DMS3-42: the Secret to CRISPR-Dependent Biofilm Inhibition in Pseudomonas aeruginosa

Abstract

Clustered, regularly interspaced short palindromic repeats (CRISPR) are a topic of intense interest in microbiology. Described en masse for sequenced prokaryotic genomes in 2000 and 2002 (7, 11), a functional role for CRISPR in Streptococcus thermophilus phage defense was reported in 2007 (2). That study and subsequent studies of S. thermophilus, Staphylococcus epidermidis, and Escherichia coli contribute to the commonly reported model of CRISPR as a prokaryotic immune system (1, 6, 10). In a collection of three reports (4, 5, 13), the O'Toole group has sought to vet this model in Pseudomonas aeruginosa by studying infections with the temperate phage DMS3. Instead of conclusive evidence supporting a role for P. aeruginosa CRISPR in phage defense, the work has nicely shown that CRISPR modulate group behaviors—biofilm formation and swarming motility—in DMS3 lysogens. In this issue of the Journal of Bacteriology, Cady and O'Toole (4) present a tour de force analysis of the host and phage requirements for CRISPR-dependent biofilm inhibition and in the process raise a number of intriguing questions about the role of CRISPR in P. aeruginosa.