Regulation of Host-Pathogen Interactions via the Ubiquitin System

Ubiquitination is a posttranslational modification that regulates a multitude of cellular functions. Pathogens, such as bacteria and viruses, have evolved sophisticated mechanisms that evade or counteract ubiquitin-dependent host responses, or even exploit the ubiquitin system to their own advantage. This is largely done by numerous pathogen virulence factors that encode E3 ligases and deubiquitinases, which are often used as weapons in pathogen-host cell interactions. Moreover, upon pathogen attack, host cellular signaling networks undergo major ubiquitin-dependent changes to protect the host cell, including coordination of innate immunity, remodeling of cellular organelles, reorganization of the cytoskeleton, and reprogramming of metabolic pathways to restrict growth of the pathogen. Here we provide mechanistic insights into ubiquitin regulation of host-pathogen interactions and how it affects bacterial and viral pathogenesis and the organization and response of the host cell.

Automated summary

Ubiquitination is an important posttranslational modification that regulates cellular functions. Pathogens have evolved mechanisms to evade or counteract host responses regulated by ubiquitin, and even exploit the ubiquitin system for their own benefit. Host cellular signaling networks undergo significant changes upon pathogen attack to protect the cell and limit pathogen growth. Mechanistic insights into ubiquitin regulation of host-pathogen interactions provide valuable information on bacterial and viral pathogenesis and host cell organization and response.