Studies on assembly of the bacteriophage SPP1 viral particle aim to dissect the molecular mechanisms engaged to build an infectious >30 MDa machine of homogeneous size and shape. We investigate individual reactions that lead to formation of the viral icosahedral nucleocapsid and of the long non-contractile tail that are built in independent assembly pathways.
Studies on the SPP1 nucleocapsid focus on:
– assembly of the viral procapsid with a specialized portal vertex,
– specific viral DNA packaging into the procapsid by a nanomotor assembled at the portal and
– reversible closure of the portal system.
The assembly and structure of this DNA container is conserved among viruses of the tailed phages-herpesviruses lineage.
Research on the SPP1 tail aims to understand:
– formation of its adsorption apparatus to the cell,
– construction of the helical tail tube initiated at the adsorption apparatus, and
– termination of assembly by binding of tail completion proteins
The resulting tail structure that delivers viral DNA to the host cell cytoplasm is evolutionarily related to the bacterial type VI secretion system device.
The basic knowledge produced in this research provides a rational framework for engineering viral particles and for the design of approaches to disrupt virus assembly.
Bacteriophage Infection of Gram-Positive Bacteria
Viral lytic infection disrupts host cell homeostasis. It leads to remodelling of the cell space and to hijacking of numerous cell functions to support highly efficient virus multiplication. We study the effects of bacteriophage infection on the cell biology of B. subtilis.
We aim to provide a dynamic view of the spatio-temporal re-organization of the bacterial cytoplasm space throughout the complete phage infection program. This cytological analysis is correlated with the synergistic action of host and viral effectors that are engaged at different steps of virus multiplication. Study of those effectors requires identification of host cell machineries hijacked by the virus and investigation of the mechanisms how they are diverted from their cellular function. Our research has a major focus on the essential steps of viral DNA transactions and assembly of phage infectious particles.
Phage infection is usually studied in exponentially growing bacteria, an infrequent situation in their natural ecosystems. This is well illustrated by the soil bacterium B subtilis. Its entry in stationary phase upon nutrient starvation triggers a complex decision program leading to different cellular states. We study phage infection throughout the complete B subtilis life cycle to investigate the window of opportunity for infection and the factors that either block, modulate or promote phage multiplication.