Abstract

Clustered regularly interspaced short palindromic repeats (CRISPR)-Cas-mediated immunity in bacteria allows bacterial populations to protect themselves against pathogens. However, it also exposes them to the dangers of auto-immunity by developing protection that targets its own genome. Using a simple model of the coupled dynamics of phage and bacterial populations, we explore how acquisition rates affect the probability of the bacterial colony going extinct. We find that the optimal strategy depends on the initial population sizes of both viruses and bacteria. Additionally, certain combinations of acquisition and dynamical rates and initial population sizes guarantee protection, owing to a dynamical balance between the evolving population sizes, without relying on acquisition of viral spacers. Outside this regime, the high cost of auto-immunity limits the acquisition rate. We discuss these optimal strategies that minimize the probability of the colony going extinct in terms of recent experiments.This article is part of a discussion meeting issue ‘The ecology and evolution of prokaryotic CRISPR-Cas adaptive immune systems’.

Highlights

  • Organisms have developed a wide variety of strategies to deal with pathogens [1,2,3,4,5]

  • For a fixed small value of the spacer acquisition rate h 1⁄4 0:1 hÀ1 and fixed growth and degradation rates, we explore the probability of survival as a function of the initial phage exposure and the initial size of the susceptible bacterial population [52]

  • Our approach focuses on how regulating the spacer acquisition rate affects the survival probability of bacterial populations

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Summary

Introduction

Organisms have developed a wide variety of strategies to deal with pathogens [1,2,3,4,5] Bacteria use immunity both at the population level by adopting heterogenous phenotypes with different susceptibility to varying environments [6 –9], as well as specific solutions that target invading phage viruses [10,11,12]. These strategies involve restriction enzymes that render the viral genetic material unviable [10], and the CRISPR (clustered regularly interspaced short palindromic repeats) Cas (CRISPR-associated system of proteins) system [11,12], which allows bacterial lineages to develop memory about encountered pathogens and protect future generations. Acquired spacers in type I and II systems, which are the focus of this paper, are not uniformly sampled from the viral genomes but are chosen for excision by Cas

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