Abstract
CRISPR-Cas is an adaptive prokaryotic immune system that prevents phage infection. By incorporating phage-derived ‘spacer’ sequences into CRISPR loci on the host genome, future infections from the same phage genotype can be recognized and the phage genome cleaved. However, the phage can escape CRISPR degradation by mutating the sequence targeted by the spacer, allowing them to re-infect previously CRISPR-immune hosts, and theoretically leading to coevolution. Previous studies have shown that phage can persist over long periods in populations of Streptococcus thermophilus that can acquire CRISPR-Cas immunity, but it has remained less clear whether this coexistence was owing to coevolution, and if so, what type of coevolutionary dynamics were involved. In this study, we performed highly replicated serial transfer experiments over 30 days with S. thermophilus and a lytic phage. Using a combination of phenotypic and genotypic data, we show that CRISPR-mediated resistance and phage infectivity coevolved over time following an arms race dynamic, and that asymmetry between phage infectivity and host resistance within this system eventually causes phage extinction. This work provides further insight into the way CRISPR-Cas systems shape the population and coevolutionary dynamics of bacteria–phage interactions.This article is part of a discussion meeting issue ‘The ecology and evolution of prokaryotic CRISPR-Cas adaptive immune systems’.
Highlights
Clustered regularly interspaced short palindromic repeats and their associated cas genes (CRISPR-Cas) form an adaptive immune system that is found in approximately 50% of all bacteria and 90% of archaea [1]
We examined the type of coevolutionary dynamics during this period, with a clear distinction between fluctuating selection dynamics (FSD), where the rare host and pathogen genotypes are favoured through negative frequency-dependent selection, and arms race dynamics (ARD), where host resistance and phage infectivity increase over time [21]
This mechanism of host resistance and pathogen infectivity suggests a possible scenario for coevolution, where bacteria acquire spacers over time and phage accumulate escape mutations
Summary
Clustered regularly interspaced short palindromic repeats and their associated cas genes (CRISPR-Cas) form an adaptive immune system that is found in approximately 50% of all bacteria and 90% of archaea [1]. CRISPR-Cas confers immunity to phage infection by incorporating phage-derived sequences into CRISPR loci on the host genome. These loci consist of repeating sequences (repeats) that are interspaced by sequences (spacers) derived from phage and other mobile genetic elements of typically around 30 nt in length. RNA transcripts of CRISPR loci are processed and form a ribonucleoprotein complex with Cas proteins that can recognize and cleave complementary nucleic acid sequences, preventing future infections by the same phage genotype.
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Schedule a callMore From: Philosophical transactions of the Royal Society of London. Series B, Biological sciences
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