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Phage-induced change in the stability of mRNAs

Hiroyuki Ueno1, Tetsuro Yonesaki

  • 1Department of Biology, Graduate School of Science, Osaka University, 1-1 Machikaneyama-cho, Toyonaka-shi, Osaka 560-0043, Japan.

Virology
|October 13, 2004
PubMed

Insights

Bacteriophage T4 infection destabilizes stable Escherichia coli mRNA, while stabilizing its own mRNA. A phage-encoded factor, not host factors like RNases E/G, Hfq, or polyadenylation, drives this mRNA instability.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Bacterial mRNA stability is crucial for gene expression regulation.
  • Bacteriophage infection significantly alters host cell processes.
  • Host and phage mRNA stability mechanisms are complex and interdependent.

Purpose of the Study:

  • To investigate the impact of bacteriophage T4 infection on the stability of both host and phage mRNAs.
  • To identify the host and phage factors involved in regulating mRNA stability during infection.

Main Methods:

  • Analysis of mRNA stability in Escherichia coli post-infection with bacteriophage T4.
  • Investigating the roles of host RNases E and G, Hfq protein, and 3' end polyadenylation.
  • Utilizing rifampicin treatment and a Deltatk2 deletion mutant to probe phage-encoded factors.

Main Results:

  • Phage T4 infection drastically destabilized stable host mRNAs (lpp, ompA) but stabilized unstable T4 soc mRNA.
  • Host RNases E and G contributed to mRNA destabilization.
  • Known host destabilization factors (Hfq, polyadenylation) were ineffective post-infection.
  • Phage-encoded factors, not host factors, were responsible for host mRNA destabilization, as shown by rifampicin treatment and Deltatk2 mutant experiments.
  • Similar destabilization was observed with phages T2 and T7 infections.

Conclusions:

  • Bacteriophage infection induces a significant shift in mRNA stability within Escherichia coli.
  • A phage-encoded factor is the primary driver of host mRNA destabilization during infection.
  • These findings reveal a novel mechanism of host-phage interaction at the post-transcriptional level.

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