About this Research Topic
All living organisms requires protein homeostasis to survive and proliferate. As pathogens encounter environmental fluctuations during infection, they must maintain protein homeostasis in order to adapt to host environments. Pathogens regulate protein synthesis, post-translational modifications, protein folding, and protein degradations in host tissues. Host cells sequester essential metal ions from pathogens and promote oxidative stresses to kill pathogens. Furthermore, host cells attach ubiquitin to pathogens to promote pathogen cell death by autophagic pathways. Thus, hosts and pathogens interact and battle continuously to interfere with pathogen protein homeostasis during infections.
Legionella, for example, disrupts and inhibit host ubiquitination mechanisms to compromise host immune system. However, this is a poorly understood inhibition mechanism of the host's proteolytic pathway. This Research Topic will investigate how pathogens maintain protein homeostasis in response to host immune cells. Pathogens reduce protein synthesis in hostile environments, such as the host phagosome. pathogens also reduce protein folding and degradation in unfavored environments. However, it is unknown which factors regulate these activities in pathogens during infection. This Research Topic also aims to shed light on underlying mechanisms of host-pathogen interactions, such as protein synthesis, post-translational modification, protein folding and proteolysis, which are central survival mechanisms. It has been suggested that toxin and effector proteins control host cells during infections, however, it is poorly understood how these systems work.
This Topic therefore welcomes Original Research, Reviews and Perspectives on protein homeostasis in bacteria, virus, and fungal pathogens in the context of infection. Specifically, our research topic deals with protein degradation, protein synthesis, protein folding and post-translational modifications in pathogens and host cells, in particular:
- Protein degradation mechanisms by proteases in bacteria, virus and fungi
- The mechanisms of proteasome and autophagy during infections
- Post-translational modification mechanisms of pathogens and host cells during infections
- Ubiquitylation, deubiquitylation, sumolylation, acetylation, phosphorylation mechanisms in pathogens and host cells during infections
- Functions and modifications of pathogen’s effector and toxin proteins
Legionella, for example, disrupts and inhibit host ubiquitination mechanisms to compromise host immune system. However, this is a poorly understood inhibition mechanism of the host's proteolytic pathway. This Research Topic will investigate how pathogens maintain protein homeostasis in response to host immune cells. Pathogens reduce protein synthesis in hostile environments, such as the host phagosome. pathogens also reduce protein folding and degradation in unfavored environments. However, it is unknown which factors regulate these activities in pathogens during infection. This Research Topic also aims to shed light on underlying mechanisms of host-pathogen interactions, such as protein synthesis, post-translational modification, protein folding and proteolysis, which are central survival mechanisms. It has been suggested that toxin and effector proteins control host cells during infections, however, it is poorly understood how these systems work.
This Topic therefore welcomes Original Research, Reviews and Perspectives on protein homeostasis in bacteria, virus, and fungal pathogens in the context of infection. Specifically, our research topic deals with protein degradation, protein synthesis, protein folding and post-translational modifications in pathogens and host cells, in particular:
- Protein degradation mechanisms by proteases in bacteria, virus and fungi
- The mechanisms of proteasome and autophagy during infections
- Post-translational modification mechanisms of pathogens and host cells during infections
- Ubiquitylation, deubiquitylation, sumolylation, acetylation, phosphorylation mechanisms in pathogens and host cells during infections
- Functions and modifications of pathogen’s effector and toxin proteins
Keywords: Pathogens, Macrophage, Host immune cells, Protein degradation, Translation, Post-translational modifications, Protein folding, Gene expression, Effector
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
