Global Transcriptional Analysis of Virus-Host Interactions between Phage ϕ29 and Bacillus subtilis

J Virol. 2016 Sep 29;90(20):9293-304. doi: 10.1128/JVI.01245-16. Print 2016 Oct 15.


The study of phage-host relationships is essential to understanding the dynamic of microbial systems. Here, we analyze genome-wide interactions of Bacillus subtilis and its lytic phage ϕ29 during the early stage of infection. Simultaneous high-resolution analysis of virus and host transcriptomes by deep RNA sequencing allowed us to identify differentially expressed bacterial genes. Phage ϕ29 induces significant transcriptional changes in about 0.9% (38/4,242) and 1.8% (76/4,242) of the host protein-coding genes after 8 and 16 min of infection, respectively. Gene ontology enrichment analysis clustered upregulated genes into several functional categories, such as nucleic acid metabolism (including DNA replication) and protein metabolism (including translation). Surprisingly, most of the transcriptional repressed genes were involved in the utilization of specific carbon sources such as ribose and inositol, and many contained promoter binding-sites for the catabolite control protein A (CcpA). Another interesting finding is the presence of previously uncharacterized antisense transcripts complementary to the well-known phage ϕ29 messenger RNAs that adds an additional layer to the viral transcriptome complexity.

Importance: The specific virus-host interactions that allow phages to redirect cellular machineries and energy resources to support the viral progeny production are poorly understood. This study provides, for the first time, an insight into the genome-wide transcriptional response of the Gram-positive model Bacillus subtilis to phage ϕ29 infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bacillus Phages / genetics*
  • Bacillus subtilis / virology*
  • DNA Replication / genetics
  • Genes, Bacterial / genetics
  • Host-Pathogen Interactions / genetics*
  • Promoter Regions, Genetic / genetics
  • Transcription, Genetic / genetics*
  • Up-Regulation / genetics
  • Virus Replication / genetics

Grant support

This study was also supported by an institutional grant from Fundación Ramón Areces to the Centro de Biología Molecular Severo Ochoa. The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.