Premature transcription termination modulates stochastic gene expression in bacteria.

Abstract

Bacteria regulate transcription by controlling its initiation and prematurely terminating it through attenuation. Transcriptional regulation produces RNA bursts defined by size and frequency. While bursting via regulated initiation is well characterized, how attenuation shapes burst dynamics remains poorly understood. We show that in <i>Escherichia coli</i>, attenuation combined with regulated initiation in the tryptophan operon (<i>trp</i>) modulates burst size and frequency, producing switch-like transitions in transcriptional activity between the tryptophan presence and absence. In <i>Bacillus subtilis</i>, lacking regulated <i>trp</i> initiation, attenuation modulates burst size, gradually changing transcriptional activity as the tryptophan concentration increases. These distinct architectures may reflect adaptive strategies: <i>B. subtilis</i> maintains highly expressing cells over a wider tryptophan range, likely beneficial in soil where tryptophan is scarce and unevenly distributed, while <i>E. coli</i> enables rapid repression suited to fluctuating gut environments. Notably, <i>trp</i> transcription is not strictly cell-autonomous. Highly expressing cells can suppress transcription in neighboring cells, revealing intercellular regulation and supporting community-level cooperation.