Cleavage of viral DNA by restriction endonucleases stimulates the type II CRISPR-Cas immune response

Copyright © 2022 Elsevier Inc. All rights reserved..

Prokaryotic organisms have developed multiple defense systems against phages; however, little is known about whether and how these interact with each other. Here, we studied the connection between two of the most prominent prokaryotic immune systems: restriction-modification and CRISPR. While both systems employ enzymes that cleave a specific DNA sequence of the invader, CRISPR nucleases are programmed with phage-derived spacer sequences, which are integrated into the CRISPR locus upon infection. We found that restriction endonucleases provide a short-term defense, which is rapidly overcome through methylation of the phage genome. In a small fraction of the cells, however, restriction results in the acquisition of spacer sequences from the cleavage site, which mediates a robust type II-A CRISPR-Cas immune response against the methylated phage. This mechanism is reminiscent of eukaryotic immunity in which the innate response offers a first temporary line of defense and also activates a second and more robust adaptive response.

Errataetall:

CommentIn: Trends Microbiol. 2022 Jun;30(6):513-514. - PMID 35469710

Medienart:

E-Artikel

Erscheinungsjahr:

2022

Erschienen:

2022

Enthalten in:

Zur Gesamtaufnahme - volume:82

Enthalten in:

Molecular cell - 82(2022), 5 vom: 03. März, Seite 907-919.e7

Sprache:

Englisch

Beteiligte Personen:

Maguin, Pascal [VerfasserIn]
Varble, Andrew [VerfasserIn]
Modell, Joshua W [VerfasserIn]
Marraffini, Luciano A [VerfasserIn]

Links:

Volltext

Themen:

Bacteriophage
CRISPR
Cas9
DNA, Viral
DNA Restriction Enzymes
EC 3.1.-
EC 3.1.21.-
Endonucleases
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Restriction-modification
Spacer acquisition
Staphylococcus

Anmerkungen:

Date Completed 02.05.2022

Date Revised 04.03.2023

published: Print-Electronic

CommentIn: Trends Microbiol. 2022 Jun;30(6):513-514. - PMID 35469710

Citation Status MEDLINE

doi:

10.1016/j.molcel.2022.01.012

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM336666950