Type I CRISPR-Cas systems are the most abundant and widespread adaptive immune systems of bacteria and can greatly enhance bacterial survival in the face of temperate phage infection. However, it is less clear how these systems protect against virulent phages. Here we experimentally show that type I CRISPR immunity of Pectobacterium atrosepticum leads to rapid suppression of two unrelated virulent phages, ΦTE and ΦM1. However, unlike the case where bacteria are infected with temperate phages, this is the result of an abortive infection-like phenotype, where infected cells do not survive the infection but instead become metabolically inactive and lose their membrane integrity. Our findings challenge the view of CRISPR-Cas as a system that protects the individual cell and supports growing evidence of an Abi-like function for some types of CRISPR-Cas systems.

CRISPR-Cas systems provide bacteria and archaea with adaptive, heritable immunity against their viruses (bacteriophages and phages) and other parasitic genetic elements. CRISPR-Cas systems are highly diverse, and we are only beginning to understand their relative importance in phage defense. In this review, we will discuss when and why CRISPR-Cas immunity against phages evolves, and how this, in turn, selects for the evolution of immune evasion by phages. Finally, we will discuss our current understanding of if, and when, we observe coevolution between CRISPR-Cas systems and phages, and how this may be influenced by the mechanism of CRISPR-Cas immunity.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Bacteria are under immense evolutionary pressure from their viral invaders—bacteriophages. Bacteria have evolved numerous immune mechanisms, both innate and adaptive, to cope with this pressure. The discovery and exploitation of CRISPR–Cas systems have stimulated a resurgence in the identification and characterization of anti-phage mechanisms. Bacteriophages use an extensive battery of counter-defence strategies to co-exist in the presence of these diverse phage defence mechanisms. Understanding the dynamics of the interactions between these microorganisms has implications for phage-based therapies, microbial ecology and evolution, and the development of new biotechnological tools. Here we review the spectrum of anti-phage systems and highlight their evasion by bacteriophages.

Type I CRISPR-Cas systems are abundant and widespread adaptive immune systems in bacteria and can greatly enhance bacterial survival in the face of phage infection. Upon phage infection, some CRISPR-Cas immune responses result in bacterial dormancy or slowed growth, which suggests the outcomes for infected cells may vary between systems. Here we demonstrate that type I CRISPR immunity of Pectobacterium atrosepticum leads to suppression of two unrelated virulent phages, ɸTE and ɸM1. Immunity results in an abortive infection response, where infected cells do not survive, but viral propagation is severely decreased, resulting in population protection due to the reduced phage epidemic. Our findings challenge the view of CRISPR-Cas as a system that protects the individual cell and supports growing evidence of abortive infection by some types of CRISPR-Cas systems.