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Although the key promoter elements necessary to drive transcription inEscherichia coli have long been understood, we still cannot predict thebehavior of arbitrary novel promoters, hampering our ability to characterizethe myriad of sequenced regulatory architectures as well as to design novelsynthetic circuits. This work builds upon a beautiful recent experiment byUrtecho et al. who measured the gene expression of over 10,000 promotersspanning all possible combinations of a small set of regulatory elements. Usingthis data, we demonstrate that a central claim in energy matrix models of geneexpression - that each promoter element contributes independently andadditively to gene expression - contradicts experimental measurements. Wepropose that a key missing ingredient from such models is the avidity betweenthe -35 and -10 RNA polymerase binding sites and develop what we call a refinedenergy matrix model that incorporates this effect. We show that this therefined energy matrix model can characterize the full suite of gene expressiondata and explore several applications of this framework, namely, howmultivalent binding at the -35 and -10 sites can buffer RNAP kinetics againstmutations and how promoters that bind overly tightly to RNA polymerase caninhibit gene expression. The success of our approach suggests that avidityrepresents a key physical principle governing the interaction of RNA polymeraseto its promoter.

How the Avidity of Polymerase Binding to the -35/-10 Promoter Sites Affects Gene Expression