Bacterial Pathogenesis: Neisseria Meningitidis: Hit And

RESEARCH HIGHLIGHTS

BACTERIAL PATHOGENESIS Neisseria meningitidis: hit and run The pathogen Neisseria meningitidis solid medium and that this fraction used the known structure of PilE initially proliferates on the host cell increases when bacteria are grown to model the formation of type IV surface in tight aggregates known as microcolony in contact with host cells. When the pili bundles and showed that the microcolonies; infection ensues detachment is authors deleted the NM_0885 gene, phosphoglycerol on Ser93 would as individual bacteria detach from regulated by which encodes an orthologue of cause a negative charge to protrude the microcolony and disseminate post-translational known phosphoglycerol transferases, from the pilus, which would destabi- throughout the body. Now, Chamot- they found that the phosphoglycerol lize the bundle-forming interactions modification of Rooke et al. show that microcolony modification of PilE was lost. between pili. This destabilization was detachment is regulated by post- type IV pili with Interestingly, this gene (which the confirmed by transmission electron translational modification of phosphoglycerol authors renamed pptB, for pilin microscopy of pili from wild-type type IV pili with phosphoglycerol, phosphotransferase B) had been bacteria and ΔpptB bacteria. Thus, which destabilizes the pili bundles previously shown to be upregulated the increased production of PptB that hold the colonies together. in response to adhesion to host cells. during the initial stages of micro- The major component of Furthermore, the authors showed colony growth leads to an increase N. meningitidis type IV pili, PilE, that bacteria lacking pptB have a in the modification of Ser93 of PilE was previously known to be reduced ability to detach from an with phosphoglycerol, and this post-translationally modified infected monolayer and are deficient results in loss of bacterial aggrega- by phosphoglycerol, but in transmigrating across an epithelial tion. This mechanism may allow the role of this modifica- monolayer, a step that is known N. meningitidis to time its spread tion was unknown. Using to be important for invasive through the host. mass spectrometry and disease. These findings underline Joanna E. Huddleston two-dimensional gel the critical role of PptB in cell electrophoresis, the detachment. ORIGINAL RESEARCH PAPER Chamot-Rooke, J. authors found that a frac- How does modification at one et al. Post-translational modification of pili upon cell contact triggers N. meningitidis tion of PilE is modified at residue lead to such a drastic change dissemination. Science 331, 778–782 (2011). Ser93 in bacteria grown on in bacterial behaviour? The authors