Abstract
Transcription is fundamentally noisy, leading to significant heterogeneity across bacterial populations. Noise is often attributed to burstiness, but the underlying mechanisms and their dependence on the mode of promotor regulation remain unclear. Here, we measure E. coli single cell mRNA levels for two stress responses that depend on bacterial sigma factors with different mode of transcription initiation (σ70 and σ54). By fitting a stochastic model to the observed mRNA distributions, we show that the transition from low to high expression of the σ70-controlled stress response is regulated via the burst size, while that of the σ54-controlled stress response is regulated via the burst frequency. Therefore, transcription initiation involving σ54 differs from other bacterial systems, and yields bursting kinetics characteristic of eukaryotic systems.
Highlights
Transcription is fundamentally noisy, leading to significant heterogeneity across bacterial populations
Specificity factors comprise two distinct classes: the σ70 family combines all sigma factors that bind to −10/−35 promoter elements and in E. coli includes σ70, σ19, σ24, σ28, σ32 and σ38; in contrast, σ54 binds to −12/−24 promoter elements and forms a class of its own
Open complex formation on σ54-dependent promoters strictly requires the action of cognate transcription factors, activators termed bacterial Enhancer Binding proteins, for the promoter DNA opening event[13,15,16,17,18,19] (Fig. 1)
Summary
Transcription is fundamentally noisy, leading to significant heterogeneity across bacterial populations. We measure E. coli single cell mRNA levels for two stress responses that depend on bacterial sigma factors with different mode of transcription initiation (σ70 and σ54). Noise underpins bacterial bet hedging whereby genetically identical cells display population-wide divergent phenotypes[8,9,10,11]. One major aspect of transcription initiation in bacteria is the need for a specificity factor termed sigma (σ) to direct RNA polymerase to the promoter[1,2,13]. Understanding noise and bursting during σ54-dependent gene expression will enable determination of how heterogeneously these stress-related phenotypes are established across a cell population and where noise and bursting arises within the transcription time series. One response manages stress arising from exposure to oxidants[28] and iron starvation[29], the other manages membrane stress[23,27]
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