Escherichia coli phage-inducible chromosomal island aids helper phage replication and represses the LEE pathogenicity island.

In this study, we identify and characterize a novel phage-inducible chromosomal island found in commensal Escherichia coli MP1. This novel element, EcCIMP1, is induced and mobilized by the temperate helper phage vB_EcoP_Kapi1. EcCIMP1 contributes to superinfection immunity against its helper phage, impacting bacterial competition outcomes.

Complete genome sequence of MP1.

Here, we report the complete genome sequence of strain MP1, consisting of one circular chromosome and one circular plasmid. Long-read assembly was performed using a consensus approach, followed by long- and short-read polishing, and gene annotation.

Bacterial envelope stress responses: Essential adaptors and attractive targets.

Millions of deaths a year across the globe are linked to antimicrobial resistant infections. The need to develop new treatments and repurpose of existing antibiotics grows more pressing as the growing antimicrobial resistance pandemic advances. In this review article, we propose that envelope stress responses, the signaling pathways bacteria use to recognize and adapt to damage to the most vulnerable outer compartments of the microbial cell, are attractive targets.

Isolation and Characterization of a Novel Temperate Escherichia coli Bacteriophage, Kapi1, Which Modifies the O-Antigen and Contributes to the Competitiveness of Its Host during Colonization of the Murine Gastrointestinal Tract.

In this study, we describe the isolation and characterization of novel bacteriophage vB_EcoP_Kapi1 (Kapi1) isolated from a strain of commensal Escherichia coli inhabiting the gastrointestinal tract of healthy mice. We show that Kapi1 is a temperate phage integrated into tRNA of strain MP1 and describe its genome annotation and structure. Kapi1 shows limited homology to other characterized prophages but is most similar to the seroconverting phages of Shigella flexneri and clusters taxonomically with P22-like phages.