhard Ø. Palsson

Document Type

Article

Original Publication Date

2009

Journal/Book/Conference Title

Genome Biology

Volume

10

DOI of Original Publication

10.1186/gb-2009-10-10-r118

Comments

Originally published at http://dx.doi.org/10.1186/gb-2009-10-10-r118

Date of Submission

August 2014

Abstract

Background

Short-term laboratory evolution of bacteria followed by genomic sequencing provides insight into the mechanism of adaptive evolution, such as the number of mutations needed for adaptation, genotype-phenotype relationships, and the reproducibility of adaptive outcomes.

Results

In the present study, we describe the genome sequencing of 11 endpoints of Escherichia coli that underwent 60-day laboratory adaptive evolution under growth rate selection pressure in lactate minimal media. Two to eight mutations were identified per endpoint. Generally, each endpoint acquired mutations to different genes. The most notable exception was an 82 base-pair deletion in the rph-pyrE operon that appeared in 7 of the 11 adapted strains. This mutation conferred an approximately 15% increase to the growth rate when experimentally introduced to the wild-type background and resulted in an approximately 30% increase to growth rate when introduced to a background already harboring two adaptive mutations. Additionally, most endpoints had a mutation in a regulatory gene (crp or relA, for example) or the RNA polymerase.

Conclusions

The 82 base-pair deletion found in the rph-pyrE operon of many endpoints may function to relieve a pyrimidine biosynthesis defect present in MG1655. In contrast, a variety of regulators acquire mutations in the different endpoints, suggesting flexibility in overcoming regulatory challenges in the adaptation.

Rights

© 2009 Conrad et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited

Is Part Of

VCU Computer Science Publications