Anti-phage islands force their target phage to directly mediate island excision and spread

Abstract

Mobile genetic elements called PLEs protect Vibrio cholerae from infection with phage ICP1 by unclear mechanisms. Here, McKitterick and Seed show that a PLE-encoded large serine recombinase exploits an ICP1 protein as a recombination directionality factor to excise this PLE in response to phage infection.