In this section
@article{Chee:2023:10.1016/j.cell.2023.07.001,
author = {Chee, MSJ and Serrano, E and Chiang, YN and Harling-Lee, J and Man, R and Bacigalupe, R and Fitzgerald, JR and Penadés, JR and Chen, J},
doi = {10.1016/j.cell.2023.07.001},
journal = {Cell},
pages = {3414--3426.e16},
title = {Dual pathogenicity island transfer by piggybacking lateral transduction},
url = {http://dx.doi.org/10.1016/j.cell.2023.07.001},
volume = {186},
year = {2023}
}
TY - JOUR
AB - Lateral transduction (LT) is the process by which temperate phages mobilize large sections of bacterial genomes. Despite its importance, LT has only been observed during prophage induction. Here, we report that superantigen-carrying staphylococcal pathogenicity islands (SaPIs) employ a related but more versatile and complex mechanism of gene transfer to drive chromosomal hypermobility while self-transferring with additional virulence genes from the host. We found that after phage infection or prophage induction, activated SaPIs form concatamers in the bacterial chromosome by switching between parallel genomic tracks in replication bubbles. This dynamic life cycle enables SaPIbov1 to piggyback its LT of staphylococcal pathogenicity island vSaα, which encodes an array of genes involved in host-pathogen interactions, allowing both islands to be mobilized intact and transferred in a single infective particle. Our findings highlight previously unknown roles of pathogenicity islands in bacterial virulence and show that their evolutionary impact extends beyond the genes they carry.
AU - Chee,MSJ
AU - Serrano,E
AU - Chiang,YN
AU - Harling-Lee,J
AU - Man,R
AU - Bacigalupe,R
AU - Fitzgerald,JR
AU - Penadés,JR
AU - Chen,J
DO - 10.1016/j.cell.2023.07.001
EP - 3426
PY - 2023///
SN - 0092-8674
SP - 3414
TI - Dual pathogenicity island transfer by piggybacking lateral transduction
T2 - Cell
UR - http://dx.doi.org/10.1016/j.cell.2023.07.001
UR - https://www.ncbi.nlm.nih.gov/pubmed/37541198
UR - https://doi.org/10.1016/j.cell.2023.07.001
VL - 186
ER -