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Rho-dependent transcriptional switches regulate the bacterial response to cold shock.

Mildred Delaleau1, Nara Figueroa-Bossi2, Thuy Duong Do3

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Bacterial Rho helicase controls gene expression during cold shock by terminating transcription. RNA structure changes at different temperatures regulate Rho helicase activity, impacting the cold-shock response (CSR).

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Area of Science:

  • Bacterial transcription regulation
  • Molecular mechanisms of cold-shock response
  • RNA thermosensing

Background:

  • Rho-dependent transcription termination (RDTT) is triggered by Rho helicase binding to nascent transcripts.
  • Cellular signals modulate mRNA structure and Rho utilization (Rut) sites, influencing RDTT.
  • The link between RDTT and bacterial temperature shifts was previously unexplored.

Purpose of the Study:

  • To investigate the role of Rho helicase in the bacterial cold-shock response (CSR).
  • To identify Rho utilization sites in CSR genes and their temperature-dependent regulation.
  • To elucidate how RNA restructuring directs Rho activity during temperature changes.

Main Methods:

  • Identification of Rut sites in 5'-untranslated regions of key CSR genes (cspA, cspB, cspG, nsrR-rnr-yjfHI).
  • Assessing RDTT efficiency at different temperatures (37°C vs. 15°C).
  • Evaluating the impact of RNA chaperone CspA concentration and mRNA leader nucleotide changes on RDTT.

Main Results:

  • Rho helicase is a key regulator in the bacterial CSR, challenging its purely posttranscriptional view.
  • Specific Rut sites in CSR genes trigger premature RDTT at 37°C but not at 15°C.
  • RNA restructuring, influenced by CspA and mRNA leader sequences, modulates RDTT efficiency.

Conclusions:

  • Rho-dependent transcription termination is a critical mechanism in the bacterial cold-shock response.
  • RNA thermosensors in mRNA leaders direct Rho helicase activity to control CSR gene expression.
  • This study establishes a new paradigm for RNA-mediated temperature sensing in bacteria.