Bacteriophage cooperation suppresses CRISPR-Cas3 and Cas9 immunity

Autor: Joseph Bondy-Denomy, Adair L. Borges, Beatriz A. Osuna, Blake Wiedenheft, MaryClare F. Rollins, Jenny Y. Zhang
Jazyk: angličtina
Rok vydání: 2018
Předmět:
anti-CRISPR
0301 basic medicine
viruses
Cell
host-pathogen interaction
Genome
Medical and Health Sciences
Bacteriophage
0302 clinical medicine
bacteriophage
CRISPR
Bacteriophages
skin and connective tissue diseases
Genetics
0303 health sciences
education.field_of_study
biology
CRISPR-Cas immunity
Biological Sciences
medicine.anatomical_structure
Infectious Diseases
Pseudomonas aeruginosa
Host-Pathogen Interactions
CRISPR-Cas9
Infection
musculoskeletal diseases
Evolution
Host–pathogen interaction
Population
cooperation
virus
General Biochemistry
Genetics and Molecular Biology

Virus
Article
Evolution
Molecular

Viral Proteins
03 medical and health sciences
Immune system
Immunity
medicine
education
030304 developmental biology
030306 microbiology
Cas9
Inflammatory and immune system
Molecular
biology.organism_classification
Virology
Emerging Infectious Diseases
030104 developmental biology
altruism
CRISPR-Cas Systems
030217 neurology & neurosurgery
Developmental Biology
Zdroj: Cell, vol 174, iss 4
Popis: SUMMARY>Bacteria utilize CRISPR-Cas adaptive immune systems for protection from bacteriophages (phages), and some phages produce anti-CRISPR (Acr) proteins that inhibit immune function. Despite thorough mechanistic and structural information for some Acr proteins, how they are deployed and utilized by a phage during infection is unknown. Here, we show that Acr production does not guarantee phage replication, but instead, infections fail when phage population numbers fall below a critical threshold. Failing infections can be rescued by related phages that act as Acr donors, demonstrating that infections succeed if a sufficient Acr dose is contributed to a single cell by multiple phage genomes. The production of Acr proteins by phage genomes that fail to replicate leave the cell immunosuppressed, which predisposes the cell for successful infection by other phages in the population. This “cooperative” phage mechanism for CRISPR-Cas inhibition demonstrates inter-virus cooperation that may also manifest in other host-parasite interactions.
Databáze: OpenAIRE