How ubiquitination and autophagy participate in the regulation of the cell response to bacterial infection

Bacterial infection relies on the micro-organism's ability to orchestrate the host's cell signalling such that the immune response is not activated. Conversely, the host cell has dedicated signalling pathways for coping with intrusions by pathogens. The autophagy of foreign micro-organisms (known as xenophagy) has emerged as one of the most powerful of these pathways, although the triggering mode remains largely unknown. In the present paper, we discuss the role that certain post-translational modifications (primarily ubiquitination) may play in the activation of xenophagy and how some bacteria have evolved mechanisms to subvert or hijack this process. In particular, we address the role played by P62/SQSTM1 (sequestosome 1). Finally, we discuss how autophagy can be subverted to eliminate bacteria-induced danger signals.