  Cell growth is determined by substrate availability and the cell's metabolic
capacity to assimilate substrates into building blocks. Metabolic genes that
determine growth rate may interact synergistically or antagonistically, and can
accelerate or slow growth, depending on the genetic background and
environmental conditions. We evolved a diverse set of Escherichia coli
single-gene deletion mutants with a spectrum of growth rates and identified
mutations that generally increase growth rate. Despite the metabolic
differences between parent strains, mutations that enhanced growth largely
mapped to the core transcription machinery, including the $\beta$ and $\beta'$
subunits of RNA polymerase (RNAP) and the transcription elongation factor,
NusA. The structural segments of RNAP that determine enhanced growth have been
previously implicated in antibiotic resistance and in the control of
transcription elongation and pausing. We further developed a computational
framework to characterize how the transcriptional changes that occur upon
acquisition of these mutations affect growth rate across strains. Our
experimental and computational results provide evidence for cases in which RNAP
mutations shift the competitive balance between active transcription and gene
silencing. This study demonstrates that mutations in specific regions of RNAP
are a convergent adaptive solution that can enhance the growth rate of cells
from distinct metabolic states.
