Abstract
Microbial populations founded by a single clone and propagated under resource limitation can become polymorphic. We sought to elucidate genetic mechanisms whereby a polymorphism evolved in Escherichia coli under glucose limitation and persisted because of cross-feeding among multiple adaptive clones. Apart from a 29 kb deletion in the dominant clone, no large-scale genomic changes distinguished evolved clones from their common ancestor. Using transcriptional profiling on co-evolved clones cultured separately under glucose-limitation we identified 180 genes significantly altered in expression relative to the common ancestor grown under similar conditions. Ninety of these were similarly expressed in all clones, and many of the genes affected (e.g., mglBAC, mglD, and lamB) are in operons coordinately regulated by CRP and/or rpoS. While the remaining significant expression differences were clone-specific, 93% were exhibited by the majority clone, many of which are controlled by global regulators, CRP and CpxR. When transcriptional profiling was performed on adaptive clones cultured together, many expression differences that distinguished the majority clone cultured in isolation were absent, suggesting that CpxR may be activated by overflow metabolites removed by cross-feeding strains in co-culture. Relative to their common ancestor, shared expression differences among adaptive clones were partly attributable to early-arising shared mutations in the trans-acting global regulator, rpoS, and the cis-acting regulator, mglO. Gene expression differences that distinguished clones may in part be explained by mutations in trans-acting regulators malT and glpK, and in cis-acting sequences of acs. In the founder, a cis-regulatory mutation in acs (acetyl CoA synthetase) and a structural mutation in glpR (glycerol-3-phosphate repressor) likely favored evolution of specialists that thrive on overflow metabolites. Later-arising mutations that led to specialization emphasize the importance of compensatory rather than gain-of-function mutations in this system. Taken together, these findings underscore the importance of regulatory change, founder genotype, and the biotic environment in the adaptive evolution of microbes.
Highlights
Evolutionary biologists have long sought to understand mechanistically how adaptive genetic variation arises and persists
When we adjusted d to reflect a natural break in the data, we found that a total of 91 genes from 64 transcription units significantly differ in steady state expression levels in at least one isolate at a false discovery rate of 0%
When we compared the consortium’s transcriptional profile to the 4-class Significance Analysis of Microarrays [111] (SAM) (Figure 5) we were surprised to find that many of the transcripts that distinguished CV103 from the other evolved clones in monoculture had expression patterns similar to CV101, CV115 and CV116, even though reconstruction experiments show that CV103 always emerges as the numerically dominant consortium member [14,15]. To ascertain whether this phenomenon was a general feature of the dataset, we looked at transcript levels across all samples for genes that were either (A) significant in the consortium analysis but not in the monoculture experiments, or (B) significant in the monoculture experiments but not in the consortium profile
Summary
Evolutionary biologists have long sought to understand mechanistically how adaptive genetic variation arises and persists. Long generation times, sexual recombination and practical limits on lab population size make higher eukaryotes imperfectly suited to study the tempo, trajectory and mechanisms by which evolution occurs in asexual species and in the somatic cells of sexual organisms. There, new genetic variation is limited by the rate of mutation supply and, in bacteria, by the incidence of horizontal gene transfer. Evolution in asexual species and cells can be studied using microbial models [7,8]. Microbial studies helped lead to two generalizations concerning the emergence and persistence of genetic variation in large, asexual populations. Over evolutionary time variation arising by mutation is subject to ‘‘periodic selection’’
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