title: Parasite Exposure Drives Selective Evolution of Constitutive versus Inducible Defense.
abstract: In the face of infectious disease, organisms evolved a range of defense mechanisms, with a clear distinction between those that are constitutive (always active) and those that are inducible (elicited by parasites). Both defense strategies have evolved from each other, but we lack an understanding of the conditions that favor one strategy over the other. While it is hard to generalize about their degree of protection, it is possible to make generalizations about their associated fitness costs, which are commonly detected. By definition, constitutive defenses are always "on," and are therefore associated with a fixed cost, independent of parasite exposure. Inducible defenses, on the other hand, may lack costs in the absence of parasites but become costly when defense is elicited through processes such as immunopathology. Bacteria can evolve constitutive defense against phage by modification/masking of surface receptors, which is often associated with reduced fitness in the absence of phage. Bacteria can also evolve inducible defense using the CRISPR-Cas (clustered regularly interspaced short palindromic repeat, CRISPR associated) immune system, which is typically elicited upon infection. CRISPR-Cas functions by integrating phage sequences into CRISPR loci on the host genome. Upon re-infection, CRISPR transcripts guide cleavage of phage genomes. In nature, both mechanisms are important. Using a general theoretical model and experimental evolution, we tease apart the mechanism that drives their evolution and show that infection risk determines the relative investment in the two arms of defense.
authors.affiliation: Environment and Sustainability Institute, Biosciences, University of Exeter, Penryn Campus, Penryn TR10 9FE, UK. Electronic address: westra.edze@gmail.com.
authors.forename: Edze R
authors.initials: ER
authors.lastname: Westra
authors.affiliation: Environment and Sustainability Institute, Biosciences, University of Exeter, Penryn Campus, Penryn TR10 9FE, UK.
authors.forename: Stineke
authors.initials: S
authors.lastname: van Houte
authors.affiliation: Environment and Sustainability Institute, Biosciences, University of Exeter, Penryn Campus, Penryn TR10 9FE, UK.
authors.forename: Sam
authors.initials: S
authors.lastname: Oyesiku-Blakemore
authors.affiliation: Environment and Sustainability Institute, Biosciences, University of Exeter, Penryn Campus, Penryn TR10 9FE, UK.
authors.forename: Ben
authors.initials: B
authors.lastname: Makin
authors.affiliation: Environment and Sustainability Institute, Biosciences, University of Exeter, Penryn Campus, Penryn TR10 9FE, UK.
authors.forename: Jenny M
authors.initials: JM
authors.lastname: Broniewski
authors.affiliation: School of Mathematics and Physics, University of Sheffield, Hicks Building, Sheffield S10 2TN, UK.
authors.forename: Alex
authors.initials: A
authors.lastname: Best
authors.affiliation: Departments of Molecular Genetics and Biochemistry, University of Toronto, 1 King's College Circle, Toronto, ON M5S 1A8, Canada.
authors.forename: Joseph
authors.initials: J
authors.lastname: Bondy-Denomy
authors.affiliation: Departments of Molecular Genetics and Biochemistry, University of Toronto, 1 King's College Circle, Toronto, ON M5S 1A8, Canada.
authors.forename: Alan
authors.initials: A
authors.lastname: Davidson
authors.affiliation: Biosciences, University of Exeter, Penryn Campus, Penryn TR10 9FE, UK.
authors.forename: Mike
authors.initials: M
authors.lastname: Boots
authors.affiliation: Environment and Sustainability Institute, Biosciences, University of Exeter, Penryn Campus, Penryn TR10 9FE, UK.
authors.forename: Angus
authors.initials: A
authors.lastname: Buckling
mesh_terms: D000818:Animals; D001419:Bacteria / Q000821:virology*; D001435:Bacteriophages / Q000235:genetics*; D064113:CRISPR-Cas Systems / Q000235:genetics* / Q000276:immunology; D064112:Clustered Regularly Interspaced Short Palindromic Repeats / Q000235:genetics* / Q000276:immunology; D003674:Defense Mechanisms; D019143:Evolution, Molecular; D016678:Genome; D054884:Host-Pathogen Interactions / Q000235:genetics; D010271:Parasites / Q000235:genetics / Q000276:immunology