TY - JOUR
T1 - Centrality in the host-pathogen interactome is associated with pathogen fitness during infection
AU - Crua Asensio, Núria
AU - Munõz Giner, Elisabet
AU - De Groot, Natalia Sánchez
AU - Torrent Burgas, Marc
PY - 2017/1/16
Y1 - 2017/1/16
N2 - © 2017 The Author(s). To perform their functions proteins must interact with each other, but how these interactions influence bacterial infection remains elusive. Here we demonstrate that connectivity in the host-pathogen interactome is directly related to pathogen fitness during infection. Using Y. pestis as a model organism, we show that the centrality-lethality rule holds for pathogen fitness during infection but only when the host-pathogen interactome is considered. Our results suggest that the importance of pathogen proteins during infection is directly related to their number of interactions with the host. We also show that pathogen proteins causing an extensive rewiring of the host interactome have a higher impact in pathogen fitness during infection. Hence, we conclude that hubs in the host-pathogen interactome should be explored as promising targets for antimicrobial drug design.
AB - © 2017 The Author(s). To perform their functions proteins must interact with each other, but how these interactions influence bacterial infection remains elusive. Here we demonstrate that connectivity in the host-pathogen interactome is directly related to pathogen fitness during infection. Using Y. pestis as a model organism, we show that the centrality-lethality rule holds for pathogen fitness during infection but only when the host-pathogen interactome is considered. Our results suggest that the importance of pathogen proteins during infection is directly related to their number of interactions with the host. We also show that pathogen proteins causing an extensive rewiring of the host interactome have a higher impact in pathogen fitness during infection. Hence, we conclude that hubs in the host-pathogen interactome should be explored as promising targets for antimicrobial drug design.
U2 - 10.1038/ncomms14092
DO - 10.1038/ncomms14092
M3 - Article
SN - 2041-1723
VL - 8
JO - Nature Communications
JF - Nature Communications
M1 - 14092
ER -