The evolution of a counter-defense mechanism in a virus constrains its host range
Name
elife-79549-v2.pdf
Description
Published version
Size
2.21 MB
Format
Adobe PDF
Checksum (MD5)
c8a10d80d1af52f673f531b5943abf57
Author(s)
Srikant, Sriram
Guegler, Chantal K
Laub, Michael T
Date Issued
2022
Journal
eLife
Publisher
eLife Sciences Publications, Ltd
Citation
Srikant, Sriram, Guegler, Chantal K and Laub, Michael T. 2022. "The evolution of a counter-defense mechanism in a virus constrains its host range." eLife, 11.
Version
Final published version
Abstract
Bacteria use diverse immunity mechanisms to defend themselves against their viral predators, bacteriophages. In turn, phages can acquire counter-defense systems, but it remains unclear how such mechanisms arise and what factors constrain viral evolution. Here, we experimentally evolved T4 phage to overcome a phage-defensive toxin-antitoxin system, toxIN, in Escherichia coli. Through recombination, T4 rapidly acquires segmental amplifications of a previously uncharacterized gene, now named tifA, encoding an inhibitor of the toxin, ToxN. These amplifications subsequently drive large deletions elsewhere in T4’s genome to maintain a genome size compatible with capsid packaging. The deleted regions include accessory genes that help T4 overcome defense systems in alternative hosts. Thus, our results reveal a trade-off in viral evolution; the emergence of one counter-defense mechanism can lead to loss of other such mechanisms, thereby constraining host range. We propose that the accessory genomes of viruses reflect the integrated evolutionary history of the hosts they infected.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Howard Hughes Medical Institute
Terms of Use
Creative Commons Attribution 4.0 International license
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.7554/ELIFE.79549
