Abstract
SummaryBacteria commonly exist in high cell density populations, making them prone to viral predation and horizontal gene transfer (HGT) through transformation and conjugation. To combat these invaders, bacteria possess an arsenal of defenses, such as CRISPR-Cas adaptive immunity. Many bacterial populations coordinate their behavior as cell density increases, using quorum sensing (QS) signaling. In this study, we demonstrate that QS regulation results in increased expression of the type I-E, I-F, and III-A CRISPR-Cas systems in Serratia cells in high-density populations. Strains unable to communicate via QS were less effective at defending against invaders targeted by any of the three CRISPR-Cas systems. Additionally, the acquisition of immunity by the type I-E and I-F systems was impaired in the absence of QS signaling. We propose that bacteria can use chemical communication to modulate the balance between community-level defense requirements in high cell density populations and host fitness costs of basal CRISPR-Cas activity.
Highlights
In nature, bacteria persist in myriad environments, from sparse populations to localized communities of high cell density, including cell chains, microcolonies, and biofilms (Hall-Stoodley et al, 2004)
Since bacterial defensive requirements are predicted to change relative to population density (Abedon, 2012), we hypothesized that CRISPR-Cas immunity could be integrated into the host quorum sensing (QS) circuit, allowing increased defense at higher cell densities
Quorum sensing in Gram-negative bacteria typically utilizes LuxI family proteins to generate N-acyl homoserine lactone (AHL) signals, which are sensed by LuxR-type transcriptional regulators (Miller and Bassler, 2001)
Summary
Bacteria persist in myriad environments, from sparse populations to localized communities of high cell density, including cell chains, microcolonies, and biofilms (Hall-Stoodley et al, 2004). These bacterial populations can provide collective advantages, but a trade-off may be an increased susceptibility to bacteriophage (phage) infection (Abedon, 2012) and invasion by mobile genetic elements (Babic et al, 2011; Fuqua and Winans, 1994; Pinedo and Smets, 2005). Since bacterial defensive requirements are predicted to change relative to population density (Abedon, 2012), we hypothesized that CRISPR-Cas immunity could be integrated into the host QS circuit, allowing increased defense at higher cell densities
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