Interaction of host and Staphylococcus aureus protease-system regulates virulence and pathogenicity.

Staphylococcus aureus causes various health care- and community-associated infections as well as certain chronic TH2 driven inflammatory diseases. It is a potent pathogen with serious virulence and associated high morbidity. Severe pathogenicity is accredited to the S. aureus secreted virulence factors such as proteases and host protease modulators. These virulence factors promote adhesion and invasion of bacteria through damage of tight junction barrier and keratinocytes. They inhibit activation and transmigration of various immune cells such as neutrophils (and neutrophil proteases) to evade opsono-phagocytosis and intracellular bacterial killing. Additionally, they protect the bacteria from extracellular killing by disrupting integrity of extracellular matrix. Platelet activation and agglutination is also impaired by these factors. They also block the classical as well as alternative pathways of complement activation and assist in spread of infection through blood and tissue. As these factors are exquisite factors of S. aureus mediated disease development, we have focused on review of diversification of various protease-system associated virulence factors, their structural building, diverse role in disease development and available therapeutic counter measures. This review summarises the role of protease-associated virulence factors during invasion and progression of disease.

Detection and Quantification of Protein Aggregates in Plants.

Protein quality control is an important aspect of stress recovery. It maintains protein homeostasis through a machinery of regulatory proteins such as chaperones and proteases. When the system recognizes accumulation of misfolded or aggregated proteins, the cell recruits a set of regulatory proteins to initiate protein quality control. To understand the dynamics of stress-mediated aggregate protein formation and recovery in plants, robust methods aimed at detecting and measuring such protein aggregates are needed. This will help us to deepen our understanding of protein quality control mechanisms in plants.

Robust transcriptional indicators of immune cell death revealed by spatiotemporal transcriptome analyses.

Recognition of a pathogen by the plant immune system often triggers a form of regulated cell death traditionally known as the hypersensitive response (HR). This type of cell death occurs precisely at the site of pathogen recognition, and it is restricted to a few cells. Extensive research has shed light on how plant immune receptors are mechanistically activated. However, two central key questions remain largely unresolved: how does cell death zonation take place, and what are the mechanisms that underpin this phenomenon? Consequently, bona fide transcriptional indicators of HR are lacking, which prevents deeper insight into its mechanisms before cell death becomes macroscopic and precludes early or live observation. In this study, to identify the transcriptional indicators of HR we used the paradigmatic Arabidopsis thaliana-Pseudomonas syringae pathosystem and performed a spatiotemporally resolved gene expression analysis that compared infected cells that will undergo HR upon pathogen recognition with bystander cells that will stay alive and activate immunity. Our data revealed unique and time-dependent differences in the repertoire of differentially expressed genes, expression profiles, and biological processes derived from tissue undergoing HR and that of its surroundings. Furthermore, we generated a pipeline based on concatenated pairwise comparisons between time, zone, and treatment that enabled us to define 13 robust transcriptional HR markers. Among these genes, the promoter of an uncharacterized AAA-ATPase was used to obtain a fluorescent reporter transgenic line that displays a strong spatiotemporally resolved signal specifically in cells that will later undergo pathogen-triggered cell death. This valuable set of genes can be used to define cells that are destined to die upon infection with HR-triggering bacteria, opening new avenues for specific and/or high-throughput techniques to study HR processes at a single-cell level.